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Consultant: Advances in Primary Care Medicine: Clinical Update - December 2008

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Nephrology **************************************** ( Clinical Practice Guidelines) ( Publications, Protocols, algorithms). ( Renal Protection--Pre & Post PCI) (CIN) *** (CME; NKF) (RTA--Types/ TX) (Calciphylaxis) (Calciphylaxis; with, normal -- Renal & PT function) (Overnight Dialysis; in ESRD) ( Hematuria--Tx Guidelines) (CI--Nephropathy) (ASA + Dipyradimole/ HD graft patency) (Nocturnal HD) (ATN VS. AIN) (Ferumoxytol; CKD) ( Renal Transplant/ I-S Meds) ( RTA) ( Drug-induced Nephrotoxicity)  ; ( Kidney Stones) (Teriparatide; Indications) Nephrogenic Systemic Fibrosis May Occur Years after Gadolinium Exposure. Denosumab Combo Curbs- Hyperparathyroidism in Dialysis Patients.; Iron Salt Reduces Use of Erythropoiesis-Stimulating Agent in Dialysis Patients (Decreasing the incidence of CIN)**************** (AS-RAD; Stent placement vs. Medical TX) (CKD; Hyperkalemia) (CIN; Cr & Cystatin C) (Cystatin C) (Urinary Incontinence/ Women) (BPH—TX) (Kidney Transplantation). (Algorithm for routine HCV infection surveillance in Outpatient HD units). (Diagnostic Tests for Refractory HTN—RAS) ( BPH/ When to Tx) ( Hematuria--Tx Guidelines) ( Urge Incontinence--Tolterodine/ Pelvic Exercise) ( ACR) ( U. Incontinence) ( Ac. Urinary Retention) (Kidney Failure) (CKD)--Slide - show (DM—Microvascular complications)--SS (GFR; UACR)

Renal artery stenosis (CMV prophylaxis in Transplants) (Measures of Kidney Function) (ACEI; Hyperkalemia) (NaHCO3 to prevent contrast nephropathy) (Gadolinium associated NSF)  (CKD; Intervention..) (Exercising with ESMD) (Nephrotic Syndrome)

Chronic kidney disease - identification, evaluation and management of patients (SWL) (Darifenacin; OAB) (CKD; Carotid endarterectomy) (RD: Creatinine, U/A, Renal US, GFR, Proteinuria) (Nutrition Def correction) (DASH diet; HTN, Kidney stones) (Fe therapy) (Proteinuria) (Telmisartan/ HCTZ)—CKD 2010&UID=42445 (Anemia & CKD)

Level of renal function at which to initiate dialysis.;  

Mode of dialysis at initiation.;  

Other criteria for starting dialysis. (To prevent contrast induced kidney injury) (RTA) ***** (CKD) (Mortality prediction in patients with ESRD)*******


IDENTIFICATION, DIAGNOSIS, AND MANAGEMENT OF CHRONIC KIDNEY DISEASE AND SECONDARY HYPERPARATHYROIDISM (KDOQI Guidelines) (EP: Stroke, HTN, Thrombosisi) (The Geriatric Nutrition Index) (Radiological evaluation of RV - HTN) (SE of gadolinium based contrast) (CI meds in Dialysis pts) (P, Cal, PTH---Mortality in CKD) (RAS--Revascularization vs. medical TX) (CPPS/ CP)--Men--Pelvic Pain (Correction of Fe deficiency in CKD)--ferumoxytol (TIBC, Trasferrin) (CKD: Proteinuria, GFR, Creatinine) (CKD; CRP) (Referrals for CKD) (PTX, &,Cal supplementation--CKD) (AKI/ Pneumonia) (Insulin before & after HD) ( U. Cath) ( PSA, Rectal US, Uroflowmetry--for BPH) ( Erectile Dysfunction),4047,550166,00.html ( ED) of overactive bladder in primary care practice (OAB) ( Advances in management of OAB) ( Drug Dosing/ CKD) (Nephropathy/ meds) (UT symptoms/ BPH) (NS);jama_304_4_452?node_id=amacme_course;jama304_4_452 (S. syndrome)

Polycythaemia/erythrocytosis (CKD/ PrimaryCare) (MRI/ Contrast agents) (Diuretics in HF) (Leg Cramps)

LUTS in men, age-related (prostatism) (Kidney Failure) (Restricted Cl TX—Prevents AKI) (DRI + ARB—early CKD) (Sevelamer/ P) (RI/ RFs) (Na & K excretion--Risks and benefits). (UT) (UTI) (Microscopic hematuria) (UI/ Botox) (Slow gait/ CKD) (HUS) (Robotic Surgery/ Urologic) (Embolization/ BPH) (Predictors of bad outcome in Ac. Pancreatitis) (Diuretic/ SEs). (Microscopic hematuria in adults/ prone for ESRD). (Podocyturia/ mid-gestation/ PET). (7-9 % Hgb A1C---DM--on Dialysis). (Interdialytic period/ mortality) (Urology/ Implanted cardiac devices) (CKD/ MetS) (BP changes in HD) (Kidney stones) (OAB/ Mirabegron) (IC) (Allopurinol) (Vit D/ production and activation) (Triamterene Kidney stones).,1 (Ureteral calculi -- in a middle aged woman). (CKD/ Fibrates) (Blood work in HD). (CKD--Ezetimbe/ Statins) (Cystatin C) (Kidney transplantation) (LVEDP/ IVFs/ Contrast-time) (CKD Progression/ FGF-23) (DKD/ Elderly). (Prevention of contrast AKI) (Solabegron/ OAB) (Finasteride) (“/ Dipstick test for proteinuria) ************ (OAB/ Topical OB gel) (OAB+ pyuria and negative Ur. CX; ABXs for 6 m) (OAB/ Pelvic exercises). (OAB/ fesoterodine). (ESRD--Triple markers) (Papaverine/ Renal colic). (RF/ Hep C--TX) (Avoid contrast nephropathy) (Nephrolithiasis) (Avanafil/ ED) (BPH; LUTS) (Hypercalciuria);archinte_170_21_1900?node_id=amacme_course;archinte170_21_1900 (AKI/ US);jama_305_6_592?node_id=amacme_course;jama305_6_592 (Kidney Transplantation) ( Triple RAAS blockade to slow progression of Kidney Disease)     ; ( IVF--Nacl/ to prevent contrast nephropathy) ( SRL/ MMF--Renal Transplant) ( DM & CKD--Meds) ( DM +/ - CKD)--Lipid Tx ( PTH, Cal, P) ( Steroid-Free regimen/ Renal Transplant Patients) ( Screening for CKD) ( Drug-Dosing Guidelines)*** ( SE of Erytropoietin...)  ( Anemia Management in CKD)*** ( PD--Decreasing...) (Erythropoietin Therapy: Putting Pt in Perspective) ( Cinacalcet) ( Darbepoeitin alfa) ( Management of Renal stones) *** ( Oral Activated Vit Dfor high PTH/ CKD--III, IV Stages) ( Meds to improve Kidney Transplant)*** ( Labs in Kidney Diseases) *** **************** ( Acid- Base Disorders/ RTA/ Related Chapters)  ( Renal Function) ***

Managing Anemia in Chronic Kidney Disease

CKD - A Rationale for Early Intervention Nephrogenic Systemic Fibrosis May Occur Years after Gadolinium Exposure. Denosumab Combo Curbs- Hyperparathyroidism in Dialysis Patients.; Iron Salt Reduces Use of Erythropoiesis-Stimulating Agent in

Protocol for the Prevention and Management of Renal Osteodystrophy ... ( HCV--Interferon Tx--in HD Pts) ( IV Contrast-Related ARF); ( Types of Contrasts)*** ( gadolinium) ( ARF--Definition, Types) ***  ( ARF management) ***  ( Nephrolithiasis) ***

ACE inhibitor and angiotensin II antagonist combination treatment.

Blood urea sampling methods.

Dialysis membranes.

Dose of haemodialysis.

Duration and frequency of haemodialysis therapy.

Idiopathic membranous nephropathy: use of other therapies.

Lipid lowering therapy in patients with chronic kidney disease.

Membranous nephropathy: role of cyclosporine therapy.

Metabolic acidosis and growth in children.

Treatment of secondary membranous nephropathy.

Water quality for haemodialysis. ---Anemia;    Cal/ P/ PTH, CO2 levels in CKD ******

...the awareness of the people that anemia should be treated earlier because normally anemia starts when the chronic kidney disease,

the renal function is approximately at the level of 30, 40 mL/minute renal creatinine clearance......   ( CERA vs. ESA...)              

Slide 25: ESA TherapySlide 26: What Are the Disadvantages of the Existing Products?  *********( Initiation of Dialysis...)  ( QOL)  ( DM+ HTN)

25% of CABG Patients Have CKD

The authors explain that of the more than 500,000 patients who undergo CABG each year in the United States, certain subgroups — women, the elderly, or obese patients — derive less benefit. Patients with CKD have higher in-hospital complication rates as well as other problems, such as anemia, altered mineral metabolism, etc, and comorbidities such as diabetes, which might affect their postsurgery benefits. Understanding potential postoperative quality-of-life benefits is very important for patients with CKD who are contemplating CABG, but information was lacking for this subgroup, the authors write. They aimed to shed light on this topic by examining changes in physical function and mental health scores over a 6-month period in a cohort of patients with varying degrees of CKD who underwent CABG. ( Hyperparathyroidism)


(A very interesting study published in 2004, by Rix and colleagues, randomized a small group of patients to placebo treatment or alfacalcidol, which is 1-alpha-hydroxy D3. They had about a 30% to 40% suppression of PTH over an 18-month period. Bone mineral density of the femur went up significantly at 12 and 18 months, somewhere around 3% to 4%, which really is quite high in that short period of time. This might be a way for us to actually increase BMD, which could benefit patients with stage 4 disease because once GFRs drop below 35, we do not use bisphosphonates. We might be able to address the problem of bone loss with alfacalcidol).

SlideEfficacy end points for paricalcitol vs placebo treatment



1. The current annual growth rate of dialysis patients is:
Answer: 6% to 8%
One of the factors contributing to the worldwide epidemic of chronic kidney disease (CKD) is the dialysis population, which has been growing at 6% to 8% per year.
2. The best overall measurement of kidney function is the creatinine level.
Answer: False
Glomerular filtration rate (GFR) is the best overall measure of kidney function; creatinine is less accurate. Measuring the GFR allows the severity, not just the absolute presence or absence of kidney disease, to be monitored as CKD progresses.
3. Which of the following can predict mortality in dialysis patients?
Answer: All of the above
A study of 500 dialysis patients followed for 36 months found that high PTH, low phosphate, and low calcium led to improved survival; patients with low PTH, high phosphate, and high calcium had the worst survival. When data from this study were entered into a multivariate model, dialysis duration emerged as an important confounder. Slightly different risks were associated with dialysis durations of less than 6 months, 6 to 18 months, or more than 18 months.
4. In the untreated state, parathyroid glands can enlarge and undergo genotypic change as a consequence of CKD.
Answer: True
In the untreated state, parathyroid glands can become much enlarged and undergo a genotypic change, progressing from diffuse proliferation to nodular hyperplasia.
5. Vitamin D levels begin to decrease in CKD patients in early stage 2 disease.
Answer: True
Vitamin D levels begin to decline in early stage 2 CKD. Most patients will have vitamin D levels near the lower-normal limit before they progress to stage 3 disease. This decline contributes to the development of hyperparathyroidism in some patients in late stage 2 disease.
6. How often should PTH be measured in patients with stage 3 CKD?
Answer: Every 12 months
The National Kidney Foundation Kidney Disease Outcomes Quality Initiative (KDOQI) recommends measurement of PTH every 12 months in patients with stage 3 CKD, every 3 months in patients with stage 4 disease, and every 3 months in patients with stage 5 CKD or patients undergoing dialysis.
7. The new treatment paradigm for treating patients with CKD includes all of the following except:
Answer: Using vitamin D sparingly to avoid calcium and phosphorus elevations
The new treatment paradigm, from the KDOQI guidelines, calls for monitoring PTH on a regular basis in proportion to the stage of a patient's CKD. The new treatment paradigm also recognizes that active vitamin D is crucial to maintain and re-establish bone health and cardiovascular health. Therefore, vitamin D analogs can be used at higher doses with minimal effects on calcium and phosphorus metabolism.
8. The KDOQI guidelines indicate that a glomerular filtration rate (GFR) of around __ mg/dL is the point at which phosphorus begins to rise.
Answer: 60
The phosphorus begins to rise when the GFR is around 60 mg/dL, much earlier than had been previously thought.
9. The new treatment paradigm for treating patients with CKD includes all of the following except:
Answer: Using vitamin D sparingly to avoid calcium and phosphorus elevations
The new treatment paradigm, from the KDOQI guidelines, calls for monitoring PTH on a regular basis in proportion to the stage of a patient’s CKD. The new treatment paradigm also recognizes that active vitamin D is crucial to maintain and re-establish bone health and cardiovascular health. Therefore, vitamin D analogs can be used at higher doses with minimal effects on calcium and phosphorus metabolism.
10. Newer vitamin D analogs have improved safety profiles compared with the first generation of these agents.
Answer: True
A comparison of the first-generation vitamin D analog calcitriol with second-generation (alfacalcidol, doxercalciferol) and third-generation (paricalcitol) agents reveals that overall PTH levels were suppressed 25% with calcitriol, 28% with alfacalcidol, 46% with doxercalciferol, and 42% with paricalcitol. A 30% or greater reduction in PTH levels was seen in 74% of doxercalciferol-treated patients compared with 91% of paricalcitol-treated patients. Finally, increases in urinary calcium were very high in calcitriol-treated patients (128%) compared with 41% and 42% at 6 months in alfacalcidol- and doxercalciferol-treated patients and 6% in paricalcitol-treated patients.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________  ----Topics  1)to 6)

1) The recommended starting dosage for rHuEpo is between 50 and100 U/kg TIW in adults and 50U/kg TIW in pediatric patients on dialysis.  The dose should be reduced as the hemoglobin level approaches 12g/dL or increases by more than 1g/dL in any two-week period. The dosage must be individualized to maintain hemoglobin within the suggested target range. The most common side effects are minor pain and irritation at the injection site (Abu-Alfa 2003, 31-38).

