Prevalence of calcium oxalate nephrolithiasis (CaOx-NL) is markedly increased in obese patients after malab-sorptive bariatric surgery. Mechanistically, fat malabsorption is thought to lead to increased enteric oxalate absorption with secondary enteric hyperoxaluria (SEH) and potential CaOx-stone formation. Additionally, loss of enteric colonization with oxalate-digesting bacteria, e.g. Oxalobacter formigenes, may aggravate SEH. Conversely, in primary hyperoxaluria (PH) due to biallelic mutations of either AGXT, GRHPR, or HOGA1, en-dogenous hepatic oxalate overproduction is the underlying mechanism of stone formation. Therefore, the ques-tion arises whether genetic susceptibility predisposes certain patients to develop kidney stones after bariatric surgery.