Calcium Carbimide in the Treatment of Primary Hyperoxaluria

Abstract

A DEFECT in the transamination of glyoxalate has been suggested as the metabolic abnormality responsible for the increased rate of oxalate synthesis in patients with primary hyperoxaluria (Fig. 1).¹ Some of this excess oxalate combines with calcium to form insoluble deposits in a variety of tissues, resulting, in the kidney, in extensive scarring and progressive renal failure. In a recent review article² no specific therapy for this disease was proposed. From a consideration of Figure 1 it is evident that, regardless of the site of the metabolic block, any agent that depresses the rate of oxalate formation may be expected to be . . .