An Unusual Presentation of Oxalate Nephropathy in a Kidney Transplant Patient

Introduction: Hyperoxaluria results from either inherited disorders of glyoxylate metabolism leading to hepatic oxalate overproduction (primary hyperoxaluria) or increased intestinal oxalate absorption (secondary hyperoxaluria). Case Description: A 62-year-old male with a history of deceased donor kidney transplant 7 years prior, diabetes mellitus type 2, left foot ulcer presented for acute kidney injury (AKI) evaluation. He had undergone partial ray amputation of his left 4th and 5th digits for osteomyelitis and was started on 500mg erythromycin 4 times daily and doxycycline 100 mg twice daily to complete a 6-week course. He developed diarrhea shortly after erythromycin initiation, having up to 15 bowel movements daily for 30 days. He developed an AKI with peak serum creatinine (Scr) of 3.56mg/dL (baseline 1.1 -1.4), and serum bicarb of 16mmol/L. AKI was attributed to interaction of erythromycin and tacrolimus. Scr failed to improve after discontinuation of erythromycin. Scr was 2.35mg/dL on presentation to our hospital. Renal biopsy revealed AKI and several calcium oxalate crystals, with mild interstitial fibrosis. Urine microscopy was negative for calcium oxalate crystals. He was prescribed calcium carbonate tablets to increase oxalate excretion. Chart review showed oxalate crystals had been reported on urinalysis 2 years after his kidney transplant on routine follow up without further workup. His Scr was 1mg/dL and remained as such until his recent presentation. Discussion: We suspect our patient has baseline predisposition to hyperoxaluria which was exacerbated by antibiotic use as well as a prolonged course of diarrhea, leading to alteration/ destruction of gut microbiota, including Oxalobacter formigenes, (a bacterium which metabolizes oxalate), leading to hyperoxaluria. Plasma oxalate is excreted by the kidney via glomerular filtration and tubular secretion. Increased production, dehydration and acidosis lead to accumulation and deposition in the tubules, causing AKI and oxalate nephropathy. Oxalate nephropathy should be considered in the differential for AKIHistologic sections show polarizable intratubular calcium oxalate crystals in renal medulla (A&B. H&E section, 200x).