october 2012 clinical quiz
A 73-year-old African American man complained of generalized fatigue for two weeks, prompting a lab check and subsequent hospital admission by his primary care physician.
He denied fevers, vomiting, diarrhea, dysuria, gross hematuria, or use of nonsteroidal anti-inflammatory drugs. He had no abdominal, flank, or back pain and denied any history of nephrolithiasis. There was no hesistancy or incontinence. He noted a decreased appetite over the past week. Subjective urine output was normal. He had a past history of prostate cancer diagnosed more than 10 years previously. He was treated with, and responsive to, casodex. He also had diabetes mellitus and was recently placed on insulin.
The man also had a history of carotid disease with past endarterectomy. Medications included lisinopril, atorvastatin, tamsulosin, hydrochlorothiazide, glargine insulin, amlodipine, and aspirin/dipyridamole. He took up to 2000 mg of vitamin C on a daily basis, as well as Morinda citrifolia supplements. He enjoyed blending his own vegetable purees in an effort to eat healthy.
On exam his blood pressure was 140/70. His was alert and fully oriented, lungs were clear, and there was no pericardial rub. His abdomen was non-tender, legs show minimal edema, and he was neurologically intact.
His creatinine level was 7.1 mg/dL, whereas it was 1.2 mg/dL three months previously. His sodium level was 142 mEq/L. BUN was 81 mg/dL, CO2 was 18 mEq/L, chloride level was 116 mEq/L, and potassium level was 5.2 mEq/L. His calcium level was 8.9 mg/dL and phosphorus level was 3.7 mg/dl.
There is normocytic anemia and platelets were within normal limits. Urinalysis revealed a specific gravity 1.006, trace protein, and no hemoglobin or white cells. Renal ultrasound revealed no obstruction. There were no red or white cell casts on examination of the urine sediment. A renal biopsy was performed and a representative micrograph is shown.
Submit your diagnosis to see full explanation.
The renal biopsy showed numerous intratubular crystals consistent with oxalate. There was also acute tubular necrosis with evidence of regeneration. Our patient’s renal function did not improve after admission and he eventually was started on hemodialysis (HD). Five months later there was evidence of renal recovery and HD treatments were stopped. He remains off dialysis to this day.
Acute oxalate nephropathy occurs with precipitation of calcium oxalate crystals in the tubular lumens with resultant kidney injury. Calcium oxalate crystals are a nonspecific finding in normal urine and can be seen on biopsy specimens of acute kidney injury (AKI) from various causes. However, in cases where oxalate crystal deposition is the primary cause of AKI, there is widespread intratubular deposition, as was seen in this patient. Calcium oxalate crystals are usually lacking in color and of various shapes, but they show multi-colored birefringence under plane polarized light.
Causes of oxalate nephropathy include primary hyperoxaluria, ethylene glycol poisoning, large doses of vitamin C, and pancreatic insufficiency or other gastrointestinal abnormalities that predispose to hyperoxaluria. Diet drugs that induce pancreatic insufficiency and fat malabsorption have also been linked to oxalate nephropathy.
Our patient had high sustained oral intake of vitamin C. In addition, he had higher than expected oxalate ingestion in his frequent vegetable drinks, which included large amounts of kale and other oxalate-rich foods. He was counseled to lower his overall vitamin C intake and referred to a renal dietitian for further nutritional counseling.
- Nakamoto Y, Motohashi S, Kasahara H, Numazawa, K. Irreversible tubulointerstitial nephropathy associated with prolonged, massive intake of vitamin C. Nephrol Dial Transplant 1998;13:754-756.
- Alkhunaizi AM, Chan L. Secondary oxalosis: a cause of delayed recovery of renal function in the setting of acute renal failure. J Am Soc Nephrol 1996;7:2320-2326.
This clinical case was prepared by Kevin T. Harley, MD, Assistant Clinical Professor of Medicine at the University of California in Irvine. Micrograph provided by Philip Carpenter, MD, Professor of Clinical Pathology at the University of California in Irvine.