Darbepoetin is a newer erythropoietin protein product that has a longer serum half-life than rHuEpo, and hence requires less frequent dosing (Egrie 2001, 3-13). While administration route and safety profile are similar, Darbepoetin is usually given no more often than once per week, reducing the burden of therapy on the patient. Starting dose is 0.45 mcg/kg

Hemoglobin is typically measured weekly during the initial phase of treatment for CKD-associated anemia and until the target hemoglobin level (11-12 mg/dL) has been reached. Therefore, biweekly or monthly monitoring is usually sufficient (Abu-Alfa 2003, 31-38).

The initial workup for nephrotic syndrome in adults should focus on ruling out all likely systemic disorders that may be the cause for the proteinuria. This should be done prior to performing a renal biopsy or referring the patient to a nephrologist (Obrador 1999, 1793-1800). Therefore, all patients should have their blood glucose tested to rule out diabetes mellitus (Madaio 2001, 25-34). A careful family history and history of drug use or toxin exposure should be taken. Chest radiographs, colonoscopy, and in female patients mammography should be performed as appropriate to look for evidence of solid adenocarcinomas. In patients over 50 years of age, urine protein electrophoresis should be strongly considered to exclude amyloidosis or myeloma (Madaio 2001, 25-34; Orth 1998, 1202-1211). Antinuclear antibodies are important to consider in patients for whom systemic lupus erythematosus is a possibility (Balow 2003, 386-391). Infectious causes (especially HIV, Hepatitis B, and Hepatitis C) should be considered and tested for in patients at risk (di Belgiojoso 2002 469-479; Jefferson 2003, 400-405). If after a thorough examination, there is no evidence of a systemic disorder that may be causing the proteinuria, the patient should then be referred to a nephrologist (Adu 1996, 12-14; Kassirer 1983, 561-575; Stiles 2000, 419-433; Parker 2004, 708-716).

While hypertension can be responsible for mild proteinuria, it is typically NOT a cause of nephrotic-range proteinuria (Douglas 2003, S74-S76; Agodoa 2001, 2719-2728).

On average, HbA1c varies by approximately 1% for every 30 mg/dL change in mean blood glucose (Unger 1998, 975; ADA 2003, S5-S20; ADA 2003, S33-S50).

Overt diabetic nephropathy, defined as chronic proteinuria in association with hypertension and reduced glomerular filtration rate, ultimately develops in 30%-40% of patients with either type 1 or type 2 diabetes (Strippoli 2003, 487-499; Ritz 1999, 1127-1133). Microalbuminuria (urinary albumin excretion rate of 30-300 mg/24h) represents the first clinical evidence of diabetic nephropathy. Moreover, the presence of microalbuminuria is an independent predictor of future cardiovascular morbidity and mortality in patients with type 2 diabetes (Neil 1993, 996-1003; O'Keefe 1999, 171-180). More than half of diabetic patients with microalbuminuria will eventually go on to develop macroalbuminuria and ESRD (ADA 2003, S5-S20). Therefore, the American Diabetes Association recommends assessing patients for microalbuminuria at the time of diagnosis of type 2 diabetes mellitus and annually thereafter (ADA 2003, S33-S50).


The National Kidney Foundation (NKF) recently published the Kidney Disease Outcome Quality Initiative (K/DOQI) guidelines for the evaluation and management of CKD (National Kidney Foundation 2002, S1-S266). The NKF K/DOQI guidelines specifically address the workup of anemia in CKD patients. These guidelines recommend that all patients with stage 3 or 4 CKD (ie, patients with GFR <60 mL/min/1.73m2) be evaluated for anemia

The National Kidney Foundation (NKF) recently published the Kidney Disease Outcome Quality Initiative (K/DOQI) guidelines for the evaluation and management of CKD (National Kidney Foundation 2002, S1-S266). The NKF K/DOQI guidelines recommend a hemoglobin target of 11-12 mg/dL (hematocrit levels between 33%-36%) in patients with CKD.

Iron deficiency is the most common reason for resistance to erythropoietin therapy. Upon initiation of erythropoietin therapy, the patient's iron demands increase with improved erythropoiesis. Therefore, many patients will require iron supplementation in order to maintain adequate responsiveness to erythropoietin and achieve target hemoglobin levels. These patients need to have iron indices (eg, transferrin saturation, serum ferritin) followed regularly to guide iron administration (Abu-Alfa 2003, 31-38). While both oral and intravenous iron preparations are available, intravenous administration of iron is more effective at increasing hemoglobin levels and decreasing the needed dose of erythropoietin in this population (Macdougall 1996, 1694-1699; Macdougall 1999, S40-S46).


2) Based upon these data, National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (K/DOQI) Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease (CKD) recommend that the serum levels of phosphorus should be maintained between 3.5 and 5.5 mg/dL in patients with stage 5 CKD. [K/DOQI Guidelines].  (Table 1) The serum levels of corrected total calcium should be maintained within the “normal” range for the laboratory used, preferably toward the lower end (8.4 to 9.5 mg/dL), calcium-phosphorus product < 55 mg2/dL2 and  the target range of plasma iPTH is 150-300 pg/mL These targets are  best achieved by controlling serum levels of phosphorus within the target range.

The levels of serum calcium and phosphorus, and plasma iPTH should be measured in all patients with CKD stages 3, 4 and 5 (GFR < 60 mL/min/1.73 m2). [K/DOQI Guidelines]. The minimum recommended frequency of these measurements is based upon the stage of CKD; among individuals undergoing maintenance dialysis therapy (stage 5), it is recommended that serum calcium and phosphorus levels should be monitored at least once a month, and plasma iPTH levels should be monitored every 3 months. (Table 2) These measurements should be made more frequently if the patient is receiving concomitant therapy for abnormalities in the serum levels of calcium, phosphorus or PTH.

Control of serum phosphorus (see below) and treatment with vitamin D or its analogs (such as calcitriol, alfacalcidol, paricalcitol, or doxercalciferol) and/or calcimimetics (viz., cinacalcet) form the cornerstones for the management of secondary hyperparathyroidism. The target range for plasma iPTH levels is between 150 and 300 pg/ml and it is recommended that treatment with vitamin D or its analogs should begin when the plasma iPTH levels are > 300 pg/mL [K/DOQI Guidelines]. Calcimimetic agents like cinacalcet are also appropriate for use in patients with elevated plasma iPTH levels, either in combination with vitamin D or as monotherapy. [Block 2004][Lindberg 2005]

In patients with elevated serum phosphorus, the following interventions are recommended: 1) dietary counseling and restrict dietary phosphate; 2) start or increase phosphate binder therapy; and 3) increase dialysis frequency. [K/DOQI Guidelines]

Dietary restriction of phosphorus (800 to 1,000 mg/day) should begin in all patients with chronic kidney disease and either elevated serum phosphorus or plasma iPTH levels [K/DOQI Guidelines]. Even among patients that are able to adhere to this level of dietary phosphorus restriction, dialysis regimens, as practiced today, are unable to prevent phosphorus accumulation. Thus, most patients with stage 5 CKD require phosphate binder therapy. 

Increasing the frequency of hemodialysis treatment has the potential to enhance phosphorus clearance, and is an appropriate option for patients undergoing maintenance hemodialysis who have persistent hyperphosphatemia (serum P > 5.5 mg/dL). [K/DOQI Guidelines][Raj 1999][Mucsi 1998] However, this approach has limited usefulness since, at this time, it is not consistently reimbursed and may have limited patient acceptance. Thus, increasing the frequency of hemodialysis treatment is often reserved for cases in which escalating phosphate-binder dose cannot control serum P levels or is not tolerated.

Thus, in a patient who develops an increase in serum calcium levels (the threshold used by the K/DOQI guidelines: serum Ca > 10.2 mg/dL) or whose plasma iPTH levels are < 150 pg/mL on two consecutive measurements, it is prudent to avoid calcium-based phosphate binders. [K/DOQI Guidelines]. Because serum calcium levels remained above recommended levels (Ca >10.2 mg/dL) on consecutive measurements, a trial of a non-calcium containing phosphate binder is indicated in this case. Furthermore, the recent K/DOQI guidelines have recommended limiting the amount of elemental calcium obtained through phosphate binders, to < 1500 mg/day.

The use of calcium-based phosphate binders, particularly calcium carbonate, is associated with a high incidence of hypercalcemia and may contribute to the progression of vascular calcification in patients with end-stage renal disease. [Chertow 2002][Goodman 2000][Guerin 2000]. On the other hand, substituting calcium-based phosphate binders with sevelamer hydrochloride (HCl) has been associated with lower serum bicarbonate, and in some cases, metabolic acidosis. [Gallieni 2000][Marco 2002][Qunibi 2004].  Recently, another non-calcium, non-aluminum based phosphate binder has been approved by the Food and Drug Administration for the management of hyperphosphatemia in patients with stage 5 CKD – lanthanum carbonate. [Hutchison 2005][Al-Baaj 2005][Finn 2004][Hutchison 2004]. This phosphate binder may also be appropriate to use under conditions described in this case.

Given the long-term toxicity known to result from aluminum accumulation (dementia, osteomalacia, proximal myopathy and microcytic anemia), aluminum-based phosphate binders are only recommended as short-term “rescue” therapy (= 4 weeks) in patients with serum phosphorus levels > 7.0 mg/dL. [K/DOQI Guidelines].

In patients with ESRD, calcification occurs in numerous vascular beds; with the availability of electron-beam computed tomography, coronary artery calcification is the most widely studied. Several recent studies have indicated a high prevalence and severity of coronary artery calcification among ESRD patients even among individuals < 30 years of age. [Goodman 2002]. Epidemiologic studies indicate that the severity of vascular calcification is related to the serum levels of calcium, [Kimura 1999][Oh 2002][Raggi 2002][Nitta 2003]  phosphorus, [Raggi 2002] and PTH level, [Kimura 1999][Oh 2002][Shigematsu 2003] as well as the use of calcium-based phosphate binders. [Goodman 2000][Guerin 2000.

Clinically, vascular calcification can be manifested in a range of adverse cardiovascular correlates. In a cross-sectional analysis of 205 maintenance hemodialysis patients, EBCT-determined coronary artery calcium scores were directly related to the history of previous myocardial infarction (P<0.0001) and angina (P<0.0001), and the aortic calcium scores were directly related to the prevalence of claudication (P = 0.001) and aortic aneurysm (P = 0.02). [Raggi 2002].

Bone pains, fractures and hypercalcemia can occur in both high- and low-turnover bone diseases. With increasing severity of renal disease, there is a progressive decrease in bone mineral density. Furthermore, patients with ESRD have a significant increase in the risk for fractures, including of the hip, when compared to the general population. [Stehman-Breen 2000][Coco 2000] Age, dialysis vintage, female gender, and diabetes mellitus appear to confer an increased risk for fracture. On the other hand, renal osteodystrophy is typically not associated with enthesopathy.

According to the K/DOQI Guidelines, levels of iPTH as determined by immunoradiometric assay (IRMA) or immunochemiluminometric assay (ICMA) are an adequate screening tool to separate high-turnover bone disease (osteitis fibrosa) from low-turnover bone disorders (adynamic bone disorder). [K/DOQI Guidelines]. However, in patients with plasma iPTH levels between 100 and 500 pg/ml, plasma iPTH has limited discriminating power in diagnosing low- and high-turnover bone disease. [Qi 1995] [K/DOQI Guidelines]. A definitive diagnosis of the nature of bone disease can be made only by the use of bone biopsy, particularly when the plasma iPTH is in the intermediate range. However, the lack of local resources to properly procure, process, and reliably interpret the bone biopsy, and reimbursement difficulties undermine the routine use of this diagnostic procedure. Thus, in most circumstances, clinicians depend upon indirect methods, rather than bone biopsy, to diagnose the type of bone disease associated with CKD. A similar position has been adopted by the K/DOQI Working Group. [K/DOQI Guidelines].

Similarly, bone radiographs are not indicated for the assessment of bone disease of CKD. Bone mineral density (BMD) evaluation, measured by dual energy X-ray absorptiometry (DEXA), should be reserved for patients with fractures and in those with known risk factors for osteoporosis.

