Baylis P H, Heath D A
Ann Intern Med. 1978 May;88(5):607-9. doi: 10.7326/0003-4819-88-5-607.
Forty-eight patients treated with oral lithium carbonate and 20 control subjects were studied to define the causes of lithium-induced water disturbances. Measurement of plasma immunoreactive arginine vasopressin, plasma osmolality, and urine osmolality after a period of dehydration separated nephrogenic diabetes insipidus, cranial diabetes insipidus, and primary polydipsia, the three postulated mechanisms of lithium-induced polyuria. Seventeen patients had a urinary concentrating defect despite serum lithium concentrations in the therapeutic range. Ten of these patients had nephrogenic diabetes insipidus, one had results suggestive of cranial diabetes insipidus, but none had evidence of primary polydipsia. Symptoms of thirst and polyuria were poor indicators of the degree of hypo-osmolar urine. No patient had electrolyte abnormalities, and none had sufficiently severe polyuria to stop lithium treatment.
对48例接受口服碳酸锂治疗的患者和20例对照受试者进行了研究，以确定锂诱导的水代谢紊乱的原因。在一段时间的脱水后，测量血浆免疫反应性精氨酸加压素、血浆渗透压和尿渗透压，区分了锂诱导多尿的三种假定机制，即肾性尿崩症、中枢性尿崩症和原发性烦渴。17例患者尽管血清锂浓度在治疗范围内，但仍存在尿浓缩功能缺陷。其中10例患者患有肾性尿崩症，1例患者的结果提示中枢性尿崩症，但均无原发性烦渴的证据。口渴和多尿症状并不能很好地反映低渗尿的程度。没有患者出现电解质异常，也没有患者因多尿严重到需要停止锂治疗。
