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MOUNTING evidence indicates that two disorders, idiopathic hypercalciuria and hyperuricosuria, account for approximately 65 per cent of calcium stones in patients without a better known cause of nephrolithiasis. Of 230 patients studied during the past five years in the Michael Reese Hospital kidney-stone program, only 84 had a well established cause of stones (Table 1). The urine of the remaining 146 patients, who would usually be considered to have idiopathic recurrent stone formation,1 contained excessive amounts of calcium and uric acid. Because it has become clear that both hypercalciuria and hyperuricosuria can participate in the formation of calcium stones, it . . .

Renal stones is not one of the "in" topics of medical research. Historical importance it has aplenty, but glamour and excitement none. Research in the stone field has been ploddingly slow and carried out in relatively few laboratories. Nevertheless, genuine, valuable accor plishments have been made in the past decade leading to better understanding of pathogenetic mechanisms and rational therapy of stone disease. Witness the increased knowledge of factors affecting calcium excretion, the careful descriptions of cystinuria and the hyperoxaluric states, the successful treatment of uric acid stones with allopurinol and alkali, and the reduction of calcium stone formation with . . .