This tested

whether these probiotic preparations can increase oxalate metabolism in the intestine and/or decrease oxalate absorption from the gut. Patients were maintained on a controlled diet to remove the confounding variable of differing oxalate intake from food. Urinary oxalate excretion and calcium oxalate supersaturation on the controlled diet were significantly lower compared with baseline on a free-choice diet. Neither study preparation reduced urinary oxalate excretion nor calcium oxalate supersaturation. Fecal lactobacilli colony counts increased on Panobinostat molecular weight both preparations, whereas enterococcal and yeast colony counts were increased on the synbiotic. Total urine volume and the excretion of oxalate and calcium were all strong independent determinants of urinary calcium oxalate supersaturation. Hence, dietary oxalate restriction reduced urinary oxalate excretion, Selleck GW4869 but the tested probiotics did not influence urinary oxalate levels in patients on a restricted oxalate diet. However, this study suggests

that dietary oxalate restriction is useful for kidney stone prevention. Kidney International (2010) 78, 1178-1185; doi: 10.1038/ki.2010.310; published online 25 August 2010″
“Diabetes mellitus is the most common and rapidly growing cause of end-stage renal disease. A classic hallmark of diabetes pathology is the activation of the intrarenal renin-angiotensin system (RAS), which may lead to hypertension and renal tissue injury, but the mechanism of RAS activation has been elusive. Recently, we described the intrarenal localization of the novel metabolic receptor GPR91 and established some of its functions in diabetes. These include the triggering of renin release in early diabetes via both vascular (endothelial) and tubular

(macula densa) sites in the juxtaglomerular apparatus as well as the activation of MAP kinases in the distal nephron-collecting duct, which are important Ketotifen signaling mechanisms in diabetic nephropathy (DN) and renal fibrosis. GPR91 is a cell surface receptor for succinate and during the past few years it has provided a new paradigm for the mechanism of cell stress response in many organs. Beyond its traditional role in the tricarboxylic acid cycle, succinate now has an unexpected hormone-like signaling function, which may provide a feedback between local tissue metabolism, mitochondrial stress, and organ functions. Succinate accumulation in the local tissue environment and GPR91 signaling appear to be important early mechanisms by which cells detect and respond to hyperglycemia and trigger tissue injury in DN. Also, the distal nephron-collecting duct system, which is the major source of (pro) renin in diabetes and has the highest level of GPR91 expression in the kidney, may have an important, active, and early role in the pathogenesis of DN in contrast to the existing glomerulus-centric paradigm. Kidney International (2010) 78, 1214-1217; doi:10.1038/ki.2010.