Controversy exists over whether metabolic factors or urinary stasis predominate in the pathogenesis of calyceal diverticular calculi. We performed a study to better define the effects urinary stasis and metabolic abnormalities have in the pathogenesis of calyceal diverticular stones. Twenty-nine patients who underwent percutaneous treatment of calyceal diverticular calculi were studied. All patients underwent 24 h urine collection to evaluate metabolic risk factors. In three patients, urine was sampled directly from the diverticulum for metabolic studies. The urinary stone risk parameters of the patients with calyceal diverticular stones (Tic SF) were similar to those of a well-characterized cohort of calcium oxalate stone formers (CaOx SF). When compared to a group of normal people, the Tic SF and CaOx SF were significantly more hypercalciuric and their urine was significantly more supersaturated with calcium oxalate. Urine aspirated directly from the diverticulum had the lowest SSCaOx when compared to ipsilateral and contralateral renal pelves. The urinary risk profiles of patients with diverticular calculi are similar to those of CaOx SF, suggesting a metabolic etiology of diverticular stones. However, the SS CaOx of urine aspirated directly from the diverticula is significantly lower than that of the renal pelves; these data support the hypothesis that urinary stasis significantly contributes to the pathogenesis of calyceal diverticular calculi. Taken together, it seems likely that calyceal diverticular calculi arise from a combination of metabolic abnormalities and urinary stasis.