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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To better understand the pathogenesis of nephrolithiasis, we developed a new animal model that closely mimics human calcium oxalate stone disease. Rats were treated with a regimen that combines moderate hyperoxaluria (produced by 10 days of feeding with 3% ammonium oxalate) with mild proximal tubular injury/dysfunction (produced by 8 daily injections of gentamicin sulfate -40 mg./kg.). This combined treatment caused a marked increase in the incidence of calcium oxalate crystals and stones over that seen in animals treated with oxalate or gentamicin alone. Using a semiquantitative scoring system for estimating the abundance of crystals in coronal sections of kidneys, we found that 63% of animals receiving gentamicin plus oxalate showed "moderate" numbers of crystal, as compared to 8% of animals receiving oxalate alone; and the majority of the crystals occurred in the papilla, a pattern similar to that seen in human stone disease. Untreated rats and rats treated with gentamicin alone did not exhibit calcium oxalate crystals or stones. Despite the abundance of crystals and stones, animals receiving gentamicin plus oxalate retained relatively normal renal function as judged by creatinine clearance. Thus, the model has several advantages over preexisting models of nephrolithiasis. Crystal and stone deposition develop rapidly (within 14 days). The pattern of deposition resembles that seen in human stone disease and renal function remains relatively normal. These findings indicate that this model of nephrolithiasis may prove useful for studies of the pathogenesis of stone disease. Moreover, they suggest that renal tubular injury and/or dysfunction may produce conditions conducive to the formation and growth of calcium oxalate stones.
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PMID:A new model of nephrolithiasis involving tubular dysfunction/injury. 194 7

A 54-year old man who had been taking triamterene (150 mg daily) over a period of 8 months, passed a 3 mm stone partly coated with mustard-colored substance. Metabolic evaluation showed only mild-hyperoxaluria. Through IR spectrography after microdissection, thin-layer chromatography, UV light examination, and mass spectrometry, the stone if found to consist of 70% whewellite, 5% protein, 5% carbapatite and 20% triamterene and hydroxylated triamterene, and perhaps also the sulfate conjugate of this metabolite. In spite of the few number of observations (two cases have been reported previously), triamterene seems likely to induce stone formation, both alone and associated with urate or oxalate, and triamterene should be used cautiously in patients with a predisposition for nephrolithiasis.
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PMID:[Drug induced nephrolithiasis: observation of an oxalate and hydroxylated triamterene stone (author's transl)]. 730 Oct 28

Lactic acid bacteria (LABs) are being used as a probiotic very often for various enteric problems. Many genetically modified LABs are created by different workers for various novel applications. In this study we examine the expression of heterologous oxalate decarboxylase (oxdc) in Lactobacillus plantarum NC8. Generally, this enzyme is not present in Lactobacillus spp. Oxdc gene from Bacillus subtilis was polymerase chain reaction-amplified and cloned in a shuttle vector pSIP400 series, downstream of the inducible promoter, P(orfx). In the presence of an inducing peptide, Sakacin-P, the expression of OxdC was observed in sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The cell-free extract and the purified protein from the recombinant LABs showed the presence of OxdC activity. The above recombinant LABs, with desired modifications, can be used as a possible probiotic for the degradation of intestinal dietary oxalate for preventing enteric hyperoxaluria.
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PMID:Heterologous expression of oxalate decarboxylase in Lactobacillus plantarum NC8. 1894 1

