#6180 OXALATE NEPHROPATHY SECONDARY TO ENTERIC HYPEROXALURIA: A RARE CAUSE OF END STAGE RENAL FAILURE – A REPORT OF 2 CASES

Abstract

Abstract Background and Aims Oxalate nephropathy is a rare cause of renal failure which is usually due to primary or secondary hyperoxaluria. Secondary hyperoxaluria results from increased intake or increased intestinal oxalate availability (enteric hyperoxaluria), increased intestinal oxalate degradation, or increased colonic permeability to oxalate [1]. Little is known about the burden of end stage kidney disease in this group of patients as most of the initial literature was from case reports and case series. More recently, prevalence of 1- 4.01% was reported from biopsy studies suggesting that this entity is indeed a cause of kidney failure that needs to be considered [2,3]. Method We present two cases of oxalate nephropathy secondary to enteric hyperoxaluria following small bowel resections. Results CASE ONE 82 year old man with a solitary kidney who was admitted in the ED on account of a decline in renal function on a background of episodes of loose stools. This was his second admission in two months on account of decline in renal function. He had emergency laparotomy and adhesiolysis as a result small bowel obstruction from volvulus 12 months earlier. Other past medical history include left nephroureterectomy for renal cancer, transurethral resection of bladder tumour, hypertension, Barretts and appendectomy. His medications were Omeprazole(which was switched to Famotidine due to hypomagnesaemia 7 months postop), Atenolol and Adcal D3. Renal immunology and myeloma screen were negative. Urine was bland and ultrasound did not show any obstruction. His AKI was initially thought to be pre-renal and there was some improvement in renal function with fluids during his first admission although renal function didn't return to baseline. His renal function progressively worsened in a spate of a few months. He had a baseline creatinine of 130 prior to his laparotomy which worsened to 184 post surgery bur the improved to about 109 few days post op. However, his renal function was noticed to decline 9 months post op and eventually his creatinine peaked at 751, fourteen months post op. He eventually had a renal biopsy 13 months post op that showed oxalosis, acute tubular injury and patchy interstitial fibrosis. His renal function continued to deteriorate and he was eventually commenced on haemodialysis. CASE TWO A 75-year-old man who was referred to the renal clinic on account of a decline in renal function. He had a past medical history of Crohn's disease, previous right hemicolectomy 26 years ago with revision 4 years ago, ileostomy(with subsequent reversal), inguinal herniorrhaphy, hypertension and BPH. He was on Azathioprine for his Crohn's and his initial decline in renal function was thought to be attributable to Azathioprine. Other medications include: Amlodipine 5 mg, Finasteride 5 mg, Loperamide 2 mg bd, Tamsulosin 400mcg od. At referral, his renal function had progressively deteriorated over the previous few months from a baseline creatinine of 145 to 303, 44 months after his last surgery. Urinalysis showed trace of protein and + of blood however, urine ACR was normal. Vasculitis and myeloma screen were also normal. Ultrasound ruled out any obstruction. Despite pausing Azathioprine, renal function continued to deteriorate with creatinine peaking at 561 over the next 2 months. He subsequently had a renal biopsy that showed chronic damage with oxalate casts. He was subsequently commenced on haemodialysis. Conclusion These two cases highlight the need to consider enteric hyperoxaluria in patients presenting with unexplained decline in renal function who have had bowel surgery or have risk factors for fat malabsorption. This is important due to the usual poor prognosis in this group of patients [1].