Abstract
Over the past 10 years, a variety of reports have linked bariatric surgery to metabolic changes that alter kidney stone risk. Most of these studies were retrospective, lacked appropriate controls, or involved bariatric patients with a variety of inclusion criteria. Despite these limitations, recent clinical and experimental research has contributed to our understanding of the pathophysiology of stone disease in this high-risk population. This review summarizes the urinary chemistry profiles that may be responsible for the increased kidney stone incidence seen in contemporary epidemiological bariatric studies, outlines the mechanisms of hyperoxaluria and potential therapies through a newly described experimental bariatric animal model, and provides a focused appraisal of recommendations for reducing stone risk in bariatric stone formers.