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Renal Stone Formation (renal + stone_formation)
Selected AbstractsHeterogeneous Disease Modeling for Hardy-Weinberg Disequilibrium in Case-Control Studies: Application to Renal Stones and Calcium-Sensing Receptor PolymorphismsANNALS OF HUMAN GENETICS, Issue 2 2009D. C. Hamilton Summary Renal stone formation due to hypercalciuria is a relatively common disorder with clear evidence for genetic predisposition, but cryptic phenotypic heterogeneity has hampered identification of candidate genes. The R990G single-nucleotide polymorphism (SNP) of the calcium sensing receptor (CASR) gene has been associated with hypercalciuria in stone formers and shows the appropriate functional phenotype in cell culture. In our preliminary association analysis of a case-control cohort, however, we observed significant Hardy-Weinberg disequilibrium (HWD) for the cases (n= 223), but not controls (n= 676) at the R990G locus, pointing us toward the general disease model incorporating HWD. Because there is an adjacent CASR SNP, A986S, which is in negative linkage disequilibrium with R990G, we extended the general disease model to enable testing of a two-site hypothesis. In our data set, there is no lack of fit (P= .345) for the single-locus model for the R990G genotype, and likelihood ratio testing favors a recessive effect with an eight-fold increase in risk (P < .001) for GG homozygotes, relative to wild-type, based on a population prevalence of 2%. Addition of the A986S genotype provides no additional information either by itself or when included in our two-site model. [source] Mechanism of calcium oxalate renal stone formation and renal tubular cell injuryINTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2008Masao Tsujihata Abstract: Formation of calcium oxalate stones tends to increase with age and begins from the attachment of a crystal formed in the cavity of renal tubules to the surface of renal tubular epithelial cells. Though most of the crystals formed in the cavity of renal tubules are discharged as is in the urine, in healthy people, crystals that attach to the surface of renal tubular epithelial cells are thought to be digested by macrophages and/or lysosomes inside of cells. However, in individuals with hyperoxaluria or crystal urine, renal tubular cells are injured and crystals easily become attached to them. Various factors are thought to be involved in renal tubular cell injury. Crystals attached to the surface of renal tubular cells are taken into the cells (crystal,cell interaction). And then the crystal and crystal aggregates grow, and finally a stone is formed. [source] Chronic acid ingestion promotes renal stone formation in rats treated with vitamin D3INTERNATIONAL JOURNAL OF UROLOGY, Issue 1 2007Naohiko Okamoto Objective: Although hypercalciuria, a well-established adverse effect of vitamin D3, can be a risk factor of renal stone formation, the risk of nephrolithiasis has not been well defined. The consumption of a diet high in acid precursors is often cited as a risk factor for the development of calcium-based kidney stones. In the present study, we investigated the effect of chronic acid ingestion on kidney stone formation in rats treated with calcitriol (1,25[OH]2 D3). Methods: Control rats (C-C), calcitriol-treated rats (C-V; three treatments of 0.5 µg of calcitriol per week) and acid-ingested (water containing 0.21 mol/L NH4Cl), calcitriol-treated (three treatments of 0.5 µg of calcitriol per week) rats (A-V) were fed in metabolic cages. After 1 month, urine, blood, kidney and bone samples were analyzed. Results: The A-V rats exhibited elevated serum calcium concentrations, urinary calcium and phosphate excretion, urinary type I collagen cross-linked N-peptide (NTx)/creatinine values, mRNA expression of osteopontin in the kidney, and renal calcium contents as well as decreased bone mineral densities, compared with the C-C and C-V rats. Urinary citrate excretion was lower and NaDC-1 mRNA expression in the kidney was higher in the A-V rats than in the C-C and C-V rats. Calcium phosphate kidney stones were found in the A-V rats. Conclusions: The ingestion of NH4Cl, an acid precursor, promotes calcium phosphate kidney stone formation in calcitriol-treated rats. The chronic intake of a diet rich in acid precursors may be a risk factor for the development of kidney stones in subjects who are being treated with calcitriol. [source] Prophylaxis effect of Trigonella foenum graecum L. seeds on renal stone formation in ratsPHYTOTHERAPY RESEARCH, Issue 10 2007Amine Laroubi Abstract Despite considerable progress in medical therapy, there is no satisfactory drug to treat kidney stones. Therefore, the current study aimed to look for an alternative by using Trigonella foenum graecum (Tfg) on nephrolithiasic rats as a preventive agent against the development of kidney stones, which is commonly used in Morocco as a phytotherapeutic agent. The inhibitory effect of the aqueous extract of Tfg seeds was examined on the formation of calcium oxalate renal stones induced by ethylene glycol (EG) with ammonium chloride. At the end of the experiment all kidneys were removed and examined microscopically for possible crystal/stone locations and the total calcium amount in the renal tissue was evaluated. The blood was recovered to determine the levels of calcium, phosphorus, creatinine and urea. The results showed that the amount of calcification in the kidneys and the total calcium amount of the renal tissue in rats treated with Tfg were significantly reduced compared with the untreated group. Consequently, Tfg may be a useful agent in the treatment of patients with calcic urolithiasis. Copyright © 2007 John Wiley & Sons, Ltd. [source] The effect of Phyllanthus niruri on urinary inhibitors of calcium oxalate crystallization and other factors associated with renal stone formationBJU INTERNATIONAL, Issue 9 2002A.M. Freitas Objective,To evaluate the effect of an aqueous extract of Phyllanthus niruri (Pn), a plant used in folk medicine to treat lithiasis, on the urinary excretion of endogenous inhibitors of lithogenesis, citrate, magnesium and glycosaminoglycans (GAGs). Materials and methods,The effect of chronic (42 days) administration of Pn (1.25 mg/mL/day, orally) was evaluated in a rat model of urolithiasis induced by the introduction of a calcium oxalate (CaOx) seed into the bladder of adult male Wistar rats. The animals were divided into four groups: a sham control (16 rats); a control+Pn (six); CaOx+water instead of Pn (14); and CaOx+Pn (22). Plasma and urine were collected after 42 days of treatment for biochemical analysis and the determination of urinary excretion of citrate, magnesium and GAGs. The animals were then killed and the calculi analysed. Results,The creatinine clearance or urinary and plasma concentrations of Na+, K+, Ca2+, oxalate, phosphate and uric acid were unaffected by Pn or the induction of lithiasis. Treatment with Pn strongly inhibited the growth of the matrix calculus and reduced the number of stone satellites compared with the group receiving water. The calculi were eliminated or dissolved in some treated animals (three of 22). The urinary excretion of citrate and magnesium was unaffected by Pn treatment. However, the mean (sd) urinary concentration of GAGs was significantly lower in rats treated with CaOx+Pn, at 5.64 (0.86) mg/g creatinine, than when treated with CaOx + water, at 11.78 (2.21) mg/g creatinine. In contrast, the content of GAGs in the calculi was higher in the CaOx + Pn rats, at 48.0 (10.4) g/g calculus, than in the CaOx + water group, at 16.6 (9.6) g/g calculus. Conclusion,These results show that Pn has an inhibitory effect on crystal growth, which is independent of changes in the urinary excretion of citrate and Mg, but might be related to the higher incorporation of GAGs into the calculi. [source] | ||||||||||