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

Hyperabsorption of dietary oxalate is a major factor in the pathogenesis of enteric hyperoxaluria and a frequent complication of inflammatory bowel disease and ileojejunal bypass surgery. Successful treatment requires reduction in oxalate intake or inhibition of absorption of dietary oxalate by oral ingestion of oxalate binding agents. To identify such agents, oxalate binding by anion-exchange resins, gums, and aluminum hydroxide was measured under conditions that simulated those present in the intestinal lumen. Of the agents tested, those that bound oxalate best were colestipol and aluminum hydroxide. Strongly basic anion-exchange resins readily bound oxalate only in the absence of chloride. These results suggest that colestipol and aluminum hydroxide administration might reduce dietary oxalate absorption in patients with enteric hyperoxaluria.
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PMID:Effective therapy of enteric hyperoxaluria: in vitro binding of oxalate by anion-exchange resins and aluminum hydroxide. 610 Nov 57

Hyperoxaluria occurs in most patients after the conventional jejunoileal bypass procedure for obesity. The mechanism of hyperoxaluria is complex, involving persistence of dietary oxalate in solution as well as increased colonic permeability to oxalate. Endogenous oxalate formation also contributes to hyperoxaluria. Treatment is unsatisfactory and involves a low-oxalate diet and simultaneous administration of agents which bind oxalate and bile acids, such as aluminum hydroxide. Hyperoxaluria was not present in 21 of 22 patients who had undergone the pancreato-biliary bypass procedure.
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PMID:Hyperoxaluria associated with intestinal bypass surgery for morbid obesity: occurrence, pathogenesis and approaches to treatment. 679 33

The urinary excretion of oxalate, calcium, magnesium and citrate as well as the inhibition of calcium oxalate crystal growth in diluted urine was studied in seven patients with hyperoxaluria following jejunoileal bypass. The study was performed on an outpatient basis before and during daily administration of 38 or 113 mmol calcium, 28 mmol of aluminum, 20 mmol of magnesium or 16 g of cholestyramine. Each substance was administered for seven days with a free interval of at least seven days. The mean urinary oxalate excretion was not reduced with any of these regimens. Administration of 38 mmol of calcium per day resulted in increased oxalate and magnesium excretion. Increased excretion of both calcium and citrate was observed during administration of 113 mmol of calcium per day. Calcium and magnesium excretion was increased with aluminium. An increased magnesium excretion was also observed during administration of magnesium, resulting in a decreased calcium/ magnesium ratio. Cholestyramine resulted in increased oxalate and decreased citrate excretion.
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PMID:Effects of calcium, aluminium, magnesium and cholestyramine on hyperoxaluria in patients with jejunoileal bypass. 683 29

Calcium oxalate monohydrate crystals are responsible for the kidney injury associated with exposure to ethylene glycol or severe hyperoxaluria. Current treatment strategies target the formation of calcium oxalate but not its interaction with kidney tissue. Because aluminum citrate blocks calcium oxalate binding and toxicity in human kidney cells, it may provide a different therapeutic approach to calcium oxalate-induced injury. Here, we tested the effects of aluminum citrate and sodium citrate in a Wistar rat model of acute high-dose ethylene glycol exposure. Aluminum citrate, but not sodium citrate, attenuated increases in urea nitrogen, creatinine, and the ratio of kidney to body weight in ethylene glycol-treated rats. Compared with ethylene glycol alone, the addition of aluminum citrate significantly increased the urinary excretion of both crystalline calcium and crystalline oxalate and decreased the deposition of crystals in renal tissue. In vitro, aluminum citrate interacted directly with oxalate crystals to inhibit their uptake by proximal tubule cells. These results suggest that treating with aluminum citrate attenuates renal injury in rats with severe ethylene glycol toxicity, apparently by inhibiting calcium oxalate's interaction with, and retention by, the kidney epithelium.
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PMID:Aluminum citrate prevents renal injury from calcium oxalate crystal deposition. 2313 89

Primary hyperoxaluria type 1 (PH1), an inherited rare disease of glyoxylate metabolism, arises from mutations in the enzyme alanine-glyoxylate aminotransferase. The resulting deficiency in this enzyme leads to abnormally high oxalate production resulting in calcium oxalate crystal formation and deposition in the kidney and many other tissues, with systemic oxalosis and ESRD being a common outcome. Although a small subset of patients manages the disease with vitamin B6 treatments, the only effective treatment for most is a combined liver-kidney transplant, which requires life-long immune suppression and carries significant mortality risk. In this report, we discuss the development of ALN-GO1, an investigational RNA interference (RNAi) therapeutic targeting glycolate oxidase, to deplete the substrate for oxalate synthesis. Subcutaneous administration of ALN-GO1 resulted in potent, dose-dependent, and durable silencing of the mRNA encoding glycolate oxidase and increased serum glycolate concentrations in wild-type mice, rats, and nonhuman primates. ALN-GO1 also increased urinary glycolate concentrations in normal nonhuman primates and in a genetic mouse model of PH1. Notably, ALN-GO1 reduced urinary oxalate concentration up to 50% after a single dose in the genetic mouse model of PH1, and up to 98% after multiple doses in a rat model of hyperoxaluria. These data demonstrate the ability of ALN-GO1 to reduce oxalate production in preclinical models of PH1 across multiple species and provide a clear rationale for clinical trials with this compound.
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PMID:An Investigational RNAi Therapeutic Targeting Glycolate Oxidase Reduces Oxalate Production in Models of Primary Hyperoxaluria. 2953 12