We have previously reported that heparan sulfate (HS) / heparan sulfate proteoglycan (HSPG, syndecan-1) expression significantly increased in the rat kidney during calcium oxalate (CaOx) nephrolithiasis. Although the exact mechanism of the increased syndecan expression still remains unclear, HS/syndecan is thought to have some important roles in CaOx crystal formation. The present study examined the role of HS during oxalate exposure by using a newly developed cell line (KIC-synd-1) that expresses human heparan sulfate proteoglycan (syndecan-1). Quantitative competitive (QC)-RT-PCR was used to examine change of syndecan-1 mRNA expression in KIC-synd-1 cells. Production of syndecan-1 core protein and glycosaminoglycans (GAGs) were also confirmed by Western blot, immunohistochemistry and HPLC, respectively. Wild type Mardin-Darby canine kidney (MDCK) cells were also examined in the same manner. The stable expression of syndecan-1 gene and production of both core protein and HS chains were confirmed in the newly developed KIC-synd-1 cell line. Increased syndecan-1 mRNA expression and production of core proteins were confirmed in KIC-synd-1 cells during oxalate exposure. MTT assay revealed that the cell viability decreased significantly in the MDCK cells after 1 mM oxalate exposure (p<0.05). On the other hand, there was no significant difference in the oxalate exposed KIC-synd-1 cells. However, the cell viability in KIC-synd-1 cells pretreated with heparitinase digestion decreased significantly before oxalate exposure (p<0.05). The present data suggests that both exogenous and endogenous HS exerts protective effect against oxalate-induced cell injuries. Previous studies in our laboratory have indicated that hyperoxaluria and deposition of CaOx crystals resulted in renal tubular cellular injury inducing the synthesis of HSPG to protect and repair the damaged epithelial cell surface. The present data offers strong support for this hypothesis. Finally, HS could be potent inhibitor of CaOx nephrolithiasis and the absence of this substance on the tubular surface may increase the risk of CaOx crystal formation and retention.
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PMID:Increased expression of heparan sulfate proteoglycan on the cultured renal epithelial cells during oxalate exposure. 1898 81

We studied the effects of oral magnesium (Mg) salts either alone or in combination with pyridoxine hydrochloride in rats on pyridoxine-deficient diet. Fifty-four male rats were randomized into two groups and were fed either a standard diet or a pyridoxine-deficient diet for 3 weeks. A significant rise of the EGOT index ( > 1.5), oxaluria (from 74.8 +/- 5.2 to 117.9 +/- 12.3 mcM/l, p = 0.035), and crystalluria in rats fed with pyridoxine deficient diet were revealed. Oral Mg chloride, Mg L-aspartate either alone or in combination with pyridoxine in comparison with magnesium sulfate, magne B6 (Mg lactate with pyridoxine) and pyridoxine alone were administered (50 mg of magnesium and/or 5 mg of pyridoxine per kg body weight). Magnesium salts in combination with pyridoxine lowered an oxalate level and crystalluria whereas magnesium salts alone reduced only crystalluria. Antilithis effects of Mg L-aspartate and Mg chloride in combination with pyridoxine were comparable with those observed in magne B6 or pyridoxine treatment and were significantly higher than in magnesium sulfate treatment.
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PMID:[Effects of mangesium salts and their combinations with vitamin B6 on oxalates crystalluria in rats fed with pyridoxine-deficient diet]. 1967 Aug 11

Urolithiasis, a condition in which stones are present in the urinary system, including the kidneys and bladder, is a poorly understood yet common disorder worldwide that leads to significant health care costs, morbidity, and work loss. Acetaminophen-induced liver damage is a major cause of death in patients with acute liver failure. Kidney and urinary stones and liver toxicity are disturbances linked to alterations in oxalate and sulfate homeostasis, respectively. The sulfate anion transporter-1 (Sat1; also known as Slc26a1) mediates epithelial transport of oxalate and sulfate, and its localization in the kidney, liver, and intestine suggests that it may play a role in oxalate and sulfate homeostasis. To determine the physiological roles of Sat1, we created Sat1-/- mice by gene disruption. These mice exhibited hyperoxaluria with hyperoxalemia, nephrocalcinosis, and calcium oxalate stones in their renal tubules and bladder. Sat1-/- mice also displayed hypersulfaturia, hyposulfatemia, and enhanced acetaminophen-induced liver toxicity. These data suggest that Sat1 regulates both oxalate and sulfate homeostasis and may be critical to the development of calcium oxalate urolithiasis and hepatotoxicity.
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PMID:Urolithiasis and hepatotoxicity are linked to the anion transporter Sat1 in mice. 2252 12

