OXALATE NEPHROPATHY AS A COMPLICATION AFTER ROUX- EN- Y GASTRIC BYPASS

Oxalate nephropathy is a rare cause of kidney disease and can be missed when triggers go unrecognized. In this era of consciousness and management of obesity epidemic, one needs to be cognizant of unfavorable consequences of bariatric surgery.

Case presentation

62 yr old male with history of type 2 diabetes for past 6 years, chronic NSAID use and PPI use, morbid obesity was evaluated for chronic kidney disease. At that time his creatinine was 1.53. He underwent gastric bypass surgery and developed acute kidney injury with a peak creatinine of 3.04 post surgery. Subsequently his creatinine improved to 1.23.He lost 144 pounds with gastric bypass and kept it off and was not on any medications for diabetes and hypertension. In follow up, his creatinine was stable around 1.3 for  up until  1.5 yrs after surgery. However, 4 months later his creatinine went up to 3.96 and failed to improve with supportive care. He has not been on any nephrotoxic medications and was hydrating well. UA was benign. Imaging revealed no hydronephrosis or stones. At this time, kidney biopsy was done to delineate etiology of his kidney failure, and it showed significant interstitial fibrosis of 50 to 60% with prominent oxalate casts suggestive of oxalate nephropathy.  Also seen were patchy interstitial inflammation moderate arteriosclerosis. Glomeruli were normal-appearing and EM showed no subepithelial or endothelial immune deposits. 24-hour urine showed 160 mg oxalate. He was instructed on high fluid intake of at least 2-3 L daily, low oxalate diet, low fat diet, normal dietary calcium and was started on calcium carbonate and oxalate level did come down to 116.He was then started on Ox free which contains calcium citrate which reduces oxalate and also on probiotic with oxalobacter formigenes which will help with degradation of oxalate in bowel. Unfortunately, his kidney dysfunction progressed, and transplantation evaluation is ongoing.

Discussion

Oxalate Nephropathy is defined as syndrome of decreased renal function associated with deposition of calcium oxalate crystals in the renal tubules.  There is also typical acute tubular necrosis with associated chronic/acute interstitial nephritis or fibrosis.  Calcium oxalate crystals are birefringent under polarized light. It can cause progressive renal dysfunction and there is a significant risk of end-stage kidney disease.  Most cases of oxalate nephropathy have hyperoxaluria defined by 24-hour urine oxalate of more than 40 to 45 mg/day.

It is hyperoxaluria occurring in the setting of fat malabsorption or due to steatorrhea.  Normally calcium binds oxalate in the bowel to form insoluble calcium oxalate and that is excreted in the feces.  In the state of fat malabsorption calcium is bound by free fatty acids and becomes unavailable for oxalate binding.  Then there is increased oxalate that will be absorbed by the bowel and free fatty acids and bile acid salts also directly increase colonic permeability to oxalate.

Take home points

Diagnostic criteria for oxalate nephropathy.

•      Progressive kidney disease

•      Deposition of calcium oxalate (birefringent on polarized light) within the tubular epithelial cells, tubular lumen

•      Exclusion of other causes of kidney disease like diabetes associated glomerular disease

•      Cause of hyperoxaluria condition - Both nephrolithiasis and oxalate nephropathy are complications of surgical treatment for obesity like Roux-en-Y gastric bypass