Gotloib L, Servadio C
Am J Med. 1976 Oct;61(4):465-70. doi: 10.1016/0002-9343(76)90324-7.
Six patients with chronic uremia in whom ascites developed during maintenance hemodialysis are described. Their clinical and biochemical findings are reviewed and compared with data of 10 hemodialyzed patients without ascites. Liver cirrhosis was the origin of ascites in only one case. Hypoalbuminemia, liver cirrhosis, congestive heart failure, peritonitis, peritoneal tuberculosis and carcinomatosis were uniformly absent in the other patients. Long-term and marked overhydration seems to be at the origin of ascites. Lack of peripheral edema, probably due to ascites compartmentalization, was a constant finding in every noncirrhotic patient with ascites. When long-term overhydration was stopped after successful kidney transplantation or by means of diminished water and salt ingestion, reversal of the syndrome was attained. Nevertheless, ascites because of liver cirrhosis was not influenced by means of kidney transplantation. In three patients with ascites who did not receive a transplant, a significant reduction in water and salt ingestion was reached after intensive psychotherapy which led to reversal of the ascitic syndrome. In one anephric patient ascites did not develop despite water overloading. Survival has not been influenced by the formation of ascites. Further research is needed to determine the mechanism of sodium transfer across the peritoneal membrane. Influence of humoral factors can be considered, if an active transport mechanism could be demonstrated.
本文描述了6例在维持性血液透析期间出现腹水的慢性尿毒症患者。回顾了他们的临床和生化检查结果，并与10例无腹水的血液透析患者的数据进行了比较。仅1例患者腹水的原因为肝硬化。其他患者均无低蛋白血症、肝硬化、充血性心力衰竭、腹膜炎、腹膜结核和癌转移。长期且明显的水钠潴留似乎是腹水的根源。在每例非肝硬化性腹水患者中，均持续存在因腹水分隔而可能导致的外周水肿缺失。在成功进行肾移植后或通过减少水盐摄入停止长期水钠潴留后，该综合征得以逆转。然而，肝硬化所致腹水不受肾移植的影响。在3例未接受移植的腹水患者中，强化心理治疗后水盐摄入量显著减少，腹水综合征得以逆转。1例无肾患者尽管存在水负荷过重但未出现腹水。腹水的形成未影响患者的生存率。需要进一步研究以确定钠跨腹膜转运的机制。如果能证明存在主动转运机制，则可考虑体液因素的影响。