In general, parathyroidectomy is recommended for the management of patients with severe secondary hyperparathyroidism (persistent serum iPTH > 800 pg/mL), associated with hypercalcemia and/or hyperphosphatemia that are refractory to medical therapy. [K/DOQI Guidelines]. Calcimimetics like cinacalcet have recently become available. Treatment with cinacalcet lowers plasma parathyroid levels; this is associated with a decrease in serum calcium and phosphorus levels [Block2004][Lindberg 2005]. A trial of treatment with cinacalcet is probably appropriate in any patient being referred for parathyroidectomy.

Persistent iPTH > 800 pg/mL with refractory hypercalcemia and/or hyperphosphatemia   

Effective surgical therapy of severe hyperparathyroidism can be accomplished by subtotal parathyroidectomy, or total parathyroidectomy with parathyroid tissue autotransplantation. Imaging of parathyroid glands with 99Tc-Sestamibi scan, ultrasound, CT scan, or MRI should be done prior to re-exploration parathyroid surgery.


3) Levin and colleagues reported that there is a 30% increase in risk of LVH for every 0.5-g/dL drop in hemoglobin (odds ratio [OR], 1.32 for each 0.5-g/dL decrease; P=0.004) even in patients with early renal insufficiency [Levin 1999].

There is a great variability in the doses of EPO needed to achieve the target hemoglobin in patients with CKD. Because the final dose of EPO cannot be predicted, therapy can be initiated with the average dose needed to achieve the target hemoglobin in 4 to 8 weeks. The route of administration will determine the amount of initial and final doses. According to K/DOQI guidelines, the initial dose for SC therapy should be 80 U/kg/wk to 120 U/kg/wk (typically 6000 U/wk). For IV therapy, doses should be 120 U/kg/wk to 180 U/kg/wk (typically 9000 U/wk) in 2 to 3 doses per week. [K/DOQI Guidelines, 2001].

The EPO dose needed to achieve target hemoglobin levels is about 33% lower when administered SC compared with IV administration (range, 0% to 68%) [K/DOQI Guidelines. 2001]. In a meta-analyses of 27 prospective studies with a total of 916 patients, the dose of EPO required to reach target levels was an average of 48 U/kg/wk lower when administered SC compared with IV administration [Besarab 2002]. For this reason, the K/DOQI and EPBG recommend SC administration over the IV route.

The dose-response range to EPO is wide and cannot be predicted in patients with ESRD. For this reason, it is important to monitor the response by frequently measuring hemoglobin and hematocrit. Using the initial doses recommended by the Anemia Work Group of K/DOQI will result in an average increase in hemoglobin levels of 0.3 g/dL/wk [K/DOQI, 2001].  Hemoglobin and hematocrit should be monitored every 1 to 2 weeks to adjust the dose if necessary. 

Because absolute or functional iron deficiency is common and supplemental iron is critical for successful EPO therapy in maintenance dialysis patients, routine monitoring of iron stores and the availability of iron is an important component in managing patients with ESRD. The Anemia Work Group of the K/DOQI recommends that when initiating or dose escalating EPO, percent TSAT and serum ferritin be checked monthly in patients not receiving IV iron, and at least once every 3 months in patients receiving IV iron until target hemoglobin and hematocrit are achieved [K/DOQI Guidelines. 2001]. Once the target hemoglobin and hematocrit are achieved, TSAT and serum ferritin should be evaluated at least once every 3 months.

Adequate iron stores are important to ensure a sustained response to EPO therapy. The threshold for diagnosing absolute iron deficiency (ie, serum ferritin <100 ng/mL and TSAT <20%) differs from that in the general population. Iron supplementation is the therapeutic intervention of choice in patients with absolute iron deficiency [K/DOQI Guidelines, 2001; EBPG 1999]. For this reason, iron supplementation should be the initial pharmacologic intervention for this patient.

There are at least 3 different formulations of parenteral iron available in the United States—iron dextran (Infed®, Dexferrum®), ferric sodium gluconate (Ferrlicit®), and iron sucrose (Venofer®). Each of the formulations is effective in treating iron deficiency. Because iron dextran is associated with rare but fatal anaphylactoid reactions, ferric sodium gluconate and iron sucrose have supplanted iron dextran as the agents of choice for treating iron deficiency in maintenance dialysis patients. Patients with absolute iron deficiency typically require 1000 mg of elemental iron over 8 to 10 hemodialysis sessions.

Uncorrected or partially corrected uremia that occurs in patients receiving inadequate solute clearances also can negatively affect EPO therapy. Although rare, aluminum overload can interfere with iron metabolism and reduce the efficacy of EPO. In addition, deficiencies in vitamin B12, folic acid, and potentially vitamin C can reduce the efficacy of EPO treatment.

Uncorrected or partially corrected uremia that occurs in patients receiving inadequate solute clearances also can negatively affect EPO therapy. Although rare, aluminum overload can interfere with iron metabolism and reduce the efficacy of EPO. In addition, deficiencies in vitamin B12, folic acid, and potentially vitamin C can reduce the efficacy of EPO treatment.

Data suggest that hemoglobin levels should be maintained at levels >11 g/L. Anemia increases cardiovascular morbidity and mortality and may increase the risk of mortality. Data show mortality increases with every decrease in hemoglobin <12 g/dL. EPO deficiency is the major cause of anemia in patients with chronic kidney disease. Whether absolute or functional, iron deficiency is the most important cause of hyporesponsiveness to EPO therapy. Inflammation, infection, hyperparathyroidism, and carnitine deficiency also can contribute to hyporesponsiveness to EPO therapy. In functional iron deficiency, percent TSAT may decrease to levels consistent with iron deficiency despite a normal or elevated serum ferritin.



Numerous studies have documented the progressive increase in risk associated with a decrease in GFR. The preponderance of evidence suggests that the increase in cardiovascular risk is apparent at a GFR level <70 mL/min, which often is equivalent to a serum creatinine >1.4 mg/dL [Keane, 2001; Go, 2004; Anavekar, 2004].

Similarly, recent evidence suggests there is increased cardiovascular risk associated with albuminuria even when the urine albumin excretion rate is not high enough for the patient to be diagnosed with microalbuminuria [Gerstein, 2001]. A patient with any urine albumin therefore has a greater cardiovascular risk when compared with an individual with no urinary albumin excretion.

The preponderance of evidence suggests that best clinical outcomes are achieved by maintaining serum phosphorous between 3.5 mg/dL and 5.5 mg/dL, which is supported by the K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease (Table 1).

Studies reporting achieved levels of serum phosphorus in patients undergoing maintenance dialysis show that only 50% to 60% of patients achieve targets recommended by the K/DOQI guidelines [Block, 1998][Young, 2005][Moe, 2005]. A significantly smaller proportion of patients maintain all variables of disordered mineral metabolism (including serum calcium, phosphorus, calcium phosphorus product, and PTH) within the range recommended by the K/DOQI guidelines. In addition, only a negligible proportion of patients can sustain the variables within the recommended range [Kim, 2003].

Observational studies also have demonstrated that the presence and/or severity of vascular calcification may be associated with a higher dose of calcium-based phosphate binders [Goodman, 2000][Guerin, 2000]. In addition, in the secondary analysis of the Treat to Goal study, sevelamer hydrochloride treatment was associated with a significantly slower rate of progression in vascular calcification when compared with calcium-based phosphate binders [Chertow, 2002]. Based on these data, the K/DOQI have recommended limiting the total daily intake of calcium in patients with ESRD to <2000 mg.

Although it is effective in reducing morbidity in patients with CHF, digitalis is poorly dialyzed and eliminated by the kidneys. For this reason, it is probably prudent to use digitalis for compelling indications such as rate control in patients with atrial fibrillation or suboptimal response to maximally tolerated doses of beta blockers and ACE inhibitors or ARBs.

ACE inhibitors and angiotensin receptor blockers are proven effective in the general population for treating CHF. Even though the agents have not formally been tested for CHF in maintenance dialysis patients, they may be used for LV systolic dysfunction or LVH.

While managing hypervolemia is specific to patients undergoing maintenance dialysis, the ACC/AHA Guidelines for Managing CHF recommend beta blockers, ACE inhibitors, digitalis, and diuretics for routine use in stage C heart failure (structural heart disease with prior or current heart failure symptoms) [Hunt 2004]. Several clinical trials have demonstrated the safety and efficacy of beta blockers in patients with CHF [Packer 1996; CIBIS-II 1999;  MERIT-HF, 1999; Packer 2001] (Figure 1). In addition, beta blockers such as carvedilol are the only class of agents proven effective in improving LV function, decreasing hospitalizations, and reducing mortality in randomized, controlled trials in maintenance dialysis patients [Cice 2001; Cice 2003].

Because most patients with ESRD produce little or no urine after 1 to 2 years of dialysis therapy, diuretics are ineffective. Even though spironolactone reduces morbiditiy and mortality in patients with CHF, its efficacy and safety has not been studied. Spironolactone should probably be reserved for patients who have a suboptimal response to agents such as beta blockers, ACE inhibitors, ARBs, and digitalis. Each of these agents may require special dosing regimens to facilitate ultrafiltration during dialysis therapy and drug selection must be tailored to manage potential effects of therapeutic agents on intradialytic hemodynamics.



Hemodialysis treatment is associated with an increased risk for nosocomial transmission of blood-borne infections. Because transmitting HBV and HCV is a particular concern in patients treated with hemodialysis, the Centers for Disease Control (CDC) recommends that all patients starting maintenance hemodialysis undergo routine testing for both infections.

Numerous serologic and virologic tests for detecting HCV infection have been developed. Demonstrating the presence of circulating HCV RNA by RT-PCR is considered the gold standard for diagnosing HCV infection. Using RT-PCR for HCV RNA as the primary test for routine screening, however, is not recommended [CDC Guidelines, 2001]. With a sensitivity exceeding 97%, the third generation EIA is the most widely used and recommended test for screening patients for HCV [Colin, 2001]. As with any screening test, the positive predictive value of EIAs for anti-HCV is related to the prevalence of infection in the population and low in populations with a prevalence of HCV infection <10% [CDC. MMWR. 1991; Kleinman, 1992]. Using the third generation EIA, the average time from exposure to seroconversion is 8 to 9 weeks [Alter, 1991]. Anti-HCV can be detected in 80% of patients within 15 weeks, >90% within 5 months, and >97% within 6 months of exposure [Alter, 1991; Alter, 1992].

Testing for HCV RNA should be considered in patients with a persistently elevated ALT but a negative EIA for HCV who are highly likely to have HCV. HCV RNA can be detected in serum or plasma within 1 to 2 weeks after exposure and weeks before onset of ALT elevations or the appearance of anti-HCV, which significantly reduces the serologic window before seroconversion during acute HCV infection.

HCV causes acute and chronic hepatitis. The incubation period ranges from 14 to 180 days, with an average of 6 to 7 weeks [CDC. MMWR. 1998]. Acute infection with HCV is usually asymptomatic. Approximately 1 to 2 weeks after incubation, HCV RNA can be detected in the plasma [Pawlostsky, 2002], which is followed by a fluctuating elevation in serum ALT and seroconversion (or the appearance of anti-HCV antibodies) [Mondelli, 2005].

There is no correlation between the appearance of anti-HCV antibodies and the elimination of HCV from the body. Only about 15% to 20% of individuals with normal immune status appear to resolve their infection, which is defined by sustained absence of HCV RNA in serum and normalization of ALT. Chronicity and persistent infection appears common in patients with HCV infection, with 75% to 85% of patients with acute HCV infection showing evidence of persistent infection and 60% to 70% percent of those with chronic HCV infection showing persistent or fluctuating ALT elevations that indicate active liver disease [Alter, 2000]. Most studies have reported that cirrhosis develops in 10% to 20% of HCV patientswho have had chronic hepatitis C for 20-30 years, and hepatocellular carcinoma occurs in 1%-5% [Alter, 2000]. The probability of chronic complications such as cirrhosis and/or hepatocellular carcinoma is increased with HCV. In addition, the conditions occur sooner in patients with concomitant alcohol use.

There are limited data on the natural history of HCV infection in patients undergoing maintenance dialysis therapy partly because of the progressive nature of HCV and reduced life expectancy in patients with ESRD. In addition, patients on dialysis might be less likely to have biochemical evidence of liver disease [Pol, 1993]. Based on liver biopsy results, rates of chronic liver disease in HCV-infected patients undergoing maintenance dialysis appear similar to those in the general population.

Epidemiologic investigations have indicated substantial deficiencies in recommended infection control practices [CDC. MMWR, 1996; Favero, 1996]. For example, a December 2002 survey of all US chronic hemodialysis centers found that routine anti-HCV screening was performed on patients at only 64% of centers [Finelli, 2005]. According to the CDC, infection control practices are not being fully implemented partly because staff members are unaware of the practices and their importance. In addition, staff are confused about the differences between standard or universal precautions recommended for all health care settings and the additional precautions necessary in the hemodialysis setting. HBV vaccination is recommended for all susceptible chronic hemodialysis patients and for all staff members [CDC Guidelines, 2001]. Vaccination is recommended for pre-ESRD patients before they become dependent on dialysis and for peritoneal and home dialysis patients because they might require in-center hemodialysis. Still in the early stages of development, the HCV vaccine is not available in the clinical setting [Huang, 1997].

