Kivonat:
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 evaluate cellular Na handling. The effect of chronic thiazide
administration 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 +/- 110 mu mol P/l erythrocyte per hour vs. 3,165 +/- 175, P <
0.01). Thiazide 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 period, P < 0.03). The bone mineral density
Z score rose from -1.3 +/- 0.26 to -0.8 +/- 0.22 (P < 0.03). We
conclude that IHU is accompanied by abnormalities of erythrocyte
Na+/K+-ATPase and Na+/Li+ countertransport which are corrected by
chronic hydrochlorothiazide administration. These changes could model
alterations in renal tubular transport mechanisms still to be
elucidated. Chronic thiazide treatment also has a positive effect on
bone mineral density.
