Gross P, Ketteler M, Hausmann C, Reinhard C, Schömig A, Hackenthal E, Ritz E, Rascher W
Medizinische Universitätsklinik, Pharmakologisches Institut, Heidelberg.
Klin Wochenschr. 1988 Aug 1;66(15):662-9. doi: 10.1007/BF01726923.
Because hyponatremia is frequently associated with preceding diuretic treatment and unrestricted fluid intake--conditions which have not been addressed sufficiently in published literature--we studied the pathophysiology and the clinical setting of such hyponatremia in a large group of internal medicine patients. We observed: a) Of an initial 310 patients with chemical hyponatremia only 204 (64%) had an associated plasma hypoosmolality. Since a normal plasma osmolality excludes a disturbance of water metabolism only the 204 patients with hypoosmolar hyponatremia were included in the study. This data shows that plasma osmolality is an essential measurement in any evaluation of hyponatremia. b) In 204 consecutive patients with hypoosmolar hyponatremia the electrolyte disturbance was related to advanced congestive cardiac failure in 25%, decompensated liver cirrhosis in 18%, volume contraction in 28%, syndrome of inappropriate antidiuretic hormone secretion in 19% and renal insufficiency in 4%. c) Plasma vasopressin was measurable in 90% of the 204 patients. It is known that radioimmunoassays to measure vasopressin fail to reliably detect low concentrations of circulating vasopressin (less than 0.5 pg/ml). It may therefore be stated that hypoosmolar hyponatremia was generally characterized by a failure of antidiuretic hormone suppression. d) Mean daily fluid intake of hyponatremic patients was 2.35 +/- 0.15 l. In the presence of stimulated vasopressin this large a fluid intake is bound to worsen the severity of hyponatremia. e) Of 204 patients 126 were treated with diuretics at the time of study. In these patients hyponatremia worsened during such treatments and was associated with evidence of prerenal azotemia. However there were no significant differences between diuretic-treated and -untreated patients with respect to plasma vasopressin stimulation and amount of fluid intake.(ABSTRACT TRUNCATED AT 250 WORDS)
由于低钠血症常与先前的利尿剂治疗和无节制的液体摄入有关(这些情况在已发表的文献中未得到充分探讨),我们在一大群内科患者中研究了此类低钠血症的病理生理学和临床情况。我们观察到:a)最初的310例化学性低钠血症患者中,只有204例(64%)伴有血浆低渗。由于正常的血浆渗透压可排除水代谢紊乱,因此本研究仅纳入了204例低渗性低钠血症患者。该数据表明,在任何低钠血症评估中,血浆渗透压都是一项重要的测量指标。b)在204例连续的低渗性低钠血症患者中,电解质紊乱与晚期充血性心力衰竭有关的占25%,与失代偿期肝硬化有关的占18%,与容量收缩有关的占28%,与抗利尿激素分泌不当综合征有关的占19%,与肾功能不全有关的占4%。c)204例患者中有90%可检测到血浆血管加压素。已知用于测量血管加压素的放射免疫测定法无法可靠地检测到低浓度的循环血管加压素(低于0.5 pg/ml)。因此可以说,低渗性低钠血症通常的特征是抗利尿激素抑制功能障碍。d)低钠血症患者的平均每日液体摄入量为2.35±0.15升。在血管加压素受到刺激的情况下,如此大量的液体摄入必然会加重低钠血症的严重程度。e)在研究时,204例患者中有126例正在接受利尿剂治疗。在这些患者中,低钠血症在治疗期间恶化,并伴有肾前性氮质血症的证据。然而,在血浆血管加压素刺激和液体摄入量方面,接受利尿剂治疗和未接受治疗的患者之间没有显著差异。(摘要截选至250词)