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NKF 2007 Spring Clinical Meetings Abstracts
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231 ACUTE PHOSPHATE NEPHROPATHY (APN): AN UNAPPRECIATED ETIOLOGY OF ACUTE KIDNEY INJURY Nicholas Varverelis, Saba Azhar, Richard Snyder, Robert Pursell, Easton Hospital/Drexel University College of Medicine, Easton,PA, USA. Many patients are subjected to phosphate-based enemas in preparation for GI procedures, including colonoscopy. In patients with pre-existing CKD, the deposition of calcium and phosphate within the kidney tubule is an unappreciated etiology of acute kidney injury (AKI). We present the case of a patient with CKD who was found to have this as an etiology of AKI on renal biopsy. A 74-year-old female with a baseline creatinine of 1.5 mg/dl presented with a creatinine of 3.4 mg/dl. Her past medical history consisted of atrial fibrillation. HTN, CAD, MI. Six months prior to this presentation she had undergone a colonoscopy following the use of a phosphate-based bowel preparation. A renal biopsy demonstrated multifocal distal tubular calcification consistent with nephrocalcinosis. There was also accompanying mild tubular atrophy and interstitial fibrosis and moderate arteriosclerosis. Various case series have described risk factors for APN, many of which were applicable in our patient: advanced age, a history of hypertension and the use of ACE or ARB (our patient was on Cozaar). She may have been pre-renal at the time of the procedure. We feel that use of a phosphate-based bowel preparation is an unrecognized etiology of AKI. A question about enema use should be included in the evaluation of any patient with AKI or CKD. It may also be prudent to consider withholding the use of ACE inhibitors, diuretics, ARBs, and/or NSAIDS 48 hours before a procedure if an enema preparation is to be used. Finally, an estimate of a steady state creatinine by MDRD should be calculated before such a procedure to better stratify a person’s risk of acquiring AKI.
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EFFECT OF BLOCKING THE RENIN ANGIOTENSIN ALDOSTERONE SYTEM (RAAS) ON REFRACTORY FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS) TO LOWER BLOOD PRESSURE AND DECREASE PROTEINURIA TO PRESERVE GLOMERULAR FILTRATION RATE (GFR) AND SLOW PROGRESSION TO END STAGE RENAL DISEASE (ESRD) Charanjit Vedi, Kyle Knuppel, Meenal Shah, Allan B. Schwartz, Drexel College of Medicine, Philadelphia, PA FSGS leads to rapidly progressive scarring or sclerosing of capillaries, deterioration of kidney function and ESRD, dialysis/transplantation. FSGS causes proteinuria (P) from asymptomatic microalbuminuria to large symptomatic nephrotic syndrome, >3,500mg/24h and hypertension. We treated 8 patients 3-5 years with kidney biopsy proven FSGS. Serial studies included P, BP, electrolytes, serum creatinine and GFR in response to combination therapy interfering with the RAAS. Medications were in 4 categories: I.Angiotensin-Converting Enzyme Inhibitors (ACE I), II.Angiotensin Receptor Blockers (ARB), and III.Aldosterone Receptor Antagonist (ARA) or Selective ARA (SARA) plus IV.immunosuppressives, corticosteroids and mycophenolate. Poor response to corticosteroids defined refractory. Mycophenalate was used as a last resort. As medications were added, a decrease in P occurred in 8/8 patients. Treatment with 3 drugs blocking the RAAS caused progressive reduction of BP and P preventing rapid deterioration of GFR in all 8 patients while adhering to the therapeutic regimen. In 6/8 long term compliant patients, P and BP were reduced progressively. 2/8 patients became delinquent and noncompliant leading to rapid reduction of GFR and subsequent hemodialysis within 6-9 months. FSGS prognosis correlates with BP & P reduction preventing ESRD. Anti-RAAS treatment effectively reduced P and BP in 8/8 patients while compliant, slowing down the loss of GFR. 2 Anti-RAAS noncompliant patients had rapid deterioration of kidney function requiring hemodialysis. Patients with FSGS should be treated early and continuously with combinations of Anti-RAAS medications. Frequent testing of potassium and creatinine are required. Future larger trials are in design.
