IMPAIRMENT OF RENAL CONCENTRATING ABILITY IN PROLONGED HYPERCALCEMIA AND HYPERCALCIURIA IN MAN
IMPAIRMENT OF RENAL CONCENTRATING ABILITY IN PROLONGED HYPERCALCEMIA AND HYPERCALCIURIA IN MAN
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DOI：
10.1172/jci104305
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发表时间：
1961-01-01
影响因子：
15.9
通讯作者：
BARTTER, FC
中科院分区：
文献类型：
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作者：
GILL, JR;BARTTER, FC
在高钙尿症、高钙血症或两者兼有的受试者中测量最大尿渗透压（Umax和TC H20（重吸收的溶质游离水））。对患有“高吸收性高钙尿症”、高维生素D血症和高甲状旁腺素血症的患者进行了旨在降低尿钙的治疗前后的研究。所有受试者均显示Umax和Tc H2O受损，治疗后改善。这些数据表明，过量的钙，而不是产生它的代理或疾病过程，最终是“负责的缺陷。浓缩缺陷不是由于溶质排泄增加所致，这表明改善后的变化可以忽略不计。除一名受试者外，所有受试者均表现出正常的钠保护，在此摄入量下，尿钠低于每天9毫克当量，这表明浓缩缺陷并不依赖于钠转运的严重失败。
Maximal urinary osmolality (Umax and TC H20 (solute free water reabsorbed) were measured in subjects with hypercalciuria, hypercalcemia, or both. Patients with "hyperabsorption hypercalciuria," hypervitaminosis D and hyper-parathyroidism were studied before and after treatment designed to lower urinary calcium. All subjects showed impairment in both Umax and Tc H2O and improvement in them with therapy. The data suggest that excess of Ca, rather than the agent or disease process producing it, is ultimately "responsible for the defect. The concentrating defect was not attributable to an increased solute excretion, which showed negligible changes with improvement. All subjects but one showed normal Na conservation with urinary Na less than 9 meq per day at this intake, suggesting that the concentrating defect does not depend upon gross failure of Na transport.