The CDC recommends monthly ALT testing of HCV-negative patients for timely detection of new infections [CDC Guidelines, 2001] (Figure 2). In the absence of unexplained ALT elevations, testing for anti-HCV every 6 months is sufficient to monitor for new HCV infections.

If, however, 1 or more patients seroconverts from anti-HCV negative to HCV positive during a 6-month period, more frequent (every 1 to 3 months) anti-HCV testing of HCV-negative patients is warranted for the subsequent 3 to 6 months. Semiannual testing can be resumed if no additional newly infected patients are identified.

Anti-HCV-positive seroconversions should be reported to the local health department. When a seroconversion occurs, results of each patient's routine laboratory test should be reviewed to identify additional causes. The clinician should investigate potential sources for infection to determine if transmission occurred within the dialysis unit. This review should include the newly infected patients' recent medical histories (blood transfusions, hospitalizations), history of high-risk behavior ( IV drug use), and dialysis unit practices and procedures. If ongoing HCV transmission among patients is identified, control measures should be implemented based on potential sources of transmission. In addition, infection control measures should be monitored by performing more frequent anti-HCV testing of HCV-negative patients for 6 to 12 months before resuming semiannual testing [CDC Guidelines, 2001].

CDC guidelines indicate that patients who are anti-HCV positive (or HCV RNA-positive) do not have to be isolated from other patients or dialyzed separately on dedicated machines [CDC Guidelines, 2001]. In addition, they can participate in dialyzer reuse programs because reprocessing dialyzers from HCV-positive patients does not increase staff members' risk for infection.


6) The majority of patients with ESRD are between 45 and 64 years of age. The incidence rates for individuals younger than 65 years have stabilized over the last few years. Conversely, for those individuals aged 65 years and older, the incidence rates continue to climb. From 2002 to 2003, the incident rate in individuals older than 75 years surpassed the rate for those 65 to 74 years of age (Figure 2)(USRDS, 2005).Thus, the oldest patients now account for 26% of the ESRD population.

In the United States, it is currently estimated that fewer than 10% of patients with ESRD utilize peritoneal dialysis.  In comparison, the percentage of patients with ESRD on peritoneal dialysis ranges from 20% to 30% in such countries as Australia, Denmark, Finland, Korea, the Netherlands, and Sweden, and is approximately 45% in New Zealand and as high as 80% in Mexico (USRDS, 2005). Attempts to identify reasons for this decline have focused on such factors as older age and greater comorbidity of the dialysis population, publication of studies showing a higher mortality rate associated with peritoneal dialysis, guidelines requiring an increasingly complex peritoneal dialysis regimen, a rapid increase in the number of hemodialysis units, an increase in the dominance of dialysis centers in the delivery of care to patients with ESRD, and changing patterns of reimbursement. However, increasing evidence shows that most patients starting dialysis are not offered chronic peritoneal dialysis as a method of treatment. A recent study indicated that only about one third of patients starting dialysis treatment reported that chronic peritoneal dialysis was offered as a method of renal replacement therapy (Mehrotra, 2005).  Figure 5 shows these and other responses to a question about the treatment options offered to patients requiring dialysis. Many studies suggest that when education programs are provided prior to initiating renal replacement therapy and the opportunity is given to freely choose a treatment option, up to 50% of patients will choose peritoneal dialysis, favoring its self-care component (Prichard, 1996; Korevaar, 2003; Manns, 2005). Accessibility may also be a significant factor when making the choice between maintenance hemodialysis and peritoneal dialysis. Most of the dialysis units in the United States do not have the facilities or personnel required to adequately support patients on peritoneal dialysis (O’Hare, 2006).  In addition, patient preference, contraindications for peritoneal dialysis, poor social support, and comorbidity may also contribute to low peritoneal dialysis utilization rates.

Various studies have shown a relationship between elevated serum phosphorus, calcium, and parathyroid hormone levels and increased risk for death among patients undergoing maintenance dialysis. Of the various elements of disordered mineral metabolism, the greatest increase in risk is attributable to a high serum phosphorus level (Block, 1998; Block, 2004; Young, 2005; Slinin, 2005).  Hyperphosphatemia is an inevitable consequence of progressive decrease in glomerular filtration, as seen in patients with chronic kidney disease (Mehrotra, 2006). In patients with ESRD, the dialytic removal of phosphorus is inadequate to maintain neutral balance and hyperphosphatemia is near-universal, requiring the use of phosphate binders.  Increasing evidence, however, points to the potential role of hyperphosphatemia and hypercalcemia in the pathogenesis of vascular calcification (Block, 2000) — a problem that is nearly universal and often severe among patients with ESRD (Mehrotra, 2006). The severity of coronary artery calcification is related to the angiographic severity of stenosis in patients undergoing maintenance hemodialysis. Moreover, the severity of vascular calcification (assessed either by plain radiographic examination, ultrasonography, or computed tomography) is associated with increased mortality (Blacher, 2001; Matsuoka, 2004).

Some physicians have defined nonadherence among patients with ESRD as interdialytic weight gain >1.5 kg, a serum phosphorus level >6 mg/dL, and a predialysis potassium level >5.5 mEq/L. Using this definition of nonadherence, as many as 86% of dialysis patients may be classified as nonadherent with one or more aspects of their treatment (Loghman-Adham, 2003). The median percent of nonadherent patients may probably be closer to 50%.


In this patient population, the most common causes of ESRD were diabetes (32%) and hypertension (33%).  More than 30% of the patients evaluated had four or more comorbid conditions, and 91% were taking six or more prescription medications. Only 15% of patients had begun dialysis within the last year, and approximately 22% had been on dialysis for more than five years. Overall medication adherence rates were very low (Table 2).

The investigators acknowledged that estimates of patient adherence as measured by self-report, pill count, and microelectronic monitoring may not sufficiently measure adherence. However, they also noted that the study results confirm that nonadherence is a significant problem for patients on dialysis.

_____________________________________________________________________________________________________________________________________________________________________________________________  ---CKD Part 2--( CKD---P, Cal, PTH, Meds...)
1. In a study comparing sevelamer with calcium acetate for control of hyperphosphatemia in pediatric dialysis patients, which of the following was not a finding?
Answer: A decreased incidence of hypercalcemia was observed with calcium acetate treatment
Serum phosphorus levels at 8 weeks were not significantly different between groups. Total cholesterol (-27%) and low-density lipoprotein cholesterol (-34%) levels decreased significantly with sevelamer treatment (P < .02 and P < .005, respectively). An increased incidence of hypercalcemia (P < .0005) was observed with calcium acetate treatment (6 patients vs 1 patient in the sevelamer group), whereas metabolic acidosis was more frequent with sevelamer treatment (11 patients vs 1 patient in the calcium acetate group, P < .005).
2. Recent safety and efficacy studies of lanthanum carbonate produced the following findings:
Answer: Exposure-adjusted adverse events were remarkably similar between lanthanum and comparison treatment groups
Exposure-adjusted adverse events were remarkably similar between treatment groups in a study by Finn comparing lanthanum carbonate, calcium acetate, calcium carbonate, and sevelamer. In this same study, average treatment exposure was greater in the standard-therapy group. Hutchison and colleagues found that after discontinuation of calcium carbonate and initiation of lanthanum carbonate, the hypercalcemia incidence was 2.7% compared with 20.2% in patients receiving calcium carbonate.
3. What type of dialysis was shown to reduce over time the need for medications to treat renal osteodystrophy?
Answer: Daily nocturnal home hemodialysis
Grabbe and colleagues demonstrated that daily nocturnal home hemodialysis was associated with the virtual absence over time of the need for medication to treat renal osteodystrophy. At the end of 24 months using this dialysis method, the average number of bone medications in 47 patients given a total of 1700 prescriptions was only 0.17!
4. Bone disease in renal transplant recipients is characterized by all of the following except:
Answer: Osteoprotegerin is a new specific biomarker used in the diagnosis of bone disease after renal transplantation
Although bone mineral density in the kidney transplant recipient improves with discontinuation of corticosteroid therapy, the risk of fracture does not seem to correlate with bone mineral density. Bone disease, as defined by histomorphometry and subsequent clinical outcome correlates including fracture, does not exist in this population. However, a recent publication reported the changes in bone histology as patients progressed from maintenance dialysis to transplantation. Although most patients retained abnormal bone histology for 6 months after the transplantation, their adynamic bone disease appeared to transition to hyperparathyroid bone disease. Unfortunately, there are no specific biomarkers to aid in the diagnosis of bone disease after kidney transplantation.
5. Which of the following is a hormone or hormone-like substance shown to be important in the control of overall phosphate homeostasis?
Answer: Phosphatonin
Phosphatonins are hormone or hormone-like substances that have been shown to be important in the control of overall phosphate homeostasis. The phosphatonins include fibroblast growth factor 23 (FGF-23), MEPE (matrix extracellular phosphoglycoprotein), soluble FRP-4, and, perhaps most recently described, circulating klotho protein.
6. According to Dr. Malluche and the K/DOQI guidelines, which of the following laboratory parameters should physicians monitor regularly in patients with chronic kidney disease?
Answer: Calcium, phosphate, intact parathyroid hormone (PTH)
Physicians should refer to the National Kidney Foundation Kidney Disease Outcomes Quality Initiative guidelines for detailed recommendations. Briefly, physicians should monitor calcium and phosphorus and also PTH levels periodically. Bone-specific alkaline phosphatase might also be valuable. In most dialysis units, it is standard to perform monthly laboratory tests for routine parameters including calcium and phosphorus, and PTH should be measured at least twice a year. Parathyroid hormone may need to be more frequently monitored immediately after changing therapies. One has to keep in mind that results of total PTH levels (intact) do not only include the active PTH (1.84 PTH) but also inhibitory fragments. Therefore, regardless of which assay you're using, you need to have an idea how much of the PTH results reflect active vs antagonistic fragments.
7. What is the end result of compensatory mechanisms in chronic kidney disease?
Answer: Increase in parathyroid hormone level and decrease in 1,25 vitamin D level
With chronic reduction in kidney function, there is an increase in the levels of PTH and eventually a decrease in levels of 1,25 vitamin D.
1. According to Dr. De Broe, a multicenter bone biopsy study in dialysis patients demonstrated:
Answer: That lanthanum carbonate treatment during 1 year did not result in any aluminum-like effect on bone (adynamic bone disease, osteomalacia)
It is well documented that powerful phosphate binders at very high doses may, in the long term, induce a relative phosphate depletion and subsequent demineralization of bone in the presence of maintained and intact bone formation/turnover. However, by preventing phosphate depletion and giving the same high doses of lanthanum carbonate, the mineralization defect did not occur. In a prospective controlled (calcium acetate) multicenter bone biopsy study (repeated biopsies: basal condition and at the end of the study) in dialysis patients, lanthanum carbonate treatment during 1 year did not result in any aluminum-like effect on bone (adynamic bone disease, osteomalacia). A second analogous prospective study over 2 years of treatment came to the same conclusions.
2. According to Dr. De Broe, a lanthanum concentration of 1.0 micrograms (mcg)/g to 2.4 mcg/g in the liver:
Answer: Is not of concern because it is several hundred times lower than concentrations of iron in the liver
A concentration of 1.0 mcg/g to 2.4 mcg/g (17 nmol/g) of lanthanum is several hundred times lower than concentrations of iron (1400 nmol/g) in the liver, and it is known that in normal situations, lysosomal iron is not hepatotoxic. It is only when iron achieves the characteristic concentration of several thousand micrograms (as in the case of primary hemochromatosis) that hepatotoxicity may occur.
3. Hyperphosphatemia contributes to cardiovascular disease in which of the following ways?
Answer: All of the above
High serum phosphorus concentration contributes to worsening hyperparathyroidism and resultant renal osteodystrophy, while also contributing directly to pathologic changes in the heart and arterial vascular system. London noted that elevated serum phosphorus and calcium levels stimulate osteoblast-like changes in vascular smooth muscle. This in turn results in medial vascular calcification, which accounts for the arterial stiffening observed in most dialysis patients. Arterial stiffening contributes to the development of left ventricular hypertrophy and is an independent predictor of all-cause and cardiovascular mortality in dialysis patients.
4. With regard to active vitamin D therapy, which of the following statements is not true?
Answer: Paricalcitol is substantially more calcemic and phosphatemic than doxercalciferol and calcitriol
Dr. Stuart Sprague noted that animal studies indicate paricalcitol is substantially less calcemic and phosphatemic than doxercalciferol and calcitriol. A blinded, randomized trial of calcitriol and paricalcitol demonstrated a lower frequency of hypercalcemia and hyperphosphatemia with paricalcitol than with calcitriol. Doxercalciferol in patients with stage 3 and 4 CKD showed PTH suppression and significantly less alteration in serum calcium and phosphorus, while a trial of paricalcitol in similar patients showed minimal differences in serum calcium and phosphorus compared with placebo. Historical cohort data on calcitriol and paricalcitol in dialysis patients showed that patients receiving exclusively paricalcitol had substantially better survival than those receiving calcitriol.
5. Which statement about effects of lanthanum therapy is not true?
Answer: Better control of serum phosphate level was achieved in hemodialysis patients compared with peritoneal dialysis patients
The study by Al-Baaj and colleagues found that lanthanum carbonate decreases levels of serum phosphate and calcium X phosphate product in hemodialysis and peritoneal dialysis patients. Among the patients who had achieved adequate phosphate control during the titration period, 64.7% of those who continued to receive lanthanum maintained control of serum phosphate levels in the double-blind phase, compared with 21.4% in the placebo group. Results in patients receiving continuous ambulatory peritoneal dialysis were similar to those in the group as a whole. Finn and colleagues reported that the most commonly reported adverse events during the extension study were nausea (26.0%), peripheral edema (23.4%), and myalgia (20.8%). No treatment-related serious adverse events occurred.
6. Compared with calcium carbonate, treatment with sevelamer resulted in:
Answer: Lower serum calcium concentration
The study by Salusky and colleagues found that in children with end-stage renal disease and secondary hyperparathyroidism on peritoneal dialysis, calcium carbonate and sevelamer both limit bony lesions. Treatment with sevelamer is associated with lower concentrations of serum calcium and calcium X phosphorous product compared with treatment with calcium carbonate. The study by Block and colleagues demonstrated that those taking calcium-containing phosphate binders had greater increases in coronary calcification than those taking sevelamer hydrochloride.


