Abstract: FR-PO627
A Surprise Diagnosis: Oxalate Nephropathy
Session Information
- Trainee Case Reports - IV
October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Reports
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Shah, Deep, Ohiohealth Riverside Methodist Hospital, Columbus , Ohio, United States
- Jordan, Kim, Ohiohealth Riverside Methodist Hospital, Columbus , Ohio, United States
Introduction
Hyperoxaluria can cause acute kidney injury (AKI) or chronic kidney disease (CKD) from oxalate crystal deposition. We present a surprising diagnosis of oxalate nephropathy in an elderly female.
Case Description
A 75-year-old female presented with dyspnea, weight gain, and edema. She had diastolic heart failure, CKD stage 3 attributed to insulin-requiring diabetes, and prior partial colectomy for ulcerative colitis. Furosemide was increased two weeks prior because of symptoms, but no other medication changes were noted. Admission serum creatinine was 8.1 mg/dl, (1.6 mg/dl baseline). AKI was attributed to cardiorenal syndrome, but she failed to improve with intravenous furosemide, and hemodialysis was started. Echocardiography showed mild left ventricular hypertrophy and atrial dilation, EF 60-65%, and grade 2 diastolic dysfunction. Protein and moderate blood were noted on urinalyis, but casts and crystals were not reported. Renal ultrasound found mild asymmetry in kidney size, few simple renal cysts, and hyperechoic cortices. Serum complement levels, anti-GBM, ANA, ANCA, urine protein electrophoresis and serum immunofixaton studies were normal. Kidney biopsy revealed acute tubular necrosis with prominent oxalate crystals, urine eosinophils, mild fibrosis, and interstitial changes consistent with oxalate nephropathy. The patient reported consumption of one gallon of iced tea daily for 20 years. While on hemodialysis, plasma oxalate was 15.4 micromol/L (normal <11) with urinary oxalate excretion of 11.4 mg/24 h (normal <40 mg/24 h). Calcium supplementation was started and she was instructed to maintain high water intake, avoid iced tea consumption, and begin a low oxalate, low vitamin C, calcium-enriched diet. The patient remains on hemodialysis post-discharge.
Discussion
Hyperoxaluria can be primary from enzymatic deficiency, or secondary from gastrointestinal disease, malabsorption syndromes, excessive vitamin C ingestion, and ethylene glycol toxicity. However, ingestion of oxalate-rich foods, including spinach, beets, rhubarb, peanuts, star fruit, and iced tea should also be considered. Despite documented excess dietary oxalate intake in individuals in the United States, reports speculate that oxalate nephropathy is under-recognized. Physicians should consider oxalate nephropathy in the right clinical scenario, in this case, excessive iced tea and underlying gastrointestinal disease.