NKF 2015 Spring Clinical Meetings Abstracts
269 USE OF RENIN ANGIOTENSIN ALDOSTERONE SYSTEM BLOCKADE (RAASB) MAY BE BENEFICIAL IN PATIENTS WITH ACUTE KIDNEY INJURY (AKI): C. Suarez-Fuentes, K.Rausa, J. Kreimerman, L. Golestaneh, M. Melamed, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, NY, USA RAASB has protective effects in patients with diabetic nephropathy and congestive heart failure (CHF). Animal models suggest that RAAS inhibition has renoprotective effects on ischemic AKI. Exposure to RAASB is associated with AKI in hospitalized patients and early discontinuation is recommended. Based on animal data, we hypothesized that exposure to RAASB has a protective effect in patients with hospital acquired AKI. Medical records were obtained for all patients admitted between 2008 and 2010 at Montefiore Medical Center. AKI was defined as a 50% increase in serum creatinine over a pre-admission value and mortality data was collected via linkage to the Social Security Death Index. There were 46,580 admissions meeting our eligibility criteria. 2,104 patients developed AKI (5%) and 33% had exposure to RAASB. Those developing AKI were more likely to have higher Charlson scores (2.3 versus 2.0, p=0.001), diabetic complications (5.8% versus 4.4%, p<0.001) or an eGFR that was less than 60 ml/min/1.73 m(2) (37% versus 22% p<0.001). RAASB was not associated with a higher risk of developing AKI (OR 0.95, 095% CI 0.85, 1.07). In a multivariable model, patients who developed AKI had higher risk of mortality (OR 1.37, 95% CI 1.16, 1.60). Patients that had exposure to RAASB had a lower risk of mortality overall compared to patients who did not receive RAASB (OR 0.72, 95% CI 0.66, 0.78) independent of AKI status. We identified 653 patients who developed AKI and were on RAASB. Of these, 306 patients were continued on the RAASB and 51 died (17%) while RAASB was discontinued in 347 patients and 72 (21%) died (p=0.18). Hospital acquired AKI is common and has a high risk of mortality. Our data suggest that RAASB did not increase the risk of AKI in hospitalized patients and RAASB in hospitalized patients was associated with a lower risk of mortality. Studies are needed to examine whether stopping RAASB upon the development of AKI has an effect on mortality and severity of AKI outcomes.
270 COCCIDIODOMYCOSIS MASQUERADING AS BREAST MASS Sukumaran Nair S, Patron RL, Niska JR, Huskey JL, Pockaj BA, Chakkera HA Mayo Clinic, Phoenix, Arizona Coccidioides immitis is a dimorphic fungus endemic to the southwestern United States. Disseminated coccidioidomycosis occurs in 1 in 200 infected patients and can infect skin, bones and joints, lymph nodes, and meninges. Though it can infect almost any part of the body, infection of the breast tissue is reportedly uncommon. We describe a patient with end stage renal disease (ESRD) being evaluated for kidney transplantation who was found to have an unusual manifestation of disseminated Coccidiomycosis presenting as elevated serum titers and a breast nodule found on imaging work-up. A 42-year-old Navajo male with history of type 2 diabetes ESRD on dialysis for a year presented for kidney transplant evaluation. He had good functional capacity and no constitutional symptoms. As part of his pre-transplant work-up, a laboratory test revealed Coccidioides complement fixation titer to 1:64 that subsequently led to a CT scan of the chest. CT chest demonstrated a 2.3 cm soft tissue mass in the right breast with enlarged right axillary adenopathy and 3 small subcentimeter subpleural nodules on left lung. Mammogram with targeted right-sided ultrasound demonstrated a well-circumscribed mixed echogenicity oval mass with a thick vascular periphery, measuring 1.7 x 2.7 x 1.3 cm, and a lymph node in the R axilla with an eccentricallyshaped cortex measuring 10 x 6 mm. Percutaneous core biopsy of the breast mass and axillary lymph node were performed. Pathology revealed foci of necrobiotic granulomatous inflammation in both the breast mass and lymph node with GMS stain demonstrating spherules of Coccidioides immiti in the lymph node but not breast mass. Given the fact that he had extrapulmonary manifestations with a high antibody titer, it was assumed he had disseminated Coccidioides and an MRI of the brain, spinal tap, and bone scan was ordered. He was started on fluconazole while awaiting the results of the above-mentioned studies. This case highlights the ubiquitous presentation of Coccidiomycosis, especially in immunosuppressed milieu, which both diabetes and ESRD represent. The case also emphasizes the importance of screening and adequately treating patients residing in endemic areas prior to their exposure to immunosuppression after transplantation.
