Abstract: PUB339
Enteric Hyperoxaluria (EH) Causing Kidney Allograft Loss
Session Information
Category: Transplantation
- 2102 Transplantation: Clinical
Authors
- Seethanadi, Aashish, NU Hospitals, Bengaluru, KA, India
- Patro, Kiran Chandra, NU Hospitals, Bengaluru, KA, India
- Modi, Shakuntala, NU Hospitals, Bengaluru, KA, India
- Nayak, Nitin, NU Hospitals, Bengaluru, KA, India
Introduction
EH is characterized by increased absorption of oxalate in the gut. Following kidney transplantation, the allograft is exposed to higher plasma oxalate, leading to a risk of deposition of calcium oxalate with adverse outcomes
Case Description
A 51 year old gentleman first presented with chronic kidney disease and renal calculi. Calculi were removed surgically. Stone analysis showed calcium oxalate. Serum creatinine was 2.79 mg/dL. Kidneys were not amenable for biopsy. He had no recurrence of calculi. Hemodialysis was initiated 9 months later for progressive disease. There was past history of exploratory laparotomy 5 years ago for possible inflammatory bowel disease – the details of which were unavailable. There were no gastrointestinal symptoms at presentation. Renal transplant was done after a dialysis vintage of 5 months. Serum creatinine was 1.41 mg/dL at discharge. Allograft biopsy in 3rd post transplant week for raised creatinine showed acute tubular injury (ATI). Second biopsy 5 months later for worsening kidney functions reported ATI with oxalate crystals in tubules. He had BK viruria 8 months post transplant period, following which immunosuppression was reduced. He developed BK viremia and cytomegalovirus viremia later. Third allograft biopsy in 9th post transplant month showed ATI with plenty of oxalate crystals in tubules with borderline T-cell mediated rejection. Ultrasound showed calculi in transplant kidney. He had allograft loss and was re-initiated on hemodialysis 10 months post transplant.
Genetic test for hyperoxaluria was negative. 24-hour urinary oxalate was <40mg in 3 consecutive samples. We did not do plasma oxalate levels. There was no systemic oxalosis.
Discussion
EH is secondary to an increase in oxalate solubility in the intestinal lumen and a rise in bowel permeability to oxalate due to bile salts and colonic mucosal inflammation as seen in IBD. Such cases may present with unexplained graft failure. Diagnosis is usually made on allograft biopsy.