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IT IS fitting that the shape of a sickled red blood cell (RBC)

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Intractable ascites is encountered with increasing frequency in patients undergoing chronic hemodialysis. Eight patients out of 68 developed moderate to massive ascites. Peritoneal dialysis antedated hemodialysis in all of them and the duration on either form of dialysis bore no relationship to the appearance of ascites. Congestive heart failure, when present, responded well to ultrafiltration by peritoneal dialysis; ascites always reaccumulated rapidly. There was no evidence of liver dysfunction; liver and peritoneal histology did not reveal any specific pattern. Therapy with increased dialysis time, and repeated infusions of albumin and whole blood proved futile. Five out of eight patients died 2-18 months after onset of ascites, two of them from entirely unrelated events. Two patients were cured of ascites following renal transplantation and another (not transplanted) is alive and well 21 months later even though the ascites is persistent. We conclude that intractable ascites of idiopathic origin is not uncommon in patients on chronic hemodialysis and renal transplantation is the only definitive treatment.

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