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271 IMMUNOTACTOID GLOMERULOPATHY WITH MEMBRANOUS PATTERN IN PATIENT WITH RHEUMATOID ARTHRITIS AND MONOCLONAL GAMMOPATHY G. Sultan, G. Agarwal, K. Dah, B. Wagner and S. Werner. Department of Nephrology, University of Texas, San Antonio, TX, United States; Department of Pathology, University of Texas, San Antonio, TX, United States and Department of Nephrology, South Texas Veterans Health Care System, San Antonio, TX. Immunotactoid Glomerulopathy (IMTG) is a rare cause of glomerular renal disease and frequently leads to end stage renal disease within a few years. The optimal treatment is still uncertain although steroids and other immunosuppressive agents have been tried with variable success. Proteinuria and microscopic hematuria occurred in a 69 year old male with history of rheumatoid arthritis receiving infliximab and sulfasalazine. Past medical history was significant for ground glass changes of the lungs (by computed tomography imaging), hypertension and monoclonal gammopathy of undetermined significance. Serum chemistries were non–contributory. Urine sediment was notable for one dysmorphic red blood cell and no casts. A 24 hour urine collection revealed 600 mg of protein. His serologic evaluation for proteinuria was negative for hepatitis B panel, hepatitis C, human immunodeficiency virus, rapid plasma reagin, cryoglobulins, anti– nuclear antibody, double–stranded DNA antibody and anti–neutrophil cytoplasmic antibody. Complement C3 and C4 were normal. His serum protein electrophoresis showed an increased beta and gamma fractions with a possible monoclonal spike in the beta region. Immunofixation electrophoresis showed monoclonal bands in IgA/kappa and free kappa chains. Kidney biopsy showed morphologic changes consistent with immunotactoid glomerulonephritis with a membranous pattern. Most cases of ITGN are reported as idiopathic but screening for occult malignancy, paraproteinemia and autoimmune diseases should be always considered once the diagnosis is established, as the treatment of the underlying disease will have great impact on the renal prognosis.
272 PERITONEAL DIALYSIS-RELATED PERITONITIS CAUSED BY STREPTOCCUS BOVIS BIOTYPE-II/1: G. Sultan, H. Manickam, K. Dah, T. Auger, R. Kessler and S. Bansal. Department of Medicine/Nephrology, University of Texas, San Antonio, Texas, USA. Streptococcus bovis subspecies are rarely reported to cause PD related peritonitis. S. bovis biotype-I infection has been associated with endocarditis or intestinal pathologies. Contrary, S. bovis biotype-II associates with chronic liver disease. To our knowledge, we present the first case of S. bovis biotype-II/1 (S.infantarium) related peritonitis. A 57-year-old male presented to PD clinic with abdominal pain and hazy peritoneal fluid for 1 day. The patient was recently diagnosed with ESRD due to diabetic nephropathy and had undergone manual PD training. He had been discharged from the clinic 48 hours prior to presentation to perform manual PD independently at home. Physical exam showed temperature 99.3 F, BP 92/50 mmHg and HR of 85/minute. Abdomen was soft but tender on palpation. Peritoneal catheter exit site had no erythema or discharge. Dialysis fluid was extremely hazy with visible sediment. The patient was given empirical treatment with intraperitoneal (IP) vancomycin, cefepime and heparin and admitted to the hospital. Examination of peritoneal fluid showed white blood cell count of 26,630/ mm3 (90% neutrophils). Culture of the peritoneal effluent revealed Streptococcus bovis biotype II. He improved clinically within 48 hours. Peritoneal effluent became clear and cell count decreased to 161/mm3 within 72 hours. The patient was treated with 1 gram IP vancomycin every 4 days for 2 weeks with complete recovery. The patient was not found to have any evidence of chronic liver disease. S. bovis biotype II is unlikely to cause infective endocarditis or colonic neoplasm; therefore it is important for the microbiology laboratory to identify the biotype of S. bovis as this can determine the necessity of performing particular investigations to rule out any underlying disease.
Am J Kidney Dis. 2015;65(4):A1-A93