Determinants of Urolithiasis in Patients With Intestinal Fat Malabsorption

Abstract

To investigate the determinants of urinary stone formation in patients with fat malabsorption, because, although the prevalence of urolithiasis is greater in patients with intestinal diseases, the pathogenetic mechanisms and risk factors associated with urolithiasis in this population remain partially unsolved. The present study retrospectively analyzed the determinants of urolithiasis in 51 patients with fat malabsorption due to different intestinal diseases. Anthropometric, clinical, blood, 24-hour urinary parameters, and dietary intake were assessed. The resection rate (ie, pancreatic and/or bowel resection) differed significantly between stone formers (SF; n=10) and nonstone formers (NSF; n=41; 70% vs 29%; P=.027). Urinary citrate was lower (1.606±1.824 vs 3.156±1.968 mmol/24 h; P=.027), while oxalate excretion (0.659±0.292 vs 0.378±0.168 mmol/24 h; P=.002) and the relative supersaturation of calcium oxalate were greater in SF than NSF (8.16±4.61 vs 3.94±2.93; P=.003). Total cholesterol and low-density lipoprotein cholesterol, but also high-density lipoprotein cholesterol, plasma β-carotene, and vitamin E concentrations, were significantly diminished, whereas serum aspartate aminotransferase activity was significantly greater in SF compared with NSF. Binary logistic regression analysis revealed resection status as a major extrarenal risk factor for stone formation (odds ratio 5.639). Increased urinary oxalate and decreased citrate excretion, probably resulting from pancreatic and/or bowel resection with mainly preserved colon, were identified as the most crucial urinary risk factors for stone formation in patients with fat malabsorption. The findings suggest that hyperoxaluria predominantly results from increased colonic permeability for oxalate due to disturbed bile acid metabolism. The impaired status of fat-soluble antioxidants β-carotene and vitamin E indicates severe malabsorptive states associated with an enhanced stone-forming propensity.