Prompt Diagnosis and Intervention of Oxalate Nephropathy to Salvage Kidney Function

ABSTRACT

Hyperoxaluria can be primary due to defective glyoxylate metabolism leading to hepatic oxalate overproduction or secondary due to increased intestinal oxalate absorption. Oxalate nephropathy is the deposition of calcium oxalate crystals leading to tubular injury, interstitial fibrosis, and AKI or CKD. This describes three cases of renal oxalosis. First is a 60 year old male with stroke, hypertension, diabetes who presented with AKI of 4.5 mg/dL from 1.6 that rose to 11 mg/dL. Serologies for glomerulonephritis and paraproteinemia were negative. Biopsy showed tubular oxalate crystal deposition with tubular injury and interstitial nephritis. His renal failure required dialysis. Second is a 58 year old female with gastric bypass surgery who presented for edema and AKI from 1.3 to 3.6 mg/dL. Serologies were also negative. Biopsy showed interstitial nephritis with tubular calcium oxalate deposition. She was started on prednisone 60 mg. Creatinine stabilized to 2.2 mg/dL, not requiring dialysis. Third is a 82 year old male with obesity and sarcoma of the scalp treated with pembrolizumab who presented with dyspnea, edema and an AKI from 1 to 8.6 mg/dL. Urine sediment was bland with negative serologies. Differential included AIN due to pembrolizumab. Patient was started on high dose prednisone and biopsy showed interstitial nephritis and calcium oxalate crystal deposition. Patient endorsed taking frequent vitamin C as prophylaxis for Covid. Creatinine stabilized to 2.9 mg/dL not on dialysis. Classic etiologies of hyperoxaluria include dietary oxalate from ascorbic acid and fat malabsorption from gastric bypass surgery. Treatment includes increased fluid intake, oral calcium supplements and low oxalate diet. Oxalate nephropathy remains an under recognized cause of kidney failure, as such, early biopsy and intervention are necessary. (Figure Presented)