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一名患有下丘脑疾病和慢性肾小球肾炎患者的周期性水肿:精氨酸血管加压素依赖性心房利钠激素释放。

Cyclical edema in a patient with hypothalamic disorders and chronic glomerulonephritis: arginine vasopressin-dependent atrial natriuretic hormone release.

作者信息

Yamamoto T, Kimura T, Ota K, Shoji M, Inoue M, Sato K, Ohta M, Saito T, Abe K, Yoshinaga K

机构信息

Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Endocrinol Jpn. 1991 Apr;38(2):137-44. doi: 10.1507/endocrj1954.38.137.

DOI:10.1507/endocrj1954.38.137
PMID:1836431
Abstract

A 28-year-old woman had hypothalamic disorders (amenorrhea, obesity, psychiatric abnormalities, polydipsia and fever) and chronic glomerulonephritis. She also suffered from general edema associated with cyclical oliguria and polyuria. Her body weight and plasma osmolality increased during the oliguria phase lasting 2 to 8 days and decreased after paroxysmal polyuria accompanied by the natriuresis. These episodes occurred repeatedly, regardless of the treatment with or without diuretics. The release of arginine vasopressin in response to increased plasma osmolality was exaggerated, but changes in plasma volume did not affect arginine vasopressin release. Plasma atrial natriuretic hormone increased in response to a rise in plasma arginine vasopressin and plasma volume during the oliguria phase, thereby resulting in the diuresis and natriuresis. The renin-angiotensin-aldosterone system was secondarily activated by body fluid depletion and diuretics, and this might play an additive role in general swelling. Plasma gonadal hormones did not change to explain the edema. The mechanism of this cyclical edema remains unknown, but it is likely that hypothalamic dysfunction related to psychiatric abnormalities may exaggerate arginine vasopressin release, and enhanced renal sympathetic activity may cause retention of Na and water, and the increase in atrial natriuretic hormone release responding to the plasma volume expansion may bring about the diuresis and natriuresis.

摘要

一名28岁女性患有下丘脑疾病(闭经、肥胖、精神异常、烦渴和发热)以及慢性肾小球肾炎。她还伴有与周期性少尿和多尿相关的全身性水肿。在持续2至8天的少尿期,她的体重和血浆渗透压升高,而在阵发性多尿伴利钠后则降低。这些发作反复出现,无论是否使用利尿剂治疗。对血浆渗透压升高的反应,精氨酸加压素的释放被夸大,但血浆容量的变化并不影响精氨酸加压素的释放。在少尿期,血浆心房利钠激素随着血浆精氨酸加压素和血浆容量的增加而升高,从而导致利尿和利钠。肾素-血管紧张素-醛固酮系统因体液耗竭和利尿剂而继发性激活,这可能在全身性肿胀中起累加作用。血浆性腺激素未发生变化,无法解释水肿情况。这种周期性水肿的机制尚不清楚,但与精神异常相关的下丘脑功能障碍可能会夸大精氨酸加压素的释放,增强的肾交感神经活动可能导致钠和水潴留,而对血浆容量扩张做出反应的心房利钠激素释放增加可能会引起利尿和利钠。

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