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The effect of chronic thiazide\nadministration on these parameters and on bone mineral density was also\nevaluated. Patients with IHU had significantly lower erythrocyte\nNa+/K+-ATPase activity than 23 age-matched healthy controls (mean + SEM\n2,156 +/- 110 mu mol P/l erythrocyte per hour vs. 3,165 +/- 175, P <\n0.01). Thiazide treatment significantly lowered urinary calcium\nexcretion; this was followed by a slight suppression of intact\nparathyroid hormone (iPTH). The urinary calcium/creatinine ratio before\nand during treatment was 0.90 +/- 0.07 mmol/mmol versus 0.51 +/- 0.06\nrespectively, P < 0.01. The corresponding iPTH levels were 5.9 +/- 0.6\npmol/l and 5.1 +/- 0.7, P < 0.05. The Na+K+-ATPase activity increased\nsignificantly (2,769 +/- 169 mu mol P/l erythrocyte per hour vs. 2,156\n+/- 110 in the control pe riod, P < 0.01) and the Na+/Li+\ncountertransport decreased (268 +/- 28 mu mol Li/l erythrocyte per hour\nvs. 328 + 26 in the control period, P < 0.03). The bone mineral density\nZ score rose from -1.3 +/- 0.26 to -0.8 +/- 0.22 (P < 0.03). We\nconclude that IHU is accompanied by abnormalities of erythrocyte\nNa+/K+-ATPase and Na+/Li+ countertransport which are corrected by\nchronic hydrochlorothiazide administration. These changes could model\nalterations in renal tubular transport mechanisms still to be\nelucidated. 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