SODIUM-TRANSPORT AND BONE-MINERAL DENSITY IN HYPERCALCIURIA WITH THIAZIDE TREATMENT

Erythrocyte sodium-potassium (Na+/K+) -ATPase and sodium-lithium (Na+/ Li+) countertransport activities were measured in 18 children (aged 9. 6 years, range 6-16 years) with idiopathic hypercalciuria (IHU) to eva luate cellular Na handling. The effect of chronic thiazide administrat ion on these parameters and on bone mineral density was also evaluated . Patients with IHU had significantly lower erythrocyte Na+/K+-ATPase activity than 23 age-matched healthy controls (mean + SEM 2,156 +/- 11 0 mu mol P/l erythrocyte per hour vs. 3,165 +/- 175, P < 0.01). Thiazi de treatment significantly lowered urinary calcium excretion; this was followed by a slight suppression of intact parathyroid hormone (iPTH) . The urinary calcium/creatinine ratio before and during treatment was 0.90 +/- 0.07 mmol/mmol versus 0.51 +/- 0.06 respectively, P < 0.01. The corresponding iPTH levels were 5.9 +/- 0.6 pmol/l and 5.1 +/- 0.7, P < 0.05. The Na+K+-ATPase activity increased significantly (2,769 +/ - 169 mu mol P/l erythrocyte per hour vs. 2,156 +/- 110 in the control pe riod, P < 0.01) and the Na+/Li+ countertransport decreased (268 +/ - 28 mu mol Li/l erythrocyte per hour vs. 328 + 26 in the control peri od, P < 0.03). The bone mineral density Z score rose from -1.3 +/- 0.2 6 to -0.8 +/- 0.22 (P < 0.03). We conclude that IHU is accompanied by abnormalities of erythrocyte Na+/K+-ATPase and Na+/Li+ countertranspor t which are corrected by chronic hydrochlorothiazide administration. T hese changes could model alterations in renal tubular transport mechan isms still to be elucidated. Chronic thiazide treatment also has a pos itive effect on bone mineral density.