[Clinical aspects of oxalate metabolism].
The daily amount of oxalate in normales is formed by about 90 per cent from endogenous sources. Approximately 10 per cent are due to intestinal absorption of dietary oxalate. The oxalate formed endogenously is derived from aminoacid-, carbohydrate- and ascorbic acid metabolism. Oxalate synthesis is increased in inherited defects of enzymes (primary hyperoxaluria) or as a consequence of exogenous factors (vitamin-B6-deficiency, ethylene glycol intoxication, high dose ascorbic acid application, possibly excessive protein and carbohydrate intake). The intestinal absorption of oxalate is increased in some diseases of the intestinal tract (Morbus Crohn, ulcerative colitis). Oxalate, that is totally excreted in urine, is the principal component for urinary calcium oxalate saturation. Oxalate accumulates in renal failure. The increased plasma oxalate level - as a consequence of impaired renal function and additional metabolic influences - is an important factor for calcium oxalate depositions in uremic patients.
D000818:Animals; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism; D010070:Oxalates / Q000378:metabolism* / Q000652:urine; D026681:Vitamin B 6 Deficiency / Q000378:metabolism; D014993:Xylitol
D010070:Oxalates; D014993:Xylitol
Klinische Aspekte des Oxalatstoffwechsels.