169HYPERCALCEMIA DUE TO VALACYCLOVIR TOXICITY Ang Li, Jharna Nitin Shah, Sreedhar Mandayam Baylor College of Medicine, Houston, Texas Hypercalcemia is a common complication in hospitalized patients. We report a case of symptomatic hypercalcemia in an elderly lady after she received 2 courses of inappropriately-dosed valacyclovir. An active 80 year old woman with CKD III (eGFR 53 mL/min) developed shingles and received 7 days of valacyclovir 1000 mg PO TID. She was subsequently admitted for severe abdominal pain and constipation. Her initial labs showed mildly elevated serum calcium of 10.7 mg/dL and her condition improved with supportive treatment. She then received 10 more days of high-dose valacyclovir for recurrent shingles, after which her hypercalcemia worsened to 13.5 mg/dL and she developed altered mental status, acute kidney injury, respiratory distress, hepatic dysfunction, anemia, and thrombocytopenia. Upon transfer to our institution, valacyclovir was immediately discontinued and a work-up for hypercalcemia was initiated (see below), including an extensive malignancy work-up with breast biopsy, thoracentesis, CT chest/abdomen/pelvis, and bone scan, all of which revealed no malignancy. Valacyclovir toxicity from inappropriate dosage for her renal function was suspected to be the culprit. She was treated with isotonic saline, IV furosemide, subcutaneous calcitonin, IV pamidronate, and IV hydrocortisone. Her serum calcium improved over the next 7 days to 9.9 mg/dL and her neurological, renal, respiratory, hepatic, and hematopoietic functions also improved. In conclusion, we report a case of severe symptomatic hypercalcemia due to valacyclovir toxicity inappropriately dosed for renal function. Practitioners need to be aware of this possible complication. Test Result Interpretation Ionized Ca 1.68 mmol/L (H) Confirms hyperCa Intact PTH 4.5 pg/mL (L) Suggests non-PTH hyperCa FeCa 14% (H) r/o familial hypocalciuric hyperCa PTHrP 20 pg/mL (N) r/o humoral hyperCa of malignancy 1,25 Vit D 40 pg/mL (N) r/o lymphomas or granulomas SPEP/ UPEP

No monoclonal/ light chains (N)

r/o multiple myeloma

170TREATMENT OF 25-OH VITAMIN D DEFICIENCY IN PATIENTS WITH MODERATE CHRONIC KIDNEY DISEASE REDUCES CARDIOVASCULAR EVENTS Anton Lishmanov, Smrita Dorairajan, Youngju Pak2, Kunal Chaudhary, Anand Chockalingam, Harry S. Truman Memorial Veterans’ Hospital1 and University of Missouri School of Medicine2,Columbia, Missouri Observational studies in healthy people suggest an inverse relationship between serum 25-hydroxyvitamin D (25OHD) levels and cardiovascular (CV) mortality. Treating vitamin D deficiency in patients with moderate chronic kidney disease (CKD) may reduce CV events in this high risk population. Study data was abstracted from Harry S. Truman Memorial Veterans Hospital electronic medical record system. Medical records of all veterans who had CKD stage 3 and 4 and had 25OHD levels determined from 4/2006 to 9/2007 were reviewed. Patients with 25OHD deficiency, serum level <30 ng/ml, were included (n= 126, all men, mean age 70 years). Successful 25OHD replacement was defined as prescription of ergocalciferol sufficient to increase serum 25OHD level by 25% from baseline within 6 months (treatment group, n=90). Otherwise patients were considered as untreated controls (n=36). During median follow up 27.2 months, 44% of controls had CV events while only 21 % of the patients in the treatment group had CV events (p= 0.001). In multivariate logistic regression analysis adjusting for CV events predictors age, initial PTH level, statin use, history of CV disease and GFR, the estimated odds ratio (OR) for 25OHD replacement status was 0.37 (95% Confidence Interval, CI : 0.14- 1.0). Both overall survival and disease specific survival were shown to be lower in the untreated group and the difference in survival curves were statistically significant (p-values=0.008, 0.02, respectively). Treatment of 25-OHD deficiency with ergocalciferol in moderate CKD patients is associated with significant reduction in cardiovascular events.

