Vitamin Be antagonist

The same authors have shown that oxalate nephrocalcinosis and hyperoxaluria can be reproduced in animals such as rats (G6) or cats (G7) by vitamin Be deficiency. The main difference between the experimental disease and patients with oxalosis is the absence of extrarenal deposits in the former (G7). The urinary excretion of oxalate in vitamin Be-deflcient rats can be enhanced by dietary supplementation with vitamin Be antagonists, such as deoxypyridoxine or isonicotinic hydra-zide, or with glycine, which appears to be the endogenous source of the excessive oxalate production, as in patients with oxalosis (G6). 

Supplement vitamin Be deficiency states, impaired absorption, therapy with vitamin Be antagonists, increased requirements (pregnancy, lactation), increased stimulation with exogenic estrogens. X-ray therapy... 

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