In summary, this conference stressed the clear need for aggressive phosphorus control and avoidance of substantial positive calcium balance (ideally by use of lanthanum carbonate or sevelamer) to minimize cardiovascular and bone disease in patients with CKD. Active vitamin D reflects both a benefit, as demonstrated by improved survival, and a risk, because phosphorus and calcium balance may be adversely affected depending on the choice of agent. Last, cinacalcet, used alone or with active vitamin D, provides significant PTH suppression with reduction in serum phosphorus and calcium levels.


Icodextrin instead of glucose during the daytime dwell ... -         Exit-site care and exit-site infection in continuous ...  ( CAPD/ CCPD)  ( Choice---HD vs. PD)

___________________________________________________________________________________________________________________________________________________________________________________________  ( CCF & RI ---Use of Ultrafiltration vs. Diuretics)


1. Which of the following associated diseases continue to gain prevalence despite increasingly successful management of HIV?
Answer: A, B, C
The improvement in treatment for HIV has resulted in a decrease in viral-mediated disease such as wasting/cachexia; however, other diseases such as cardiac, renal, and liver disease are increasing. The increasing age of the population, the side effects of long term-therapy, and lifestyle may all be contributing factors. Selik RM, Byers RH Jr, Dworkin MS. Trends in diseases reported on U. S. death certificates that mentioned HIV infection. 1987–1999. J Aquir Immune Defic Syndr. 2002;29(4):378-387.
2. HIV-Associated Nephropathy (HIVAN) is most likely to occur in which of the following groups?
Answer: African American
Several studies have shown that HIVAN occurs almost exclusively in persons of African descent. In the United States, African Americans are 12 times more likely to develop HIVAN than other ethnic groups. It is not different in Europe. Martins D, Tareen N, Norris KC. The epidemiology of end-stage renal disease among African Americans. Am J Med Sci. 2002;323:65-71.
3. Which of the following predictors of mortality for women with HIV was discussed in this program in the Szczech Study?
Answer: Proteinuria
In a study that determined hazard ratios for various parameters to predict mortality in women with HIV following HAART initiation, proteinuria and elevated serum creatinine stood out as predictors. Szczech LA , Hoover DR, Feldman JG, et al. Association between renal disease and outcomes among HIV-infected women receiving or not receiving antiretroviral therapy. Clin Infect Dis. 2004;39:1199-1206.
4. The best method to estimate Glomerular Filtration Rate (GFR) is
Answer: Modification of Diet in Renal Disease (MDRD) equation
Serum creatinine is well known to be a poor predictor of GFR. A 24-hour creatinine clearance is difficult and often inaccurate because of poor collections. The inulin clearance requires special assays. While the Cockcroft-Gault equation is useful, clinically, the MDRD provides a better estimate of GFR. It is a regression formula that incorporates creatinine, age, race, and sex. Levey AS, Bosch JP, Lewis JB, et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Ann Intern Med. 1999;130:461-470.
5. Which of the following is unusual in a patient with HIVAN?
Answer: Undetectable viral load
HIVAN presents as acute renal failure. Usually the serum creatinine is elevated. Other features of HIVAN are a decreased GFR, nephritic range proteinuria ( > 3 g), a low CD4 count, and a detectable viral load. It is unusual that the patient would have undetectable virus; however, it has been reported.
6. The definitive diagnostic test for HIVAN is
Answer: Kidney biopsy
Clinical and laboratory tests such as urine protein may suggest HIVAN; however, the definitive diagnosis requires a kidney biopsy.
7. Which of the following have been shown to have clinical benefit in patients with HIVAN?
Answer: A, B, and C
Retrospective analyses have demonstrated clinical benefit from the use of steroids and ACE inhibitors in patients with HIVAN. HIVAN has been shown to recur in patients who stop ART. Lucas GM, Eustace JA, Sozio S, et al. Highly active antiretroviral therapy and the incidence of HIV-1-associated nephropathy: a 12 year cohort study. AIDS. 2004;20:18(3):541-546.
8. What is first-line therapy for a patient newly diagnosed with HIVAN?
Answer: HAART
While corticosteroids and ACE inhibitors have been shown to result in clinical benefit in patients with HIVAN, the first line of treatment and prevention is HAART. Patients with HIVAN should be treated with HAART at diagnosis. If there is insufficient improvement with HAART, consideration should be given to ACE inhibitors and/or corticosteroids (prednisone). Gupta SK, Eustace JA, Winston JA, et al. Guidelines for Management of Chronic Kidney Disease in HIV/AIDS. Clin Infect Dis. 2005;40(11):1559-1585.
9. Which is the most common cause of acute renal failure?
Answer: Renal causes including drug toxicity, interstitial nephritis, and Acute Tubular Necrosis (ATN)?
A study that looked at the causes of acute renal failure in HIV patients found that 38% were pre-renal, 46% were renal, 7% were obstructive, and 9% were unknown. Franceschini N, Napravnik, S, Eron Jr JJ, et al. Incidence and etiology of acute renal failure among ambulatory HIV-infected patients. Kidney Int. 2005;67:1526-531.
10. The three most common causes of acute renal failure in patients with HIV are dehydration, ATN, and nephrotoxic drugs
Answer: True
Dehydration (from various causes), acute tubular necrosis, and nephrotoxic drugs are the three leading causes of acute renal failure in the HIV population. Franceschini N, Napravnik S, Eron Jr JJ, et al. Incidence and etiology of acute renal failure among ambulatory HIV-infected patients. Kidney Int. 2005;67:1526-1531.
11. The best first-line management for treating drug-induced Acute Interstitial Nephritis (AIN) is
Answer: Stopping the medication that is causing the AIN
Acute interstitial nephritis (AIN) is an idiosyncratic reaction and is not dose-dependent. The best therapeutic approach is to diagnose the disease early and stop the offending drug. Perazella MA. Acute renal failure in HIV-infected patients: a brief review of common causes. Am J Med Sci. 2000;319(6):385-391.
12. Tenofovir is structurally and chemically related to adefovir.
Answer: True
Tenofovir is structurally very similar to adefovir. A methyl group differentiates tenofovir from adefovir. Squires K, Pozniak AK, Pierone G Jr, et al. Tenofovir disoproxil fumarate in nucleoside-resistant HIV-1 infection: a randomized trial. Ann Intern Med. 2003;139:313-320.
13. The site of tenofovir nephrotoxicity is believed to be located at the
Answer: Proximal tubule
Tenofovir is freely cleared at the level of the glomerulus and is also actively secreted in the proximal tubule. There are multiple transporters that transport tenofovir through the proximal tubule. It is believed that tenofovir may be retained in the proximal tubule and become nephrotoxic. Squires K, Pozniak AK, Pierone G Jr, et al. Tenofovir disoproxil fumarate in nucleoside-resistant HIV-1 infection : a randomized trial. Ann Intern Med. 2003;139:313-320.
14. According to currently available clinical trials the average incidence of tenofovir toxicity appears to be
Answer: 18%
While registration trials have reported no tenofovir nephrotoxicity, clinical trials continue to report about an incidence of 7%. More recently two papers reported the rate of tenofovir toxicity in these populations to be 18%. Harris M, et al. 2nd IAS. Paris, France 2003. Abstract #730. Kiser J, et al. Effect of lopinavir/retonivar on the renal clearance of tenofovir in HIV infected patients. CROI Denver 2006 Abstract #L-156. Thompson M, Haubrich R, Margolis D, et al. Differences in Calculated Glomerular Filtration Rates in Efavirenz- or Tenofovir-treated Adults in ESS40006. 13th CROI February 1, 2006. Poster 777.
15. Which of the following are potential risk factors for tenofovir-associated renal failure?
Answer: All of the above
While it's not possible to predict who will develop tenofovir nephrotoxicity, there are potential risk factors. A well-recognized risk factor is a low baseline renal function when determined by GFR. Also, lower body weight, lower CD4 count, RTV-boosted PI, and didanosine are believed to be factors. While race and gender need to be more fully examined, people of African descent have a higher incidence of HIVAN and would appear to be at greater risk. Harris, et al. CROI San Fran 2004 Abs 750. Peyriere, et al. Renal tubular dysfunction associated with tenofovir therapy: report of 7 cases. J Acquir Immune Defic Syndr 2004;35:269-73. Harris, et al. IAS 2003 Abs 730. Gallant J, et al. Changes in renal function associated with tenofovir disoproxil fumarate treatment, compared with nucleoside reverse-transcriptase inhibitor treatment. CID. 2005;40:1194-8. Zimmerman, et al. Tenofovir-associated acute and chronic kidney disease: a case of multiple drug interactions. CID. 2006;42(2):283-90.
16. The presence of glucose in the urine in a patient who does not have diabetes is a positive indicator of
Answer: Renal toxicity
Glucose in the urine of a patient who is not a diabetic suggests that the proximal tubule is not functioning appropriately. This may be a good clinical marker for drugs that are associated with, or have known risk of, renal damage. Rifkin BS, Perazella MA. Tenofovir-associated nephrotoxicity: Fanconi syndrome and renal failure. Am J Med 2004;117:282-284.
17. The incidence of tenofovir nephrotoxicity has been shown to increase with the use of which of the following Antiretroviral Therapies (ARV)?
Answer: Ritonavir
In a review of 25 cases of tenofovir-induced Fanconi syndrome, ritonavir was used along with tenofovir in 18 (72%). It's possible that ritonavir exacerbates the toxicity of tenofovir by competing with the same transporters. Peyriere H, et al. J Acquir Immune Defic Syndr. 2004;35:269-73. Rifkin B, et al. Am J Med 2004;117:282-4. Karras A, et al. Clin Infect Dis. 2003;36:1070-3. Rollot F, et al. Clin Infect Dis.2003;37(12):e174-e6. Saumoy M, et al. AIDS. 2004;18(12):1741-9. Gaspar G, et al. AIDS. 2004;18:351-2.
18. Which of the following are laboratory features of tenofovir-induced Fanconi syndrome?
Answer: All of the above
The classic signs of Fanconi syndrome are hypophosphatemia, acidosis, glucosuria, aminoaciduria, and hypokalemia. A patient does not have to have all of these features to have Fanconi syndrome. In a study looking at patients with tenofovir-induced Fanconi syndrome, all had an increase in serum creatinine, 20/20 had hypophosphatemia, 12/13 had glycosuria, and all had proteinuria. Peyriere H, et al. J Acquir Immune Defic Syndr. 2004;35:269-73. Rifkin B, et al. Am J Med 2004;117:282-4. Karras A, et al. Clin Infect Dis. 2003;36:1070-3. Rollot F, et al. Clin Infect Dis.2003;37(12):e174-e6. Saumoy M, et al. AIDS. 2004;18(12):1741-9. Gaspar G, et al. AIDS. 2004;18:351-2.
19. The discontinuation of tenofovir in a patient with tenofovir-induced Fanconi syndrome would result in resolution of the following except
Answer: Elevated creatinine
In reviewing the data on tenofovir-induced Fanconi syndrome, the electrolyte abnormalities and glycosuria resolved; the proteinuria partially resolved. The resolution of these values may be lengthy. The serum creatinine did not return to baseline during the observation period. Peyriere H, et al. J Acquir Immune Defic Syndr. 2004;35:269-73. Rifkin B, et al. Am J Med 2004;117:282-4. Karras A, et al. Clin Infect Dis. 2003;36:1070-3. Rollot F, et al. Clin Infect Dis.2003;37(12):e174-e6. Saumoy M, et al. AIDS. 2004;18(12):1741-9. Gaspar G, et al. AIDS. 2004;18:351-2.
20. The Infectious Diseases Society of America (IDSA) recommends that patients taking tenofovir should have their renal function assessed every
Answer: Six months
The Infectious Disease Society of America (IDSA) state that patients using tenofovir should have their renal function monitored biannually (every six months) when:
  • GFR < 90 mL/min per m2
  • Taking other medications eliminated via renal secretion
  • Comorbid disease exists (e.g.; diabetes or hypertension)
  • Taking a ritonavir-boosted protease inhibitor regimen (creatinine along with serum phosphorus and urine analysis for proteinuria and glycosuria)
Some clinicians would monitor the renal function more frequently in patients taking tenofovir. Gupta SK, Eustace JA, Winston JA, et al. Guidelines for Management of Chronic Kidney Disease in HIV/AIDS. Clin Infect Dis. 2005;40(11):1559-1585.
___________________________________________________________________________________________________________________________________________________________________________________________________________________________________  ----Osteodystrophy  & Bone-Mineral Disorder in CKD
1. Which of the following statements best describes the current status of the science of the effect of vitamin D therapy on mortality in chronic kidney disease (CKD) patients?
Answer: Several epidemiologic studies have yielded similar findings of a survival advantage of vitamin D