This review summarizes the physiological roles of the renal sulfate transporters NaS1 (Slc13a1) and Sat1 (Slc26a1). NaS1 and Sat1 encode renal anion transporters that mediate proximal tubular sulfate reabsorption and thereby regulate blood sulfate levels. Targeted disruption of murine NaS1 and Sat1 leads to hyposulfatemia and hypersulfaturia. Sat1 null mice also exhibit hyperoxalemia, hyperoxaluria and calcium oxalate urolithiasis. Dysregulation of NaS1 and Sat1 leads to hypersulfaturia, hyposulfatemia and liver damage. Loss of Sat1 leads additionally to hyperoxaluria with hyperoxalemia, nephrocalcinosis and calcium oxalate urolithiasis. These data indicate that the renal anion transporters NaS1 and Sat1 are essential for sulfate and oxalate homeostasis, respectively.
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PMID:Physiological roles of mammalian sulfate transporters NaS1 and Sat1. 2129 88

This review will briefly summarize current knowledge on the renal anion transporters sodium-sulfate cotransporter-1 (NaS1; Slc13a1) and sulfate-anion transporter-1 (Sat1; Slc26a1). NaS1 and Sat1 mediate renal proximal tubular sulfate reabsorption and thereby regulate blood sulfate levels. Sat1 also mediates renal oxalate transport and controls blood oxalate levels. Targeted disruption of murine NaS1 and Sat1 leads to hyposulfatemia and hypersulfaturia. Sat1 null mice also exhibit hyperoxalemia, hyperoxaluria, and calcium oxalate urolithiasis. NaS1 and Sat1 null mice also have other phenotypes that result due to changes in blood sulfate and oxalate levels. Experimental data indicate that NaS1 is essential for maintaining sulfate homeostasis, whereas Sat1 controls both sulfate and oxalate homeostasis in vivo.
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PMID:Physiological roles of renal anion transporters NaS1 and Sat1. 2149 Jan 38

Experimental urolithiasis was induced in 80 white non-inbred male rats by adding 0.75% ethylene glycol and 2% ammonium chloride to drinking water by Fan et al. After significant differences in crystalluria, oxaluria and urine pH were achieved in hyperoxaluric rats vs controls one, hyperoxaluric rats were given magnesium (Mg) salts Mg chloride, Mg L-aspartate either alone or in combination with pyridoxine hydrochloride (B6) in comparison with Mg sulfate and magne B6 (mg lactate in combination with B6) in a dose of 50 mg of elementary Mg per 1 kg of body weight. All the rats were fed with Mg-adequate diet containing 0.84 g of Mg oxide (0.5 g of elementary Mg per kg of diet). Calcium-oxalate urolithiasis has developed in rats taking ethylene glycol and ammonium chloride for 28 days. An urinary oxalates levels increased threefold, oxalate/creatinine--fourfold. Calcium oxalate crystals were detected in the urine of rats drinking solution of ethylene glycol and ammonium chloride, pH decreased by 20%, fractional excretion (FE) of Mg increased by 60%, FE of phosphate--by 58.2%, FE of calcium--by 95.8%, creatinine clearance lowered by 39.2% in comparison with intact group. Magnesium salts administration resulted in reduction of urine oxalates, crystalluria, phosphate excretion, Ca/Mg and oxalate/creatinine ratios, increased urine pH and creatinine clearance. Mg L-aspartate in combination with vitamin B6 appeared the most effective salt and significantly more effective than magnesium sulfate.
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PMID:[Effects of magnesium salts on the course of experimental calcium-oxalate urolithiasis]. 2181 54

Anion transporters NaS1 (SLC13A1) and Sat1 (SLC26A1) mediate sulfate (re)absorption across renal proximal tubule and small intestinal epithelia, thereby regulating blood sulfate levels. Disruption of murine NaS1 and Sat1 genes leads to hyposulfatemia and hypersulfaturia. Sat1-null mice also exhibit hyperoxalemia, hyperoxaluria, and calcium oxalate urolithiasis. This review will highlight the current pathophysiological features of NaS1- and Sat1-null mice resulting from alterations in circulating sulfate and oxalate anion levels.
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PMID:Slc13a1 and Slc26a1 KO models reveal physiological roles of anion transporters. 2288 9


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