Case Presentation:
A 54-year-old female with hypertension, type 2 diabetes, and morbid obesity with Roux-en-Y gastric bypass (RYGB) in 2009 presented to the hospital with abdominal pain and was found to have choledocolithiasis and acute cholecystitis. She was admitted to the surgery service and underwent ERCP and laparoscopic cholecystectomy. Her post-op course was complicated by acute kidney injury resolving with IV fluids. She was transferred to the medicine service for persistent hyponatremia, diarrhea, and new onset metabolic acidosis.
Upon transfer, she had blood pressures in the 90s/50s and physical exam revealed a morbidly obese woman with 3+ pitting edema to mid-calf. Labs showed a mixed non anion-gap and anion-gap acidosis, normal lactic acid, elevated beta hydroxybutyric acid, hyponatremia to 126, and creatinine of 1.27. Her mixed metabolic acidosis was owed to starvation ketoacidosis due to malabsorption from RYGB and bicarbonate wasting from diarrhea. She was thought to have hypervolemic hyponatremia and was diuresed for four days with improvement of hyponatremia.
A gradual elevation of creatinine and progressive oliguria was observed over the next three weeks after the trial of diuresis. Urine sodium was <10 with a FENA of <0.1%. Urine sediment was bland with hyaline casts. A kidney ultrasound was unremarkable. Her rising creatinine was refractory to IV fluids on midodrine and subsequent albumin challenge, peaking to 5.20. She had gained 30 kilograms since presentation and had anasarca. A kidney biopsy revealed acute tubular injury with crystals consistent with oxalate nephropathy in a background of early diabetic nephropathy. Her course was further complicated by uremic encephalopathy secondary to acute oliguric kidney failure. She was initiated on hemodialysis for oxalate clearance and then volume removal.
Discussion:
Oxalate nephropathy is characterized by tubular crystalline deposits of calcium oxalate (CaOx) leading to acute and chronic tubular injury, interstitial fibrosis, and progressive renal insufficiency. Under normal conditions, dietary calcium and oxalate form insoluble CaOx in the intestine and are excreted in stool. In conditions with fat malabsorption – such as RYGB – excessive intraluminal free fatty acids saponify calcium and prevent CaOx formation with consequent increase in the enteric absorption of free oxalate. Low urine volume and metabolic acidosis promote CaOx crystallization with reduction of urinary citrate and magnesium, both crystallization inhibitors.
In this case, due to the patient’s multiple co-morbidities, enteric oxalate absorption and CaOx deposition was increased. Her nephropathy presented as progressive acute oliguric renal failure.
Conclusions:
Oxalate nephropathy is a rare complication of RYGB. In patients with a history of RYGB presenting with acute or chronic renal injury of unclear etiology, the differential diagnosis should include oxalate nephropathy. Renal biopsy should be considered for definitive diagnosis.