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THE EFFECT OF HYPONATREMIA ON THE SAFETY AND EFFICACY OF NESIRITIDE Raghava Velagaleti, Leslie Franke, John Clements all affiliated with Synergy Medical Education Alliance, Saginaw, MI, USA. BACKGROUND: The interaction between vasoactive therapy and serum sodium is well known. Nesiritide, when used in acute decompensated heart failure, occasionally decreases serum sodium. Whether pre-existing renal dysfunction alters the efficacy and safety of this drug is unknown.This study assessed the hypothesis that preexisting renal dysfunction does not alter the safety and efficacy of nesiritide. METHODS: Data were collected on 183 consecutive patients who were admitted to our hospital, enrolled in the ADHERE registry (Acute Decompensated Heart Failure National Registry) and received nesiritide. The data were abstracted with a prespecified data collection sheet from a combination of patient charts and the ADHERE database. Measured serum sodium was used to classify patients into tertiles of natremia and also as a continuous variable. Improvements in Cardiac Index(CI), Systemic Vascular Resistance(SVR), Thoracic Fluid Content(TFC), symptoms and Length of Stay(LOS) were used as efficacy variables. Hypotension and ventricular arrhythmias were the safety variables. ANALYSIS: Chi-square was used to determine differences in distribution of categorical outcome variables. ANOVA was used to determine differences in means of continuous outcome variables. Regression analysis and a General effects model were used to determine if baseline differences between the groups had any confounding effect on the results. RESULTS: In the sample, 52% were men, 76% were caucasian and their mean age was 72 years. No significant difference was found between different sodium groups with respect to any of the safety or efficacy variables. Secondary analysis of different sub-groups with respect to possible confounders revealed no effect on primary result. CONCLUSION: This study did not reveal any effect of baseline serum sodium on the safety or efficacy of nesiritide when administered to patients with acute decompensated heart failure.
CONVERSION TO LANTHANUM CARBONATE MONOTHERAPY MAINTAINS SERUM PHOSPHORUS CONTROL AND REDUCES TABLET BURDEN IN PATIENTS WITH CHRONIC KIDNEY DISEASE STAGE 5 Nirupama Vemuri, South Florida Nephrology Group PA, Coral Springs, FL, USA Control of serum phosphorus (SP) is important for reducing morbidity in chronic kidney disease (CKD) Stage 5. Most oral phosphate binders require a high tablet burden that may diminish compliance. Lanthanum carbonate (LC) is an effective, non-calcium phosphate binder that is well tolerated by patients with CKD Stage 5. A large Phase 4 US study assessed the conversion from other phosphate binders (sevelamer and calcium-based binders) to LC monotherapy in a clinical practice setting. After a 1-week observation period on previous binders, phosphatebinder therapy was changed (no washout) to LC for a 12-week titration period, followed by a 4-week LC maintenance period. SP, daily dose, and tablet burden were assessed at baseline and at weeks 12 and 16. A total of 2763 patients were enrolled; 2643 patients (59% men; 49% diabetic; mean age, 56.4±14.3 yrs; median dialysis vintage 2.6 yrs) were in the safety population and 2520 comprised the intent-to-treat population. Patients previously maintained on a mean calcium-based binder dose of 5.4 g/day (n=1045) were titrated to mean LC doses of 2.7 and 2.6 g/day at weeks 12 and 16, respectively; mean SP was 6.01 mg/dl on calcium binders, 5.97 mg/dl at LC week 12, and 6.09 mg/dl at LC week 16. Patients maintained on a mean sevelamer dose of 7.6 g/day (n=958) were titrated to mean LC doses of 2.8 and 2.7 g/day at weeks 12 and 16, respectively; mean SP was 5.90 mg/dl on sevelamer, 5.86 mg/dl at LC week 12, and 5.94 mg/dl at LC week 16. At week 12, tablet burden was reduced by 35% and 28% for patients previously taking sevelamer and calcium-based binders, respectively (P<0.001 for both), with similar reductions at week 16. In a clinical practice setting, conversion to LC monotherapy maintained SP with significant reductions in both daily dose and tablet burden. Effective LC doses for most patients were ≤3 g/day, which can be provided by one 1-g reformulated LC tablet with each meal, simplifying treatment and potentially improving patient compliance.