Endogenous oxalate synthesis and glycine, serine, deoxypyridoxine interrelationships in vitamin B6-deficient rats.

Attempts to study the etiology of diseases associated with oxaluria or oxalate deposition or both, have been handicapped by the misconception that very little urinary oxalate is endogenous in origin. However, Gershoff et al. (1) have demonstrated oxalate nephrocalcinosis and oxaluria in vitamin Be-deficient cats. In vitamin Bc-deficient rats consuming diets free from oxalate, renal calculi of calcium oxalate monohydrate have been observed (2). Such renal calculi and the obstructive sequelae they produce, closely resemble the conditions found in human cases of kidney disease accompanied by oxalate stones. The possibility that these findings relating oxalate production and vitamin B8 may be pertinent in human nutrition is indicated by the finding (3) that vitamin Bs supplements decreased oxalate excretion in human subjects receiving diets thought to be more than adequate in vitamin Be. In the present paper, the effect of glycine, deoxypyridoxine, and isonicotinic acid hydrazide supplements on oxaluria in vitamin Be-deficient rats is reported. The effect of L-serine and glycine on deoxypyridoxine toxicity has also been studied.