Kamoi K, Toyama M, Ishibashi M, Yamaji T
Department of Medicine, Nagaoka Red Cross Hospital, Niigata, Japan.
J Clin Endocrinol Metab. 1995 Oct;80(10):2906-11. doi: 10.1210/jcem.80.10.7559873.
To clarify the cause and pathophysiology of hyponatremia after intracranial bleeding, we analyzed the possible causative factors, and examined the response of vasopressin (AVP) secretion to osmotic stimulus in six patients. Despite hyponatremia, urinary sodium excretion persisted, with urinary osmolality exceeding plasma osmolality. Serum levels of urea nitrogen, creatinine, and uric acid were not elevated in any of them. PRA was normal or subnormal in four patients, and all had normal adrenocortical and thyroid functions. Although these laboratory findings may support the diagnosis of the syndrome of inappropriate antidiuretic hormone secretion, the cause of hyponatremia in our patients was attributed to excessive renal excretion of sodium, because water load performed in an euvolemic state showed no impairment in diuresis, and replenishment of sodium without water restriction improved hyponatremia as well as clinical conditions. Plasma AVP levels relative to plasma osmolality in these patients were constantly elevated. When challenged by an osmotic stimulus, AVP secretion increased with increasing plasma osmolality in one patient, but no consistent pattern of AVP secretion was observed in others. The potentiating effect of hypovolemia on osmotic secretion of AVP was not demonstrated in any of the patients. These results show that hyponatremia after intracranial bleeding with clinical features almost indistinguishable from those of syndrome of inappropriate antidiuretic hormone secretion may result from an impaired renal sodium-conserving mechanism of unknown cause. Persistent AVP secretion without an alteration in the sensitivity of the osmostat in this pathological state may be due to an incomplete suppression by plasma hypotonicity per se of the baroreceptor-mediated stimulation of AVP release.
为明确颅内出血后低钠血症的病因及病理生理机制，我们分析了可能的致病因素，并检测了6例患者血管加压素（AVP）分泌对渗透压刺激的反应。尽管存在低钠血症，但尿钠排泄持续存在，尿渗透压超过血浆渗透压。所有患者的血清尿素氮、肌酐和尿酸水平均未升高。4例患者的肾素活性正常或低于正常，且肾上腺皮质和甲状腺功能均正常。虽然这些实验室检查结果可能支持抗利尿激素分泌不当综合征的诊断，但我们患者低钠血症的原因归因于肾脏钠排泄过多，因为在血容量正常状态下进行的水负荷试验显示利尿功能无损害，且在不限制水的情况下补充钠可改善低钠血症及临床状况。这些患者血浆AVP水平相对于血浆渗透压持续升高。当受到渗透压刺激时，1例患者的AVP分泌随血浆渗透压升高而增加，但其他患者未观察到一致的AVP分泌模式。在任何患者中均未证实低血容量对AVP渗透压分泌的增强作用。这些结果表明，颅内出血后出现的低钠血症，其临床特征与抗利尿激素分泌不当综合征几乎无法区分，可能是由于不明原因的肾脏保钠机制受损所致。在这种病理状态下，AVP持续分泌且渗透压感受器敏感性无改变，可能是由于血浆低渗本身对压力感受器介导的AVP释放刺激抑制不完全所致。
