Renal handling of sodium and calcium in hypercalciuria

The renal handling of Ca in response to Na intake was evaluated in 12 patients with hypercalciuria and active kidney stone disease. There was no depression of urinary Ca excretion in response to the hypocalciuric effect of metolazone. Patients were hospitalized and their Ca and Na excretions measured while on a 190‐mEq Na, 800‐mg Ca, 1200‐mg PO − 4 diet. These measurements were then repeated after Na intake decreased to 35 mEq/day while other variables, including diuretic dose and Ca intake, were unchanged. Two distinct responses were elicited by patients after Na restriction. In group I or the “responders” (n = 4), Ca excretion was reduced from 255 ±31 to 62 ±6 mg/24 hr. In the control group (n = 4), Ca excretion decreased from 95 ± 8 to 57 ± 11 mg/24 hr at similar levels of Na excretion. In group II or the “nonresponders” (n = 8), Ca excretion fell from 317 ±31 to 154 ±17 mg/24 hr when Na excretion was less than 50 mEq/24 hr. Metolazone with Na restriction normalized urine Ca excretion to the same order as in control subjects in group I. This is indicative of a mild Ca leak or a salt‐sensitive leak. Despite diuretic and Na restriction most of the patients with hypercalciuria (group II) did not reabsorb Ca in a normal manner. This is indicative of a severe reabsorptive defect for Ca despite normal Na handling. Clinical Pharmacology and Therapeutics (1984) 35, 342–347; doi: 10.1038/clpt.1984.41