CHAPDELAINE A, LANTHIER A
Can Med Assoc J. 1963 Jun 15;88(24):1184-92.
Observations are presented on two patients with chronic compulsive polydipsia who showed a relative defect in renal concentrating capacity. After excluding all possible metabolic and renal causes of hyposthenuria and after obtaining normal kidney biopsies, both patients were studied in metabolic balance on a constant diet under the following conditions: (a) dehydration (loss of 3-5% body weight), (b) water loading and response to hypertonic saline, and (c) water loading and response to intravenous vasopressin (Pitressin). Throughout these studies the following parameters were observed: plasma and urine osmolality, glomerular filtration rate (inulin), renal plasma flow (P.A.H.), osmolar clearance and clearance of free water. In both patients the concentration defect was not related to variations in glomerular filtration rate or osmotic load. There was no correlation between the degree of hypoosmolality and the renal concentrating defect. Contrary to reports from other laboratories, restriction of water intake and chronic administration of intramuscular vasopressin did not correct the concentration defect.
本文报告了两例患有慢性强迫性多饮症的患者，他们的肾脏浓缩功能存在相对缺陷。在排除了所有可能导致低渗尿的代谢和肾脏原因，并获得正常的肾脏活检结果后，对这两名患者在以下条件下进行了恒定饮食的代谢平衡研究：(a) 脱水（体重减轻3-5%），(b) 水负荷及对高渗盐水的反应，以及 (c) 水负荷及对静脉注射血管加压素（垂体后叶素）的反应。在这些研究过程中，观察了以下参数：血浆和尿液渗透压、肾小球滤过率（菊粉）、肾血浆流量（对氨基马尿酸）、渗透清除率和自由水清除率。在两名患者中，浓缩功能缺陷与肾小球滤过率或渗透负荷的变化无关。低渗程度与肾脏浓缩功能缺陷之间没有相关性。与其他实验室的报告相反，限制水摄入和长期肌肉注射血管加压素并不能纠正浓缩功能缺陷。
