We have determined calcium and sodium excretion rates in three members of a kinship with familial hypocalciuric hypercalcemia (FHH) and in four patients with primary hyperparathyroidism (PHP) under control conditions and following the intravenous administration of chlorothiazide or furosemide. The characteristic hypocalciuria of FHH, evidenced by a significantly reduced urinary calcium/creatinine ratio compared with that of PHP, is present under control conditions (0.08 vs. 0.26 mg calcium/mg creatinine, respectively, P less than 0.05), and after chlorothiazide (0.14 vs. 0.53, respectively, P less than 0.01). However, after furosemide infusion the calcium/creatinine ratio is no longer lower in FHH than in PHP (1.12 vs. 1.14, respectively, P greater than 0.05). These data suggest that, in FHH, tubular calcium reabsorption is enhanced in the thick ascending limb of Henle's loop, the site of action of furosemide. However, the data do not exclude the presence of an abnormality at a more distal site in the nephron.