Reusz G S, Dobos M, Vásárhelyi B, Sallay P, Szabó A, Horváth C, Szabó A, Byrd D J, Thole H H, Tulassay T
First Department of Pediatrics, Semmelweis University Medical School, Budapest, Hungary.
Pediatr Nephrol. 1998 Jan;12(1):30-4. doi: 10.1007/s004670050398.
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 micromol 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 micromol P/l erythrocyte per hour vs. 2,156 +/- 110 in the control period, P < 0.01) and the Na+/Li+ countertransport decreased (268 +/- 28 micromol 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.
对18名特发性高钙尿症（IHU）儿童（年龄9.6岁，范围6 - 16岁）测定红细胞钠钾（Na+/K+）-ATP酶和钠锂（Na+/Li+）逆向转运活性，以评估细胞内钠处理情况。还评估了长期服用噻嗪类药物对这些参数以及骨密度的影响。与23名年龄匹配的健康对照相比，IHU患者的红细胞Na+/K+-ATP酶活性显著降低（平均±标准误：每小时每升红细胞2,156±110微摩尔磷，对照为3,165±175，P<0.01）。噻嗪类药物治疗显著降低尿钙排泄；随后血清完整甲状旁腺激素（iPTH）略有下降。治疗前和治疗期间尿钙/肌酐比值分别为0.90±0.07毫摩尔/毫摩尔和0.51±0.06，P<0.01。相应的iPTH水平分别为5.9±0.6皮摩尔/升和5.1±0.7，P<0.05。Na+/K+-ATP酶活性显著增加（每小时每升红细胞2,769±169微摩尔磷，对照期为2,156±110，P<0.01），Na+/Li+逆向转运降低（每小时每升红细胞268±28微摩尔锂，对照期为328 + 26，P<0.03）。骨密度Z评分从 - 1.3±0.26升至 - 0.8±0.22（P<0.03）。我们得出结论，IHU伴有红细胞Na+/K+-ATP酶和Na+/Li+逆向转运异常，长期服用氢氯噻嗪可纠正这些异常。这些变化可能模拟了仍有待阐明的肾小管转运机制改变。长期噻嗪类药物治疗对骨密度也有积极作用。
