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Bariatric surgery is increasingly performed on overweight individuals. A significant benefit with respect to cardiovascular (CV) events and survival has been documented. After weight loss, reduction of albuminuria/proteinuria is almost consistently seen; small studies documented retardation of the glomerular filtration rate (GFR) loss after bariatric surgery; reduction of blood pressure (BP) is less consistent. It has been known for a long time that the frequency of oxalate stones is increased after bariatric surgery. The main renal threat of hyperoxaluria is renal oxalosis, often irreversible, causing persisting renal failure. The causes are reduced oxalate binding by calcium due to saponification of calcium causing fat malabsorption, increased permeability for oxalate because of increased permeability of colon mucosa triggered by increased bile salts and reduced colonization of the colon by oxalobacter formigenes. These mechanisms are susceptible to treatment.

Background: The epidemiological incidence of oxalate nephrolithiasis is higher in men than in women. Oxalate is predominantly produced in the liver and then released into the systemic circulation by sat1, a sulfate anion transporter, which is localized in the sinusoidal membrane of hepatocytes, where it mediates exit of oxalate in exchange for sulfate. In renal proximal tubules, sat1 is responsible for basolateral uptake of oxalate into the cell and release of sulfate into systemic circulation. Finally, oxalate is extruded into the urine by the luminal chloride-formate exchanger, CFEX, which also accepts oxalate as a substrate. Methods: The model of ethylene glycol (EG)-induced oxalate nephrolithiasis in adult male and female rats was used to monitor changes in sat1, CFEX, and the rate-limiting enzymes of oxalate synthesis, alcohol dehydrogenase (Adh1) and hydroxy acid oxidase (Hao1). Protein and mRNA expression was studied by immunochemistry and real time RT-PCR. Results: As compared to controls, EG-treated animals exhibited higher concentrations of oxalate in plasma and urine, and a higher abundance of oxalate crystals in urine with male dominance. Sat1 protein in liver and kidneys was male-dominant in controls, increased only in EG-treated female rats, while sat1 mRNA stayed unchanged. CFEX mRNA in both organs was sex-independent and unaffected by EG treatment. Adh1 and Hao1 mRNA in both organs exhibited distinct sex dependency which remained unchanged upon EG treatment. A general male-dominant Hao1 expression in kidneys of untreated rats was also shown by microarray analysis. Conclusions: In conclusion, despite hyperoxaluria in EG-treated animals, the expression of sat1 in males and of CFEX in both sexes was sufficient to handle the EG-induced production and secretion of oxalate.

Studies of crystals of calcium oxalate dihydrate (COD) grown by vapor diffusion from solutions contain-ing 5.1 x 10-7, 1.5 x 10-6, and 1.0 x 10-5 M nephrocalcin (NC), indicate that NC profoundly affects COD's habit, size and structure. The decrease in COD size is such that at 1.0 x 10-5 M NC, the dimensions of the crystals are reduced about five-fold with respect to those of a NC-free control. In addition, the planes of the {101} form disappear, the original habit is lost, and the diffraction pattern deteriorates to such an extent that only the 200 reflections are recorded. The results are quite different when NC is adsorbed upon rigid substrates. Under such conditions, NC acts as a promoter and not as an inhibitor of growth and thus nucleates COD from its {100} planes. Consequently, COD grows systematically juxtaposed on NC. This effect is highly reproducible and stereospecific. COD crystals grown by vapor diffusion from solutions exposed to increasing concentrations of Tamm-Horsfall protein (THP) exhibit a drastic decrease in COD's self-association. In sharp contrast with the results obtained for NC, precession photographs taken of COD samples exposed to 1.2 x 10-5 M THP do not show evidence of deterioration of COD diffraction patterns with respect to a protein-free control. Furthermore, THP neither nucleates COD, nor does it appear to influence its growth or habit even when THP is immobilized upon a rigid substrate.