Calcium Carbimide in the Treatment of Primary Hyperoxaluria

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 . . .