1,721,439 research outputs found
Re: McPhail et al.: Nephrolithiasis in medullary sponge kidney: evaluation of clinical and metabolic features. (Urology 2012;79:277-281)
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Empirical therapy or precision medicine for kidney stone formers in the '-omics' era?
No full textIntoduction to a dedicated issue to genetic disorders in nephrolithiasi
Strategies to safely interfere with prostanoid activity while avoiding adverse renal effects: could COX-2 and COX-LOX dual inhibition be the answer?
No full textGenome-wide Association Studies Identify Genetic Loci Associated with Albuminuria in Diabetes
No full textElevated concentrations of albumin in the urine, albuminuria, are a hallmark of diabetic kidney disease and associate with increased risk for end-stage renal disease and cardiovascular events. To gain insight into the pathophysiological mechanisms underlying albuminuria, we conducted meta-analyses of genome-wide association studies and independent replication in up to 5,825 individuals of European ancestry with diabetes mellitus and up to 46,061 without diabetes, followed by functional studies. Known associations of variants in CUBN, encoding cubilin, with the urinary albumin-to-creatinine ratio (UACR) were confirmed in the overall sample (p=2.4*10(-10)). Gene-by-diabetes interactions were detected and confirmed for variants in HS6ST1 and near RAB38/CTSC. SNPs at these loci demonstrated a genetic effect on UACR in individuals with but not without diabetes. The change in average UACR per minor allele was 21% for HS6ST1 and 13% for RAB38/CTSC (p=6.3*10(-7) and 5.8*10(-7), respectively). Experiments using streptozotocin-treated diabetic Rab38 knockout and control rats showed higher urinary albumin concentrations and reduced amounts of megalin and cubilin at the proximal tubule cell surface in Rab38 knockout vs. control rats. Relative expression of RAB38 was higher in tubuli of patients with diabetic kidney disease compared to controls. The loci identified here confirm known and highlight novel pathways influencing albuminuria
Recent advances in managing and understanding nephrolithiasis/nephrocalcinosis
Full text linkUrinary stone disease is a very common disease whose prevalence is still increasing. Stone formation is frequently associated with other diseases of affluence such as hypertension, osteoporosis, cardiovascular disease, metabolic syndrome, and insulin resistance. The increasing concentration of lithogenic solutes along the different segments of the nephron involves supersaturation conditions leading to the formation, growth, and aggregation of crystals. Crystalline aggregates can grow free in the tubular lumen or coated on the wall of the renal tubule. Plugs of crystalline material have been highlighted in the tubular lumen in some patients, but crystalline growth starting from plaques of calcium phosphate within the renal papillae has been demonstrated in others. Urinary supersaturation is the result of a complex interaction between predisposing genetic features and environmental factors. Dietary intake is certainly the most important environmental risk factor. In particular, an insufficient intake of dietary calcium (<600 mg/day) can increase the intestinal absorption of oxalate and the risk of calcium oxalate stone formation. Other possible risk factors that have been identified include excessive intake of salt and proteins. The potential role of dietary acid load seems to play an important role in causing a state of subclinical chronic acidosis; therefore, the intake of vegetables is encouraged in stone-forming patients. Consumption of sugar-sweetened soda and punch is associated with a higher risk of stone formation, whereas consumption of coffee, tea, beer, wine, and orange juice is associated with a lower risk. A high fluid intake is widely recognized as the cornerstone of prevention of all forms of stones. The effectiveness of protein and salt restriction has been evaluated in some studies that still do not allow definitive conclusions to be made. Calcium stone formation can be prevented by the use of different drugs with different mechanisms of action (thiazide diuretics, allopurinol, and potassium citrate), but there is no ideal drug that is both risk free and well tolerated
Glycosaminoglycan treatment in glomerulonephritis? An interesting option to investigate.
No full textPatients with primary and secondary chronic glomerular diseases are at significant risk for progression to end-stage renal disease. Unfortunately the treatment armamentarium is relatively limited in terms both of available agents and of specificity. Experimental evidence supports the idea that heparin-derived agents and glycosaminoglycans (GAGs) favorably affect primary and secondary renal diseases. While a number of clinical exploratory studies have addressed the effect of these agents in microalbuminuric and macroalbuminuric diabetic patients, very few have investigated their activity in nondiabetic renal conditions. This paper will review the experimental and clinical evidence on the use of GAGs in renal disease other than diabetic nephropathy, following the reports of experimental findings supporting their use and the possible mechanisms involved: anticoagulant and antiproliferative activity, effect on growth factors (PDGF, FGF2 and TGF-beta1), inhibition of heparanase, macrophage renal infiltration and of the renin-angiotensin system, and decrease in proteinuria. Targeting these pathogenic loops with GAG treatment might be revealed to be very rewarding from a clinical point of view. Prospective randomized controlled trials with large case populations and definite entry criteria are clearly indicated
Regarding ‘Early postoperative serum cystatin C predicts severe acute kidney injury following pediatric cardiac surgery’
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