A historical study of dialysis patients who received vitamin D vs those who did not showed reduced overall and cardiovascular mortality rates in treated patients. A cohort study of dialysis patients showed that those who received paricalcitol had better overall and cardiovascular survival. Critics have warned against overinterpretation of these findings on the basis of their retrospective design, use of historical cohorts, and the potential for unmeasured factors that may account for mortality. In a prospective, case-control study of dialysis patients, Wolf and colleagues showed that the 90-day all-cause and cardiovascular mortality rates were significantly higher in patients who were not treated with vitamin D. Ravi Thadhani, MD, noted that the consistent findings of these studies do not imply causality, and pointed out the need for randomized controlled trials.
2. Which of the following is not an emerging risk factor that confers excess mortality from cardiovascular disease in patients with chronic kidney disease and end-stage kidney disease?
Answer: Obesity
In the past, we have looked to traditional risk factors that are associated with increased cardiovascular risk, such as obesity, hypertension, hyper-homocysteinemia, and hyperlipidemia, as explanations for the higher mortality. However, specific trials designed to intervene in many of these risk factors have been unrewarding, finding no differences at all in mortality, or paradoxically, finding that such factors as increasing obesity or higher blood pressure may be associated with better outcomes in maintenance dialysis patients. Thus, we need to turn to emerging risk factors that confer excess mortality from cardiovascular disease in patients with CKD and end-stage kidney disease (maintenance dialysis). Three general areas that may be important are: systemic alterations of mineral metabolism, malnutrition and inflammation, and anemia with associated iron deficiency.
3. Research on vitamin D therapy in patients with chronic and end-stage kidney disease has demonstrated that:
Answer: Any form of vitamin D is better than no vitamin D
Teng and colleagues indeed demonstrated a survival advantage in dialysis patients receiving any intravenous vitamin D vs none, and across all ranges of calcium, phosphorus, C X P, or PTH levels. Notably, and as yet unexplained, however, is the finding that the choice of vitamin D metabolite itself confers a distinct survival advantage. A vitamin D2-based agent (eg, paricalcitol or doxercalciferol) confers a survival advantage to new or existing dialysis patients when compared with a vitamin D3-based agent, such as calcitriol. Not only have we learned the importance of the active metabolite to patient survival, but it seems that nutritional vitamin D deficiency influences the dialysis patient's overall mortality and cardiovascular mortality as well.
4. Potential inflammatory pathways in patients with CKD include all of the following except:
Answer: Increased vagal tone
The mechanism of inflammation in CKD is not known, but several potential pathways may be involved. An inflammatory response could be stimulated by infection or low-grade exposure to microbiologic agents or toxins during the dialysis procedure. On the other hand, there could be diminished breakdown of inflammatory molecules either due to kidney dysfunction or via release of inhibitors. Kidney damage by itself might lead to an inflammatory milieu due to related stresses such as reactive oxygen species, volume overload, or sympathetic hyperactivity. Interesting observations relate decreased vagal activity with inflammation, and reduced vagal tone has been detected in CKD. Genetic factors are also likely involved in the genesis of the inflammatory state.
____________________________________________________________________________________________________________________________________________________________________________________________________________________________________  ( Anemia Management in CKD)------
The approximate conversion is 200 IU of epoetin alfa to 1 mcg of darbepoetin alfa.
1. Advantages of darbepoetin alfa over the first-generation erythropoiesis-stimulating agent epoetin alfa include all of the following except:
Answer: Less influence on hemoglobin variability
Darbepoetin alfa, a second-generation erythropoiesis-stimulating agent, contains 2 amino acid substitutions, which provide the protein with greater metabolic stability in vivo and increase the elimination half-life when compared with intravenous epoetin alfa. Darbepoetin alfa can be administered once weekly or once every other week. No clinically or statistically significant difference in median within-subject hemoglobin variance between darbepoetin alfa-treated and epoetin alfa-treated subjects was shown.
2. How do the pharmacokinetics of CERA differ from previous erythropoiesis-stimulating agents?
Answer: Longer elimination half-life compared with epoetin alfa and darbepoetin alfa
Continuous erythropoiesis receptor activator (CERA) is composed of a large methoxy polyethylene glycol polymer chain integrated into the erythropoietin molecule and linked primarily by amide bonds. As a result, the elimination half-life of CERA is substantially longer than that of epoetin alfa and darbepoetin alfa. CERA may also have different receptor binding characteristics than other erythropoietic agents. In particular, CERA has been shown to provoke a greater erythropoietic response in mice than that of epoetin alfa, despite being less tightly bound to the erythropoietin receptor. CERA has also demonstrated a 45-fold lower affinity for the erythropoietin receptor than epoetin beta.
3. Why was the Correction of Hemoglobin and Outcomes in Renal Insufficiency (CHOIR) trial stopped early?
Answer: Patients in the high-hemoglobin group had an increased risk of hospitalization for cardiovascular events and death
The CHOIR trial was an open-label, multicenter trial that randomized 1432 patients (hemoglobin of < 11 g/dL) treated with epoetin alfa to achieve target hemoglobin levels of either 13.5 or 11.3 g/dL. The trial was terminated early due to the findings of an increased risk for death and hospitalization for cardiovascular events in the high-hemoglobin group. A total of 222 composite events occurred. Of these, 125 of 715 patients in the high-hemoglobin group had an event compared with 97 of 717 patients in the low-hemoglobin group. The researchers concluded that a target hemoglobin level of 13.5 g/dL was associated with an increased cardiovascular risk and no improvement in quality of life when compared with the 11.3 g/dL hemoglobin target.
_____________________________________________________________________________________________________________________________________________________________________________________________________________________________________  ---Infection, Inflammation, Everyday HD, Comorbidities & factors associated with them...) --Cath related Infections & Tx.....
1. Longitudinal cohort analyses from patients at the Humber Rover dialysis program in Canada have revealed potential benefits of nocturnal hemodialysis compared with conventional hemodialysis to include all of the following except:
Answer: Increased survival rate
Longitudinal cohort studies from this center have confirmed that nocturnal hemodialysis (NHD) lowers the blood pressure after conversion from conventional hemodialysis (CHD) and that NHD is associated with regression of left ventricular hypertrophy and slow rates of progression of coronary calcification. The data on the cardiovascular benefits of NHD compared with CHD are favorable, but longer survival on NHD has not been confirmed.
2. Which of the following was not a finding in the analysis of trends and outcomes of the Dialysis Outcomes and Practice Patterns Study (DOPPS)?
Answer: Documented peripheral arterial disease did not predict cardiovascular mortality
The overall prevalence of clinically diagnosed peripheral arterial disease based on DOPPS I and II data was 25%. A diagnosis of peripheral arterial disease powerfully predicted both cardiovascular mortality and hospitalization risk in hemodialysis patients.
3. Potential strategies for reducing bacterial contamination of hemodialysis systems include all of the following except:
Answer: Decreased absorption of DNA fragments
Several studies point to microbiological impurity of hemodialysis water and dialysate as a significant cause of chronic inflammation in the end-stage renal disease population. Despite purification steps, there are many areas of bacterial adhesion and cell growth in the distribution system. Short bacterial-derived DNA fragments are present in dialysate and pass through dialyzer membranes and, thus, are an overlooked factor contributing to inflammation in dialysis patients. Future work will focus on additional devices or improved ultrafilters to adsorb bacterial DNA fragments.
4. Chronic inflammation plays a role in chronic kidney disease (CKD) outcomes. Which statement regarding this relationship is false?
Answer: C-reactive protein (CRP) is the best predictor of outcomes in CKD
Which inflammatory biomarker is the best predictor of outcome in patients with CKD has been debated; interleukin-6 appears to be the best predictor. Multiple studies in the general population have demonstrated that high-sensitivity CRP adds prognostic information beyond that available from traditional Framingham risk factors; other studies using the Mendelian randomization approach suggest that CRP is merely an innocent bystander.
5. Which of the following is the most prudent dialysis catheter-related strategy for a patient who develops catheter-related bacteremia (CRB)?
Answer: Apply an antibiotic lock to the existing catheter
With respect to the treatment of CRB, antibiotic locks may have a potential role in the salvage of catheters. When a patient develops a bacteremia, potential management strategies include the following: antibiotics alone, which has a low rate of catheter salvage of approximately 25%; catheter removal with delayed placement of a new catheter, the downside being the necessity for 3 procedures (removal of the infected catheter, placement of temporary access, and the final placement of a new catheter); exchange of the existing catheter over a guidewire; and because most cases of CRB are related to the biofilm on the inner lumen of the catheter, the use of an antibiotic lock may be a promising way to salvage a catheter.
(Significant predictors for the presence of HF based on multivariable analyses included older age, female sex, use of catheters and arteriovenous graft as vascular access, higher serum phosphorus, higher neutrophil count, and lower serum albumin. Not surprisingly, a diagnosis of HF was significantly associated with an elevated risk of mortality. A diagnosis of PAD powerfully predicted both cardiovascular mortality and hospitalization risk in HD patients. Importantly, PAD was strongly associated with lower quality of life scores as well as patient depression. These data provide important insights with respect to 2 major cardiovascular comorbidities among HD patients. The use of cardioprotective medications such as beta blockers, angiotensin-converting enzyme inhibitors, and long-acting calcium channel blockers is shown to be associated with lower mortality in the DOPPS and has important implications for both future clinical trials and practices in this patient population). ****************************
1. The epidemiologic studies of vitamin D therapy in hemodialysis patients, which have been conducted to date, are important for all of the following reasons except:
Answer: They have helped to elucidate the biological mechanism of a survival advantage of vitamin D
Right now, we are not sure what biological mechanisms would lead to these findings. However, there are several hypotheses. If there is a factor that is so profoundly driving the decision to give vitamin D and that factor itself is driving the survival benefit, it's surprising to me because we have no idea what that is.
2. According to this discussion, which of these arguments can be made for reevaluating the current National Kidney Foundation-Kidney Disease Outcomes Quality Initiative (K/DOQI) guideline recommendations for treatment of alterations in mineral and bone metabolism in patients with chronic and end-stage kidney disease?
Answer: All of the above
The K/DOQI guidelines were published in 2003, and the data behind them were from studies that were published up until the end of 2001, I believe. Everything we've been discussing for the last 10 or so minutes has all been published since then. Many of the guidelines that focus on PTH reduction may need to be reevaluated. Is the primary goal here PTH reduction? I think it's certainly a component of what we need to do. We want to control PTH to avoid bone complications, but there might be a benefit directly attributable to vitamin D that's not necessarily mediated by altering the PTH level.
( As Dr. Wolf and Thadhani's data showed, the advantage of vitamin D in terms of survival benefit was independent of serum calcium and phosphorus levels, as well as PTH level and/or the calcium X phosphorus product. A similar and consistent survival advantage was observed even in patients whose serum phosphorus levels were > 5.5 mg/dL, whose serum calcium levels were > 9.5 mg/dL, or whose PTH levels were > 300 pg/dL or < 150 pg/dL. Our data from the DaVita national database showed the same thing.

Currently, the K/DOQI guidelines exclude any intervention that would increase serum phosphorus or calcium beyond a certain level).

