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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

Stone disease is as old as recorded history but despite advances in diagnosis and treatment, it continues to cause significant morbidity. This review summarises the current pharmacologic management of urinary calculi based upon the stone type. All patients with stone disease are advised to increase fluid intake, limit dietary protein and limit sodium. Calcium oxalate stones can be managed on a selective or non-selective basis depending on the cause of the hypercalciuria or hyperoxaluria. Agents currently in use include sodium cellulose phosphate, thiazides, orthophosphates, oral calcium supplements, pyridoxine, cholestyramine, citrate, magnesium and allopurinol. Classically, struvite stones occur in the presence of urea splitting organisms and are composed of magnesium, ammonium phosphate and carbonate apatite. The goal of treatment is to make patients stone free as bacteria retained in stone fragments lead to stone growth. Urease inhibitors, aluminium hydroxide gel, hemiacidrin, and Suby G and M solutions are infrequently used in treatment. Cystine stones are the result of an autosomal recessive disorder. D-Penicillamine, captopril and alpha-mercaptopropionylglycine (MPG) are all oral agents that have proven to be efficacious. As more randomised trials are conducted and the understanding of endogenous stone inhibitors progresses, the medical management of stone disease will continue to improve.
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PMID:Pharmacology for renal calculi. 1124 28

Renal tubular epithelium is the major target for oxalate induced injury, and sustained hyperoxaluria together with CaOx crystal formation/deposition may induce renal tubular cell damage and/or dysfunction. This may express itself in cell apoptosis. To evaluate the possible protective effects of certain agents (vitamin E, potassium citrate, allopurinol, verapamil and MgOH) on the presence and the severity of apoptotic changes caused by hyperoxaluria on renal tubular epithelium, an experimental study in rabbits was performed. Seventy rabbits were divided into seven different groups (each group n = 10): in group I severe hyperoxaluria was induced by continuous ethylene glycol (0.75%) administration started on day 0 and completed on day 14. Histologic alterations including crystal formation together with apoptotic changes (by using the TUNEL method) were evaluated on days 21 and 42, respectively. In the remaining experimental groups (groups II-VI), animals received some agents in addition to the induction of hyperoxaluria in an attempt to limit apoptotic changes. Group VII) animals constituted the controls. Kidneys were examined histopathologically under light microscopy for the presence and degree of crystal deposition in the tubular lumen. The percentage of apoptotic nuclei in the control group was significantly different from the other group animals (2.9-2.4%) in all study phases (P < 0.05). Apart from potassium citrate and allopurinol, the other medications seemed to prevent or limit the formation of apoptotic changes in renal tubular epithelium during the early period (day 21). The percentage of positively stained nuclei in animals undergoing potassium citrate medication ranged from 24.3% to 28.6%, with an average of 27.1%. This was 18.4% in animals receiving allopurinol. On the other hand, animals receiving magnesium hydroxide (MgOH), verapamil and vitamin E demonstrated limited apoptotic changes (11.2, 9.7, 8.7%, respectively) during this phase(P < 0.05). In the long-term (day 42), the animals receiving allopurinol and vitamin E showed a decrease in the percentage of the positively stained nuclei (13.5% and 8.3%, respectively). Animals in the other groups showed an increase in the number and percentage of apoptotic cells. Although, there was a significant decrease in the mean values of apoptosis in animals receiving vitamin E (8.7%-8.3%) and allopurinol (18.4%-13.5%) (P < 0.05), animals on verapamil, MgOH and potassium citrate medication had an increase in these values or the change was not found to be significant. In the light of our findings and results from the literature, it is clear that that both hyperoxaluria and CaOx crystals may be injurious to renal epithelial cells. Apoptotic changes observed in renal tubular epithelial cells induced by massive hyperoxaluria might result in cell degradation and may play a role in the pathologic course of urolithiasis. Again, as demonstrated in our study, the limitation of both crystal deposition and apoptotic changes might be instituted by some antioxidant agents as well as urinary inhibitors. Clinical application of such agents in the prophylaxis of stone disease might limit the formation of urinary calculi, especially in recurrent stone formers.
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PMID:Limitation of apoptotic changes in renal tubular cell injury induced by hyperoxaluria. 1524 86