Thompson C J, France A J, Baylis P H
Department of Medicine, Ninewells Hospital and Medical School, Dundee.
Scott Med J. 1997 Feb;42(1):16-7. doi: 10.1177/003693309704200106.
We report the case of a patient who developed severe hypernatraemic dehydration following a head injury. Ten years previously he had been diagnosed to have lithium-induced nephrogenic diabetes insipidus, and lithium therapy had been discontinued. He remained thirsty and polyuric despite cessation of lithium and investigations on admission showed him to have normal osmoregulated thirst and vasopressin secretion, with clear evidence of nephrogenic diabetes insipidus. Lithium induced nephrogenic diabetes insipidus is considered to be reversible on cessation of therapy but polyuria persisted in this patient for ten years after lithium was stopped. We discuss the possible renal mechanisms and the implications for management of patients with lithium-induced nephrogenic diabetes insipidus.
我们报告了一例头部受伤后发生严重高钠血症性脱水的患者。十年前，他被诊断为锂诱导的肾性尿崩症，随后停用了锂治疗。尽管停用了锂，但他仍口渴且多尿，入院检查显示他的渗透压调节性口渴和抗利尿激素分泌正常，有明确的肾性尿崩症证据。锂诱导的肾性尿崩症被认为在停止治疗后是可逆的，但该患者在停用锂后多尿持续了十年。我们讨论了可能的肾脏机制以及对锂诱导的肾性尿崩症患者管理的影响。
