Oxalate deposits in the kidney of 5/6 nephrectomised rats supplemented by large doses of vitamin C.

Abstract

The secondary oxalosis of renal failure has been recognised for more than 20 years (Bennett and Rosenblum, 1961), but details of its prevalence and clinical features have been addressed only recently(Salyer and Keren, 1973; Boer et al., 1984; Pru et al., 1985). Oxalate is a non-metabolisable end product of glycine and ascorbic acid metabolism(Elder and Wyngaarden, 1960) and virtually all of it is excreted by the kidneys. Renal insufficiency can produce oxalate loads that exceed renal excretory capacity. Protein binding of oxalate is minimal and most of it should be removed by hemodialysis. However, hemodialysis does not remove oxalate as fast as it is formed, leaving patients at risk from the complications which result from systemic oxalosis (Landwehr et al., 1987).KeywordsOxalic AcidUrinary OxalateCalcium Oxalate CrystalRemnant KidneyPlasma OxalateThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.