171ANABOLIC STEROIDS:BODYBUILDER’S BEST FRIEND OR WORST ENEMY Devang Lodhavia, Jatinder Singh, Zohreh Soltani LSU-Health Sciences Center, New Orleans, LA. Introduction: The non-therapeutic use of anabolic steroids and protein supplements is common among amateur bodybuilders. Although FDA issued public health advisory warning consumers to stop using any bodybuilding product that contains anabolic steroids in 2009, unfortunately these compounds are still available and used by young adults without realizing the serious side effects.. We report a case of cholestasis-induced kidney injury (CIKI) secondary to anabolic steroid-enriched dietary supplement (testadrol). Case: A 31 year old male presented with jaundice and abdominal pain after taking testadrol supplements for 3 weeks. Labs showed total bilirubin of 34mg/dl, AST 63 u/L, ALT 222uU/L and normal renal function. Abdominal imaging studies, and other labs including acute hepatitis panel were unremarkable. Therefore, jaundice was attributed to testadrol- induced cholestasis and supportive treatment was initiated. 3 weeks later, although the steroid had been discontinued, patient’s clinical condition deteriorated and he was readmitted with persistent vomiting and nausea. Laboratory results were significant for a creatinine of 15.6mg/dl, Na 111 mmol/L, Total bilirubin 59mg/dl, AST 140 u/L, ALT 62 u/L, INR >9.7, CPK 5785u/L, Cl 71 mmol/L, HCO3 17mmol/L and positive myoglobinuria. His spun urine was consistent with acute tubular injury (ATN). Due to oliguria and metabolic acidosis, he was started on renal replacement therapy for few hours. Ursodeoxycholic acid was also initiated for liver dysfunction.. After 48 hours, the urine output improved and Na trended up to128 mmol/L.. Discussion: CIKI due to anabolic steroids is reported in few cases. The exact mechanism still remains unclear. Our case is further remarkable because it is the first report of the constellation of CIKI, hyponatremia and rhabdomyolysis. In spite of elevated CPK and myoglubinuria, our patient never reported history of recent exercise, muscle injection, and muscle pain. We believe that his severe liver injury, persistent vomiting, low oral intake, and AKI resulted in severe hyponatremia. The rhabdomyolysis would occur because of severe hyponatremia which were also reported in PUBMED.

172ERYTHROPOIESIS-STIMULATING AGENTS (ESAs) ORDER SET USAGE: IMPROVEMENT IN UTILIZATION & COST SAVINGS ACROSS CROZER KEYSTONE HEALTH SYSTEM. COMPARING PRE AND POST IMPLEMENTATION ERA Ahad Lodhi, Richard Pacitti, , David Showalter , C. Nathan Okechukwu, Crozer-Chester Medical Center, Upland PA Erythropoietin stimulating agents (ESAs) are expensive medicationswith significant impact on many health-system budgets. Payers have curtailed ESA reimbursements and excess use has been linked to increase risk of cancers and stroke. Hospitals are developing strategies to optimize ESA use. Crozer Keystone health system developed an ESA order set based on FDA recommended ESA uses along with proper dosing interval, targeting and monitoring response according to hemoglobin levels. Crozer Keystone Pharmacy and therapeutic committees approved ESA order set for use in March 2007, mandating its use in 2008. Data was obtained from CKHS Pharmacy records. Buying, utilization and ESA administration records were reviewed. Comparison was made pre and post March 2007. Cost, units of ESA use and number of treatments given were analyzed. ESA use decreased progressively 34.13%, 43.25% and 13.57% from 2006-2009, with a 58.1% (116.5 million units) reduction comparing 3 years pre and post ESA order set initiation. After ESA form initiation in March 2007, cost decreased 30.88% ($887,698), 51.23% ($928,367) and 28.67% ($253,410) respectively from 2007-2009. There was an overall cost reduction of 57.4% ($3,935,574) comparing 3 years pre and post order set implementation. ESA treatments administered remained similar; 28,826 compared to 24, 699 after order set implementation. The mandatory order set helped CKHS optimize ESA use. Most notably realizing cost savings, without significant loss of treatments provided and minimizing the complications associated with excess ESA use.

NKF 2011 Spring Clinical Meetings Abstracts

Am J Kidney Dis. 2011;57(4):A1-A108 A59