Urine kidney injury markers do not increase following gastric bypass: a multi-center cross-sectional study.

INTRODUCTION: To determine if markers of kidney injury correlate with urinary oxalate excretion. If so, such biomarkers might be early predictors of oxalate nephropathy. Gastric bypass surgery for obesity is known to be associated with postoperative hyperoxaluria, which can lead to urolithiasis and kidney damage. MATERIALS AND METHODS: Patients were recruited from four large academic centers > 6 months following completion of gastric bypass surgery. Patients provided a spot urine sample for analysis of three markers of kidney injury: 8-iso-Prostaglandin F2 α, N-acetyl- ß -D-Glucosaminidase, and Neutrophil gelatinase-associated lipocalin. Patients also provided 24 hour urine samples for stone risk analysis. RESULTS: A total of 46 study patients provided samples, the average age was 48.4 +/- 11.3. There were 40 women and 6 men. There was no difference in the level of any of the three inflammatory markers between the study group and the reference range generated from healthy non-hyperoxaluric subjects. Neither oxalate excretion nor supersaturation of calcium oxalate correlated with any of the injury markers. There was no difference noted between those with hyperoxaluria (n = 17) and those with normoxaluria (n = 29) with respect to any of the injury markers. CONCLUSIONS: Though hyperoxaluria was common after bypass surgery, markers of kidney injury were not elevated after surgery. No correlation was found between urine oxalate excretion and any of the injury markers.