(多尿症)。

T. Treutler, B. Ruf, J. Beige
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引用次数: 0

摘要

除了心因性多饮后的多尿,从更狭义上讲,这种情况可分为水再吸收受损(i)由于小管损伤或(ii)抗利尿激素(ADH)功能的相对或绝对丧失。肾小管损伤可能由不同的毒素引起,如高钙尿,药物和抗生素引起肾小管坏死。无论是绝对的还是相对的,ADH缺乏症发生在中枢性或外周性尿崩症中,其基础是由于受体功能障碍导致ADH合成失败或外周疗效丧失。多尿症的诊断依赖于口渴挑战和血清和尿液渗透压的实验室研究,这揭示了下丘脑-肾轴的无功能。抗利尿激素的使用可以区分中枢性和外周性尿崩症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Polyuria].
Beyond polyuria following psychogenic polydipsia, in a more narrow sense, this condition may be classified into impaired water re-absorption (i) due to tubular injury or (ii) relative or absolute loss of function of antidiuretic hormone (ADH). Tubular injury may be caused by different toxins affecting the ascending Henle loop as hypercalciuria, drugs and antibiotics as tubular necrosis. ADH deficiency, either absolute or relative, occurs with central or peripheral diabetes insipidus, which is based on synthesis failure or loss of peripheral efficacy of ADH due to receptor malfunction. Diagnosis of polyuria rests upon a thirst challenge in conjunction with laboratory studies of osmolality in serum and urine, which discloses the non-function of the hypothalamic-renal axis. Administration of ADH may differentiate between central and peripheral diabetes insipidus.
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