NKF 2014 Spring Clinical Meetings Abstracts

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WHEN HAVE YOU SAID TO MUCH ? COUNSELING FOR STONE PREVENTION R. Allan Jhagroo, Margaret Wertheim, Kristina L Penniston, University of Wisconsin, Madison, WI Nutrition therapy to prevent urolithiasis is endorsed. But there are questions about patients' compliance with and adherence to dietary changes, which may be significant in some cases. We sought to determine patients' recall of nutrition recommendations provided to them at a stone clinic visit. Patients were provided nutrition recommendations by a Registered Dietitian and the nephrologist in our stone clinic in our usual consultative fashion. We surveyed stone formers (SFs) who had received nutrition counseling at a clinic visit within 4 months. SFs were asked to identify the nutrition recommendation(s) provided to them from a list of possibilities. We assessed difficulty following and willingness to continue nutrition therapy using Likert scales. SFs (n=17, M:F 12:5, 61±8 y) were provided an average 3.2±1.1 recommendations each (range, 1-5). All were provided written handouts outlining their individualized plan. The most common recommendations provided by the RD were to increase fruits and vegetables to ≥5 servings/d, increase fluids by a specific amount determined for each patient, and increase and/or change the distribution of calcium intake throughout the day. All recommendations made were correctly recalled by 35% of patients. The overall recall rate was 65 ± 31%. Patients provided ≥ 3 recommendations had a 28% perfect recall rate vs. 50% in those provided ≤ 2 recommendations. Despite 24% of patients reporting difficulty in following the recommendations, 87% rated the recommendations "acceptable," 76% reported following the plan all or most of the time, and 100% said they were willing to keep trying. SFs have a strong willingness to comply with individualized nutrition therapy regimens. Adherence, however, may depend on patients' recall of the recommendations, which, in our study was 65 ± 31%. SFs provided less than 3 recommendations had a higher recall rate than those provided more.

INCIDENCE AND OUTCOME OF PATIENTS RECEIVING CRRT AT A TERTIARY CARE HOSPITAL OF UNITED ARAB EMIRATES Chandra Mauli Jha, H. Dastoor, A. Madani, A. Chaaban, S. Abouchacra, F. H. Omer, A. Saxena, Mafraq Hospital, UAE. Information on the practice of CRRT in the region of Gulf

Coordination Council) is scarce. “PubMed Search” for CRRT in different GCC counties yielded only two articles on CRRT in Saudi Arabia. There was no study of CRRT in UAE. CRRT is a costly therapy with a great impact on health care expenditure. Information on this subject shall have tremendous usefulness in health care planning and budgeting in the region. With this purpose we performed a retrospective study of patients admitted to all adult acute care units – surgical, coronary & Medical – of Mafraq Hospital and to whom CRRT was administered during one year period from 1st November 2012 to 31st October 2013. Mafraq Hospital is one of the two tertiary care Hospitals in the city of Abu Dhabi, capital of UAE. Nephrology Division record, Hospital’s statistics department record & computerized record of Hospital patients were used to obtain demographic and clinical information. Statistical Analysis was performed in “Excel”. 2.91% (total 42) of 1440 patients hospitalized in critical care area

during the study period required CRRT. Among those, 28 patients died, 10 patients recovered completely and 4 patients survived with ESRD. CRRT requiring patients were 40%, 27% & 33% from Surgical, Medical & Coronary ICU respectively. APACHE score ranged from 7 to 40. Age distribution ranged from 18 years to 101 years. Sex, age & APACHE score etc. were not predictive of survival. Hospitalization in Coronary ICU versus surgical or Medical ICU was significantly associated with mortality (14% survival in CICU patients versus 27 & 29% survival in MICU & SICI patients respectively). Finding of this study is in sharp contrast to study in Saudi Arabia

(Incidence of CRRT in Saudi Arabia 9% versus 2.9% in UAE, Females requiring CRRT: 21.5% in UAE versus 45.6% in Saudi Arabia). Difference may lie in population demographic which requires further analysis. A larger retrospective study and a prospective study at one centre or involving multiple centres are required to throw further light on this subject of great importance.

