Gastric bypass oxalosis in renal transplant: clinicopathologic correlates

Abstract

Background: Reports of oxalate nephropathy after gastric bypass (GB) leading to graft loss of kidneys causes concern for transplant professionals. We examined the clinical phenotype of GB related oxalate nephropathy (ON), its contribution to graft loss and propose a management strategy to mitigate graft loss in renal transplant recipients.

Methods: Retrospective case series of patients who had GB surgery prior to renal transplant at a single institution were studied. Oxalate burden in renal transplant biopsies was quantified by intratubular calcium/glomeruli (Ca T/G) ratio and correlated with other clinical covariates.

Results: We identified 16 GB patients; the mean BMI pre-GB was 52.5 kg/m2 (range 42-80), with a follow-up BMI of 30.9 kg/m2 (range 22-36.5) at transplant evaluation. Among 11 patients who had for cause biopsies, 3 patients had significant intra tubular allograft calcium oxalate deposition with a median time from graft to failure of 9 months. Among patients with functioning grafts, follow up creatinine averaged 1.6 mg/dl (0.9-3.4 mg/dl); median follow up was 4 years (0.5-7 years).

Conclusions: The relationship between GB and ON post renal transplant is variable. The expression of ON after acute kidney injury (AKI) suggests that mitigating strategies should be directed at preventing alloimmune and other forms of AKI in addition to managing oxalate intake.