___________________________________________________________________________________________________________________________________________________________________________________________________________________________________ ---------------------Target Hemoglobin Level and Iron Replacement Therapy in Anemic Patients With Chronic Kidney Disease

1. In the CHOIR Study, patients were randomly assigned to receive a dose of epoetin alfa targeted to achieve a hemoglobin level of either _____ g/dL or ____ g/dL.
Answer: 13.5 or 11.3
The CHOIR Study randomized 1432 subjects in 130 centers in the United States only and looked at a high target hemoglobin of 13.5 g/dL vs a low target hemoglobin of 11.3 g/dL; 1432 subjects were divided into 715 in the high target arm and 171 in the low target arm.
2. To correct anemia in patients with chronic kidney disease, what target hemoglobin level was recommended according to results from the CHOIR Study?
Answer: 11.0 to 12.0 g/dL
Data from the CHOIR Study suggest that we should be cautious about raising hemoglobin in our patients, and the investigators concluded that the goal hemoglobin in patients with chronic kidney disease should be 11 to 12 g/dL. Since the K/DOQI group does not distinguish in their guidelines between predialysis and dialysis patients, at this stage, without more data and more studies coming out, the investigators feel that the recommendation for all patients with chronic kidney disease, given the totality of randomized controlled data published so far, should be that we should maintain a hemoglobin of 11 to 12 g/dL.
3. Which of the following is not a conclusion derived from the DRIVE I and DRIVE II studies?
Answer: Neither DRIVE I nor DRIVE II provides us with useful information on how to manage patients with anemia who have high ferritin and low TSAT levels
DRIVE I and DRIVE II provide us with information on how to optimally manage patients who fit into that category of high ferritin, low TSAT and anemia, but they may have some implications about what to do with maintenance iron. In the control group, there was evidence that participants were becoming progressively iron deficient. Their ferritins steadily fell over the 6 weeks and their CHR significantly declined. And so it may be of value despite ferritin values of above 500 to continue the low maintenance dose of iron that most dialysis patients need, not with the goal to drive the ferritin even further, but to maintain iron stores because ferritin has lost its ability to tell us about their true iron stores.
( In the dialysis population in particular, the  patients have so many factors that are causing inflammation and/or malnutrition that it's increasing the ferritin and it loses its diagnostic ability for telling us that they have sufficient iron stores. As the recent K/DOQI guidelines noted, though, a very low ferritin, in fact now at 200, they have a very high rate of being overtly iron deficient, but once we get above that the ability of ferritin to tell us they have sufficient iron stores, at least in the dialysis population, really tends to go away).
( There is a tracking between EPO-hyporesponsiveness and outcome, and I think that's a very good point because we can detect these patients clinically. Not only are these patients often patients who get hospitalized a lot more than others, but they're also individuals who have laboratory parameters, use of high doses of epoetin, however you define that, uses of high markers of inflammation, whether that's ferritin or level serum albumin or high CRP level).
Slide 22: Conclusions: DRIVE I and DRIVE IISlide 17: Dialysis Patients' Response to IV Iron With Elevated Ferritin (DRIVE)
__________________________________________________________________________________________________________________________________________________________________________________________________________________________________  ---(Creatinine, GFR, Cystatin C...) ---
Cystatin C as a marker of Renal Function & CV  risk
1. Which of the following is not a characteristic of an ideal endogenous serum marker of renal function?
Answer: Expensive and slow assay for detection
An ideal endogenous serum marker would have the following characteristics: first, it must have a constant rate of production, both across individuals and within a given individual over time. Since the synthesis of many biologically active substances in vivo is modified by various external and internal stimuli, this requirement clearly limits the pool of potential candidates. Second, it must be freely filtered across the glomerular filtration barrier. Since this barrier is both size- and charge-selective, smaller neutral or positively charged substances are more likely to fit this criteria. Third, it must not undergo reabsorption by the renal tubule into the systemic circulation or tubular secretion from the circulation. Fourth, it must undergo no extrarenal clearance. Finally, it must be simple and inexpensive to measure using automated laboratory techniques.
2. Production rates of cystatin C have been found to be independent of which of the following nonrenal factors?
Answer: Age and lean body mass
Among 381 patients with a wide range of renal function, total cystatin C production was estimated using mathematical models of renal and nonrenal clearance derived from animal model experiments by Tenstad and colleagues. Production rates of cystatin C were found to be independent of both age and lean body mass, which suggests a potential advantage over creatinine, the production of which is highly dependent on these factors.
3. How does cystatin C differ from creatinine as a marker of glomerular filtration rate (GFR)?
Answer: Studies have demonstrated greater accuracy for cystatin C in detecting reduced GFR
Numerous studies have compared cystatin C with creatinine with regard to accuracy for estimating GFR. Most, but not all, have generally supported the hypothesis that cystatin C is a more accurate measure of GFR. Dharnidharka and colleagues performed a meta-analysis of studies comparing cystatin C with creatinine in predicting GFR as measured by clearance of standard exogenous tracers. Despite limitations of the study, the results do suggest a superiority of cystatin C over serum creatinine in the prediction of GFR and detection of reduced GFR. A few other studies after this study further compared the accuracy of the 2 markers and generally showed that cystatin C had greater accuracy in identifying mild renal impairment. Several studies have compared cystatin C with creatinine as markers of renal function in the elderly including one that demonstrated that among 53 geriatric outpatients aged ≥ 70 years, cystatin C was considerably more accurate than creatinine in estimating GFR.
4. As a renal function marker, in which patient population(s) can cystatin C be most useful?
Answer: Elderly and transplant patients
Cystatin C may be especially useful in situations where muscle mass (and, hence, creatinine production) is likely to be decreased (such as in the elderly) and in the detection of mild renal insufficiency, in which creatinine levels may remain normal. In addition, there is reasonable evidence that -- at least in transplant patients -- simple cystatin C-based formulae perform better than the standard Modification of Diet in Renal Disease creatinine-based formula.
5. Cystatin C has been evaluated as a prognosticator in all of the following populations, both with and without renal disease, except which of the following?
Answer: Obese patients
Cystatin C has been evaluated as a prognostic marker in 3 at-risk populations: the general population, those with prevalent heart failure, and those with a recent acute coronary syndrome. Various studies have shown cystatin C levels to be predictive of a broad range of cardiovascular end points in the elderly, where it may have found a large niche as being a valuable adjunct to GFR calculation to identify "preclinical" kidney disease. In the Health, Aging and Body Composition study of 3075 ambulatory 70- to 79-year-old participants, cystatin C was also found to be independent and a superior predictor of mortality compared with creatinine-based measures of renal function. In addition, Jernberg and colleagues found, in 726 patients admitted with non-ST-segment elevation acute coronary syndromes, that cystatin C was the most accurate predictor of mortality when compared with creatinine and creatinine clearance.
6. In elderly subjects living in the community, impaired renal function predicts all-cause death. Which of the following statements is not true regarding cystatin C, creatinine, and estimated GFR as prognosticators in this population?
Answer: Estimated GFR, but not creatinine or cystatin C, progressive quintiles have a "J" shape relationship with annual rate of death from all causes
Intriguingly, unlike cystatin C, creatinine quintiles and GFR take on a "J" relationship for mortality risk, with those in the lowest quintile having a slightly higher risk of death compared with those in the mid quintiles. When participants in the Cardiovascular Health Study (CHS) were divided into 25 subgroups defined according to quintiles of both creatinine and cystatin C, within each quintile of creatinine, higher quintiles of cystatin C appeared to be associated with increased mortality. In addition, in the CHS, cystatin C remained a significant predictor of outcome even after adjustment for inflammatory markers. Shlipak and colleagues found that the association with progression to CKD remained significant, though attenuated, even after adjustment for the baseline creatinine levels.
7. Findings that support a potential role for cystatin C in the atherosclerotic process include which of the following?
Answer: Cystatin C is an extracellular inhibitor of cysteine proteases. Cysteine proteases such as cathepsins S and K are expressed in vascular disease and can degrade elastin and fibrillar collagens
In addition to being a marker of renal function, cystatin C is an extracellular inhibitor of cysteine proteases and may have antiatherosclerotic effects. Cysteine proteases such as cathepsins S and K are expressed in vascular disease and can degrade elastin and fibrillar collagens. In clinical human studies, cystatin C has been correlated with markers of inflammation such as C-reactive protein and fibrinogen, whereas creatinine and GFR either are not associated with these inflammatory markers or are only weakly correlated at best, but the link between cystatin C and inflammation has been inconsistent in prognostic studies.
____________________________________________________________________________________________________________________________________________________________________________________________________________________________________ ---MN/ Gatroparesis, Secondary Hyperparathyroidism, P binders *************
1. According to Dr. Finn, which of the following is not a complication in patients with progressive chronic kidney disease (CKD)?
Answer: Headache
As patients progress through the various stages of CKD, various nutritional deficiencies occur, making it common for patients to develop gastroparesis and, consequently, malnutrition. Gastroparesis can lead to dysmotility problems in the upper gastrointestinal tract in the stomach. Furthermore, malnourished patients can present with decreased serum albumin concentrations as a result of hypoalbuminemia, which is a strong prognostic indicator for long-term health.
2. When choosing a phosphate binder for diabetic patients with gastroparesis, which of the following are ideal attributes of the agent?
Answer: Selective for phosphorus, disintegrates at the time of ingestion, strong binding affinity for phosphorus, noncompetitive
A phosphate binding agent should be chosen that is appropriate and safe for the patient. The ideal binding agent is one that is selective for phosphorus and one that disintegrates at the time of ingestion. It should also have a good binding affinity for phosphorus (binds phosphorus tightly and effectively) and be noncompetitive (no competition for phosphorus binding).
3. Based on recently published guidelines from the Royal College of Physicians, which of the following is not suggested for routine monitoring in patients with stage 3 CKD?
Answer: Uric acid
Recently published guidelines from the Royal College of Physicians recommend that calcium, phosphorus, and parathyroid hormone levels be measured in all patients with stage 3 CKD. An analysis was conducted to analyze adherence to this guideline in 223,000 patients; 8434 patients had stage 3 CKD. The authors concluded that adherence to the stage 3 CKD guidelines is quite poor, followed in only 8.5% to 17% of patients, but since 80% of patients tested had normal values and due to the high cost of testing, the authors believe that routine testing of calcium, phosphate, and parathyroid hormone in stage 3 CKD was not supported.
4. According to the study by Tentori and colleagues, no difference in the risk for mortality or hospitalization was found between different vitamin D analogs. Which 2 vitamin D analogs were studied?
Answer: Doxercalciferol and paricalcitol
Tentori and colleagues reported on a comparison of different vitamin D analogs with respect to risk for hospitalization and mortality. Patients on dialysis were given either doxercalciferol or paricalcitol. After adjusting for a wide variety of covariates, no difference in the risk for mortality or hospitalization was found. The authors concluded that clinical outcomes were similar for patients treated with these 2 vitamin D analogs.
5. Which of the following is not true regarding recent clinical trial data on the safety, tolerability, and efficacy of lanthanum carbonate?
Answer: Lanthanum carbonate is neither well-tolerated nor effective
Dialysis patients previously treated with calcium-containing binders, sevelamer, aluminum-based binders, or some combination of these were changed to lanthanum starting at 1500 mg per day. The investigators concluded that the majority of patients reached the Kidney Disease Outcomes Quality Initiative (K/DOQI) targets with 1000 mg of lanthanum with each meal. In a separate study, after 6 years of exposure to lanthanum, the drug was generally well tolerated and maintained good control of serum phosphate levels. Mehrotra reported on a study of a new formulation of lanthanum carbonate, a 1000-mg tablet that is approximately the same size as a previously approved 500-mg tablet of the same drug, and demonstrated that patients reported a high level of satisfaction with total pill burden and ease of taking the medication.
6. What did Katopodis and colleagues conclude regarding the efficacy of sevelamer hydrochloride in the control of hyperphosphatemia?
Answer: Sevelamer hydrochloride is well-tolerated and has similar efficacy as aluminum-based phosphate binders
Of the commonly used phosphate binders, aluminum hydroxide is associated with aluminum toxicity. Sevelamer hydrochloride is well-tolerated, controls phosphorus levels in patients on continuous ambulatory peritoneal dialysis as well as aluminum-containing binders, and also improves the lipid profile in these patients.
Hyperphosphatemia & Phosphates,  SE of P binders--acidosis?,
PTH (1-84)/ PTH (7-34) ratio;  in the presence of hypocalcemia, the ratio increased significantly while in the presence of hypercalcemia. The presence of the 7-84 PTH fragment is the most frequent reason for the relatively high PTH level (300-600 pmol/L) noted in some patients with biopsy-proven ABD. This is an important issue, because many of these patients may be still treated as HPT. The end result is the perpetuation of high incidence of ABD.
1. According to Dr. Keith Hruska, which of the following is not a complication in patients with progressive chronic kidney disease (CKD)?
Answer: Arrhythmia
Hyperphosphatemia stands out as a very significant risk factor for cardiovascular disease. Translational studies demonstrate that in CKD, hyperphosphatemia is, in fact, a direct cardiovascular risk. Second, hyperphosphatemia can be shown to directly cause not only vascular calcification but also to cause cardiac hypertrophy and perhaps cardiomyopathy, so that we have then not only a cardiovascular surrogate, which is vascular calcification, being caused by hyperphosphatemia, we also have a hard cardiac end point that is a direct outcome of hyperphosphatemia.
2. According to Dr. Keith Hruska, which of the following phosphate binders has recently been shown to decrease vascular calcification?
Answer: Lanthanum carbonate
A recent study demonstrated that through control of serum phosphorus or by reversing hyperphosphatemia, the level of vascular calcium can be decreased with lanthanum carbonate. In the no-treatment group, CKD caused progressive vascular calcification; and in the treatment group, the levels of calcium were actually decreased so we were able to demonstrate that lanthanum carbonate decreased vascular calcification in this study. Regarding sevelamer, we do know it has direct actions on the skeleton. Sevelamer also stimulates bone formation. We don't know whether that effect on a skeleton has additional actions besides improving or contributing to control of the serum phosphorus, but at this point we also don't know whether there is any difference between any of the phosphate binders in terms of potency in reducing vascular calcification.
3. Which of the following is not a possible mediator in vascular calcification?
Answer: Low dietary intake of calcium as compared with patients without calcifications
There is a high prevalence of coronary artery calcifications in end-stage renal disease patients, and studies done in the last 4-5 years have clearly established several factors as possible mediators in vascular calcifications. They include the following: higher dietary intake of calcium as compared with patients without calcifications; hyperphosphatemia with serum phosphorus higher than 6.5 mg/dL; high calcium x phosphorus product (> 65 mg/dL); duration of dialysis -- the longer the patient received dialysis, the higher the incidence of calcifications; and age of the patient -- the younger the patient, the lower the incidence and magnitude of the calcifications.
4. Which new vitamin D receptor (VDR) activator has been shown to be very effective in controlling hyperparathyroidism while avoiding hypercalcemia and hyperphosphatemia in patients with CKD?
Answer: Paricalcitol
The new VDR activator, paricalcitol, a third generation of VDR developed with the major goal of minimization of divalent ion abnormalities, has been shown, both in the experimental animal model and in extensive phase 4 studies in double blind multicenter randomized studies, to be very effective in controlling hyperparathyroidism with minimal effects on calcium and phosphorus, thus avoiding hypercalcemia and hyperphosphatemia.
5. According to a cross-sectional analysis of baseline data from the Study for the Evaluation of Early Kidney Disease, which of the following was a relationship found between vitamin D deficiency, estimated glomerular filtration rate (eGFR), and the development of secondary hyperparathyroidism (SHPT)?
Answer: A strong association was found between low 1,25 OH2 D3 levels and the prevalence of SHPT
A cross-sectional analysis of baseline data from the Study for the Evaluation of Early Kidney Disease of an unselected cohort of CKD patients not receiving vitamin D therapy and with varying levels of renal dysfunction was performed to help clarify the relationships of vitamin D deficiency, eGFR, and the development of SHPT. Serum 1,25 OH2 D3 levels were found to decline early in CKD, before significant elevations in PTH, and low 1,25 OH2 D3 and elevated PTH are more common at higher eGFRs than previously believed. Hypocalcemia and hyperphosphatemia were noted in the later stages of CKD. Notably, multivariate predictors of low 1,25 OH2 D3 levels were diabetes mellitus, elevated urinary albumin-to-creatinine ratio, and eGFR. There also appeared to be a strong association between low 1,25 OH2 D3 levels and the prevalence of SHPT.
____________________________________________________________________________________________________________________________________________________________________________________________________________________________________  ( Phosphorus, Calcium, Bone Density & Calcification 'assessment'--- in--- CKD & ESRD Pts  on Dialysis...) ********



