Clinical Geriatrics

Introduction
The incidence of acute kidney injury (AKI) is increasing. In an analysis using the Medicare 5% Sample Beneficiary Standard Analytical File for the years 1992 through 2001, Xue et al¹ noted that the incidence rate of AKI increased by approximately 11% per year. Chronic kidney disease commonly complicates AKI and may lead to end-stage renal disease (ESRD), requiring chronic renal replacement therapy. We present a case of an elderly woman who developed ESRD as a complication of absorptive hyperoxaluria, a rare and potentially reversible cause of ESRD.

Case Presentation
An 87-year-old African-American woman was admitted to a community hospital for evaluation of anorexia and polyuria. Her laboratory tests showed severe renal failure. On a previous hospitalization five months earlier for the treatment of paroxysmal atrial fibrillation, her blood urea nitrogen was 10 mg/dL and serum creatinine was 1 mg/dL. She had mild systolic hypertension and a vague history of asthma. Her current medications included enalapril 2.5 mg, carvedilol 3.125 mg, warfarin 2.5 mg, vitamin C 1000 mg, albuterol inhaler, and 3 tablets of calcium carbonate 600 mg plus vitamin D 400 IU. The patient did not take any over-the-counter medications and did not smoke or drink alcohol. She had no drug allergies.

A review of systems revealed a weight loss of 2-3 pounds since her last hospitalization and polyuria. She denied having diarrhea but admitted having a bowel movement after each meal. Physical examination showed: height, 61 inches; weight, 126 pounds; body mass index 23.8; temperature 97.0 degrees F; blood pressure 130/80 mm Hg; pulse 78 per minute; and respirations 16 per minute. The entire examination was normal except for an irregular heartbeat. The Table provides the laboratory tests.

Other results were urinalysis pH: 6.5; specific gravity, 1.010; bilirubin, ketone, and blood were negative, with a trace of protein; white blood cell count was 7400/μL; and red blood cell count was 3.59 x 10⁶/μL. Ultrasound showed both kidneys to be 9.5 cm in length with mild cortical thinning and increased echogenicity. Her daily urine volume ranged between 2000-2600 mL.

Warfarin was withheld, enalapril and vitamin C supplements were discontinued, and amlodipine 5 mg daily was started. AKI was diagnosed, and the patient received intravenous fluids at the rate of 100 mL per hour for 3 days. She did not show any signs of improvement, so therefore dialysis was initiated. On day 11, a kidney biopsy was sought. It revealed no pathological changes in the glomerulus with patent capillary lumen and unremarkable basement membrane. Proximal tubules showed diffuse degenerative and regenerative changes and displayed numerous intracytoplasmic and intraluminal polarizable calcifications consistent with calcium oxalate (Figure). Moderate tubular atrophy was noted, as well as mononuclear cell infiltrate. There was no evidence of vasculitis or tubulitis. Arterial blood vessels showed mild intimal fibrosis and medial sclerosis. Intratubular calcifications were found in the medulla. The immunofluorescence study was negative. The diagnosis of acute oxalate nephropathy (AON) was made.

The plasma oxalate level obtained after starting dialysis was 4.23 mg/mL (National Medical Service Laboratory, Willow Grove, PA). Known causes of AON were considered, namely ingestion of oxalate or substances that are metabolized to oxalate. They were excluded because of negative history. The patient was mainly vegetarian, ate a small amount of fish, and drank several cups of regular tea and an herbal tea called Jamaican Ceresse tea.