Oh M S, Carroll H J
Department of Medicine, State University of New York, Health Science Center at Brooklyn, NY 11203, USA.
Nephron. 1999 Jun;82(2):110-4. doi: 10.1159/000045385.
It is widely believed that the cerebral salt-wasting syndrome (CSWS) exists as an entity distinct from the syndrome of inappropriate ADH secretion, and that it is characterized by evidence of severe renal salt wasting that results in volume depletion and hyponatremia. Proof of the existence of CSWS as an entity requires documentation of renal salt wasting and volume depletion. The present review has been undertaken to examine the evidence that the CSWS is a separate entity. In this effort, we have discussed various methods of documentation of volume depletion, and then reviewed reported cases of CSWS to determine whether volume depletion and renal salt wasting have been clearly demonstrated. Our review has led us to conclude that not one case of purported CSWS has demonstrated clear evidence of volume depletion and renal salt wasting. If renal salt wasting had been proven in these cases, we would conclude that the likely site of renal salt transport was the proximal tubule. The proximal site of salt transport defect has been suggested by the absence of hyperreninemia and hypokalemia, which would be a distinguishing feature of Bartter's syndrome and Gitelman's syndrome.
人们普遍认为，脑性盐耗综合征（CSWS）是一种与抗利尿激素分泌不当综合征不同的独立病症，其特征是有严重肾性盐耗的证据，可导致容量耗竭和低钠血症。CSWS作为一种独立病症存在的证据需要肾性盐耗和容量耗竭的记录。本综述旨在研究CSWS是一种独立病症的证据。为此，我们讨论了记录容量耗竭的各种方法，然后回顾了报道的CSWS病例，以确定是否已明确证实存在容量耗竭和肾性盐耗。我们的综述得出的结论是，所谓的CSWS病例中没有一例显示出容量耗竭和肾性盐耗的明确证据。如果在这些病例中已证实存在肾性盐耗，我们会得出结论，肾性盐转运的可能部位是近端小管。肾素血症和低钾血症的缺乏提示了盐转运缺陷的近端部位，而这是巴特综合征和吉特曼综合征的一个显著特征。