Books ( Who killed Health Care ?) (CPT 2006; ICD-9-CM)  ( Emergency Medicine) ******* ***************** ( The Pocket Guide to Nutrition Assessment in the Patients with CKD)*** (Atlas of Orthoses--Book); (Book; Skin Diag; Photo) (Mosby’s Body Fluids & Electrolytes) (ED; Procedures)*** (An evidence-based approach to techniques & procedures) (Mosby’s Nursing Video skills) (ACLS Pocket Survival Guide : ISBN # 1-58805-056-4) ( 5 Minute EM Consult : 0-7817-3917-9) (Drug prescribing in RF:;  ISBN # 0-943126-76-2);; (Email----for Renal dosing of drugs---- Book, Dialysable drugs---- Book);; (Tarascon Pocket Pharmacopeia); (ISBN#  1-930808-07-07/ Sanford Guide to antimicrobial therapy); (Sanford Guide to HIV/ AIDS; ISBN#  1-930808-16-X). (ICU Recall/ ISBN #  0-683-08408-9;   Griffith's 5 minute Consult;  WASHINGTON MANUAL MEDICAL THERAPEUTICS;   RESIDENT'S GUIDE TO AMBULATORY CARE                   HARRISON'S PRINCIPLES OF INTERNAL MEDICINE) (Current Medical Diagnosis & Treatment)  ----Red Book (Pediatrics); The AHA Clinical Cardiac Consult (Cardiology); Harriet Lane (Pediatrics);; (Nelson's Textbook of Pediatrics); (5 minute -Pediatric Consult); (Ask for Publications Catalogue/ 1-800-227-1770)**************** (Tel # 800-924-9053; ANCC/ FNP-- Review & Resource Manual); (Practice Guidelines to FNP/ Tel# 800-924-9053);; (FP- Pearls of Wisdom). ( 5 minute- Toxicology Consult). (Psychiatry/ DSM IV criteria & Guidelines),,s1-21-0-0-0-0,00.html (PDR/ for prescribing)

Disability Analysis Handbook (ABDA)/ (ISBN#  0-7575-1591-6); (National Directory of Independent Medical Examiners). (A Physician's Guide to Anti-Kickback Rules).

Starting a practice  / Advanced Health Assessment of Women (Prenatal Assessment / Exams/ Tests)

PDR/ Nurse's Drug Handbook; 1-4018-3548-1*********

Intravenous Medications (Has Drug Compatability Chart in the last Page); ISBN#  0-323-00985-9 (Mosby's)**********

Chemotherapy Care Plans Handbook (;  ISBN#  0-7637-0424-5

Nursing IV Drug Book;  ISBN#  0-87434-387-9*********

Handbook of Infusion Therapy;  ISBN#  0-87434-941-9***********Cal,Na...replacement....

Anesthesiology & Critical Care Drug Handbook; ISBN#  1-59195-119-9*********

Drug Information Handbook for Nursing;  ISBN#  1-59195-070-8*********Lexi-Comp/ K & Mg Replacement

Mosby's Critical Care & Emergency Drug Reference;  ISBN# 0-8016-6859-X*********(gives-- Compatible Solutions-- for Drugs)

Manual of Critical Care Nursing; ISBN# 0-323-00998-0***********Fluid & Electrolyte Disorders

Nursing Drug Reference;  ISBN#  0-323-02310-X  (Mosby's).

Nurse's Drug Facts(American Nurse's Association);  ISBN#  0-932686-76-1

Drug Guide to Psychiatric Nursing;  ISBN#  0-8036-8584-X

Nurse Practitioner's Drug Handbook;  ISBN#  1-58255-129-4

Children in Intensive Care; ISBN# 0-443-06178-5 (Churchhill Livingstone)********

Primary Care of the Newborn (MOSBY);  ISBN#  0-323-0111-X

Quick Reference for Pediatric Emergency Nursing;  ISBN#  0-7216-8327-4

Mosby's Pediatric Nursing Reference;  ISBN#  0-323-00935-2

Pediatric Drug Consult (Elsevier Mosby); ISBN#  0-323-03174-9

Problems in Pediatric Drug Therapy (Drug Intelligence Publications);  ISBN# 0-914768-53-0********

Quick reference/ child abuse ;  ISBN # 1-878060-28-7

Manual & Ambulatory Pediatrics; ISBN# 0-397-55062-6

Handbook of Poisoning;  ISBN#  1-85070-038-9

Drug Abuse Handbook (Complications); ISBN#  0-8493-2637-0

Physical Exam & History Taking- Lippincott's;  ISBN# 0-397-54783-8

Handbook of Obstetrical Emergencies; ISBN#  0-7216-6431-8

Women's Health Care; ISBN#  0-8016-8013-1

Management Guidelines for NP working with women;  ISBN#  0-8036-1116-1

Advanced Health Assessment of Women (Procedures);  ISBN#  0-7817-1826-0

Mosby's Patient Teaching Guides; ISBN#  0-8151-2933-5

Nurse's Handbook of Patient Education; ISBN# 1-58255-018-2

Handbook of Patient Teaching (Mosby);  ISBN# 0-323-01103-9

Cardiac Surgical Care (Arrhythmias..);  ISBN# 0-8016-2248-4

Dysrhythmia Recognition & Management; ISBN#  0-7216-7923-4*********

Surgical Instruments;  ISBN# 0-7216-7801-7

Wound Care;  ISBN#  1-58255-169-3

HH Nursing Procedures;  ISBN#  0-323-00911-5

Ambulatory Care Procedures;  ISBN# 0-8036-0364-9

Diagnostic Criteria from DSM-IV( American Psychiatric Association);  ISBN#  0-89042-063-7********

Handbook of Psychiatric Emergencies; ISBN#  0-87434-330-5

Handbook of Diagnostic Tests;  ISBN#  0-87434-982-6

Rapid Reference to Diagnostic Lab Tests(Mosby's); ISBN# 1-5566-4515-5

Field Guide to Disease Identification & Initial Patient Management;  ISBN# 0-8493-2030-5

Quick Reference to Triage; ISBN# 0-7817-1861-9

The Cancer CT handbook;  ISBN# 0-323-01890-4

HIV Manual for Health Care Professionals; ISBN# 0-8385-0170-2

Pearls of Wisdom (Family Practice); TEL# 800-356-7537 (OSLER.ORG)************

Renal & Genitourinary Disorders; ISBN# 1-932141-10-3

Goodheart's Photo Guide of Common Skin Diseases;  ISBN#  0-7817-3741-9 (Lippincott's)*********

Critical Care Nursing Guidelines (Mosby's); ISBN# 0-8016-6118-8*********

Emergency Nursing Reference (Mosby's); ISBN# 0-323-01108-X

Lexi-Comp's Druf Reference Handbooks;  Pediatric Dosage Handbook ( ISBN # 1-59195-166-6) ************

IV Drug Reference---Intravenous Medications ( Mosby) **********ISBN# 0-323-00986-7

Pocket Guide Critical Care Assessment; ISBN# 0-8016-6697-X

Management Guidelines for Nurse Practitioners; ISBN# 0-8036-0810-1**********

Managing Chronic Disorders; ISBN#  1-58255-442-0

Home Health- Nursing Pocket Consultant(Mosby);  ISBN# 0-8151-6125-5

Nurse's Guide to the internet; ISBN#  0-7817-2459-7

Handbook of Health Assessment;  ISBN# 0-8385-3602-6

Clinical (Tarascon Adult Emergency Pocket Book)*************ACEP

BMJ: Clinical Evidence concise ---ISBN# 1-905545-00-2 (**********


BMJ  Publishing Group--Out patient Tx of DM ( by Dr. Feit)---Summer 2006 publication **********

Lab  & Diagnostic Tests ( A Pocket Guide)---ISBN # 0-7216-7303-1

Cancer Symptom Management ( ISBN # 0-7637-0689-2)

Phlebotomy Review Guide ( From ---ASCP)

Current Medical Diagnosis & Treatment ( including---OB/GYN, PEDS)

Current Surgical Diagnosis & Treatment (FP/ Book) (Preventive Med: Book store) USMLE SMASHER (9781436351607): K.G. Paul: Books

Medical Spanish: ISBN # 1-58255-291-6

Fundamentals of Nursing     Foundations Of Basic Nursing ********(Peds Magazine) ( ECG) ( Diag Test Interpretation - Book) ( Success in Phlebotomy)

PDR for Non-Prescription Drugs/ Dietary Supplements/ Herbs--ISBN # 10: 1-56363-662-X (Exercises in Arrhythmia Interpretation)

Textbook of Pediatric Emergency Procedures (LWW)

Pocket Atlas of Pediatric Emergency Procedures

ACEP Bookstore - Electrocardiography in Emergency Medicine ( Exam Prep Books/ Tips) ( DM--Guidelines)    ISBN # 1-879091-30-5 (Joslin's Insulin Deskbook)


Putting Evidence into Practice: Palliative Care---Spring 2008 ( BMJ gp.; Commissioned by -- ( RA--Pocket Educator)  ( Renal Physiology)************************** ( Children's Art) ( Effective Parenting)

Improving Prescription Drug Container Labeling in the U.S.(ACP/ United Health Foundation/ 2008 publ.) ( Pocket survival guides--EKG/ ICU Intern/ Oncology Intern) ( RXFacts: Drug Interactions)

(A manual of lab & diagnostic texts) (Treatment guidelines for Medicine & Primary Care)—ISBN # 978-1-984323-24-8

(Essentials of pathophysiology) (Exam Prep) (Kucer’s: The use of antibiotics/ book by Lindsay Grayson) (Communicable diseases manual)

Nursing Diagnosis (by Lippincott); Nursing Drug Handbook (Lippincott)

The handbook of critical care drug therapy (ISBN # 0683-30293-0) (Baby care--Book)

Handbook of commonly prescribed drugs: 0-942447484

Tarascon pocket pharmacopoeia's%20new%20world%20spanish%20dictionary&oe=utf8&cid=3052534225639364567&ei=1ZoZTLKeDaHi2wSYkbCLBQ&sa=title&ved=0CAcQ8wIwADgA#p (Spanish Dictionary) (Essentials of Phlebotomy) (Children) (Calculator) (Indian Citzenship) (Descent of a plane)


Clinical manual of emergency pediatrics - Google Books Result (Book) (EM in Peds);jsessionid=21FF56CE86BA65C055CDB7B933FA68D0.psc1705_elshsbs_001?sid=&isbn=9780323055864&lid=EHS_US_BS-DIS-3&iid= (Flip & see ECG—Mosby; ISBN: 978-0-323-05586-4)

C:\Documents and Settings\swaroopa ramdas\Desktop\Can't-Miss ECG Findings, Life-Threatening Conditions Slideshow.mht (GP in UK)


Title: Management Principles from the Indian Epics Author: Roopa Venkatesh (Joyce Meyer/ Battlefield of the mind) (Larry King)












WebMD Medical Symptom Checker – check your medical symptoms******

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