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ACUTE KIDNEY INJURY FROM MULTIPLE ETIOLOGIES FOLLOWING KIDNEY TRANSPLANTATION IN A PATIENT WITH ALPORT SYNDROME:Arksarapuk Jittirat, Heidi Schaefer, J.Harold Helderman, Paisit Paueksakon, Vanderbilt University School of Medicine, Nashville, TN, USA Alport Syndrome is a rare genetic disease caused by mutations in genes encoding the alpha-3, alpha-4, and alpha-5 chains of type IV collagen, which locate in the glomerular basement membrane of the kidney, cochlea and eye. Patients usually present with hematuria, proteinuria, hypertension and renal insufficiency associated with sensorineural hearing loss and ocular defects. Anti-glomerular basement membrane antibody (anti-GBM Ab) disease, a rare complication, can occur in up to 3% of patients with Alport syndrome who have undergone kidney transplantations. We report a case of a 32-year-old man with ESRD from Alport syndrome who underwent a 3-antigen mismatched living unrelated renal transplant in 2010. He was induced with alemtuzumab and maintained on tacrolimus and mycophenolate mofetil (MMF). The panel reactive antibody was 0%. Subsequently, MMF was switched to mycophenolic acid due to diarrhea, and prednisone was added to the immunosuppression regimen. His baseline creatinine had been 1.8-2.4 mg/dL. Two years post-transplant, his creatinine was noted to be 3.4 mg/dL with urine protein to creatinine ratio of 3.9. Kidney transplant biopsy was performed. The biopsy showed acute cellular rejection, post transplant anti-GBM antibody without crescentic glomorulonephritis, calcineurin-inhibitor toxicity, and predominantly mesangiopathic immune complex glomerulonephritis. There is also acute humoral rejection with diffuse peritubular capillary staining for C4d. The donor specific antibody was detected against DQ2. The patient was successfully treated with methylprednisone, plasmapheresis, intravenous immunoglobulin and rituximab with improvement of allograft function back to baseline. The etiologies of acute kidney injury in post transplant patients with Alport syndrome can be quite protean. We present a patient who has a combination of multiple etiologies found in kidney transplant biopsy including an evidence of anti-GBM Ab.

ACUTE ON CHRONIC HYPONATREMIA DUE TO AMIODARONE INDUCE HYPOTHYROIDISM IN A PATIENT WITH CHRONIC SYNDROME OF INAPPROPARIATE ANTIDIURETIC HORMONE (SIADH) Thanavut Jiansakul, Tamim Naber, Atlantic Care Medical Center, Atlantic City NJ Amiodarone is a class III antiarrhythmic agent with high iodine content. Hypothyroidism occurs in 8-10 % of patients. Another complication which is very rare is Amiodarone induced SIADH. We represent a complicated case of acute on chronic hyponatremia in a patient known to have SIADH after starting on Amiodarone therapy and developed severe hypothyroidism. A 67 year-old male farmer with a past history of chronic hyponatremia due to syndrome of SIADH, atrial flutter, remote history of alcohol abuse, and hypertension. Patient known to have chronic idiopathic SIADH on fluid restriction and furosemide therapy with sodium level maintained on average (130-134) mmol/L. Two months prior to this admission, he was started on Amiodarone and Dabigatran for new onset atrial flutter. This time, he presented with a sudden onset of dizziness, weakness, and change in mental status while at work. Blood pressure was 143/101 mmHg with normal exam and no edema. Serum sodium was 118 mmol/L, serum osmolality 267 mOsm/kg, potassium 3.8 mmol/L, creatinine 0.7 mg/dL, thyroid stimulating hormone 127 uIU/ml (initially was 3.75uIU/ml), Amiodarone level 1.2 mcg/ml, urine osmolality 241 mOsm/kg, urine sodium 101 meq/L, urine creatinine 54.7 mg/dl. Thyroglobuin and thyroid peroxidase antibodies were negative. Patient was treated with stopping Amiodarone, starting Levothyroxine, water restrictions, and Demeclocycline therapy. Serum sodium improved back to baseline and patient’s symptoms improved. We represent a complex case of acute hyponatremia superimposed on chronic SIADH in a patient after starting Amiodarone therapy. Although very rare, Amiodarone induced hyponatremia can be serious and complex. We would suggest having high threshold to start Amiodarone therapy in a patient with hyponatremia for any reason. We also stress the importance of monitoring sodium level and thyroid stimulating hormone for each patient on Amiodarone therapy.

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Am J Kidney Dis. 2014;63(5):A1-A121