What should be done to treat dialysis-associated ascites?

Dialysis-associated ascites (‘‘nephrogenic’’ or ‘‘nephrogenous’’ ascites) is an entity that develops in only a small number of hemodialysis patients. This entity was first described in the 1970s (1,2), and over 150 cases have subsequently appeared in the literature. The characteristics of patients with dialysis-associated ascites are reported in three major series (2,4,5) revealing a wide range of age at presentation (11–71 years of age), male predominance (3,4) but no race predilection. Ascites can appear anywhere from 18 to 69 months after the initiation of dialysis and also occurs in nondialysis requiring kidney disease (3).Most cases developed in patients with underlying primary glomerular diseases and hypertension. The number of cases has decreased since the 1970s, which might be related to better treatment of glomerular diseases, better fluid management in dialysis, more diabetic nephropathy as a primary cause of renal disease, and the universal use of angiotensin-converting enzyme inhibitors (ACEIs). Increased abdominal girth, anorexia, early satiety, and cachexia characterize the clinical presentation (6), while massive ascites with minimal lower extremity edema is found on physical examination. The ascitic fluid is straw colored, with a white blood cell count of usually 25–1600 ⁄mm and a mean serum – ascites gradient (SAAG) of 1.1 g ⁄dl. Cultures are negative. Dialysisassociated ascites is a diagnosis of exclusion and can only be established after portal hypertension or known primary liver or biliary disease, cardiac disease, peritoneal carcinomatosis, pancreatic disease, inferior vena caval obstruction, urinary extravasation, and hypothyroidism are excluded. The postulated pathogenic mechanisms for dialysisassociated ascites include peritoneal membrane changes because of uremic toxins (5), exposure to dialysis solution (1), up-regulation of the renin-angiotensin system (2), the presence of circulating immune complexes in patients with underlying glomerular diseases (2), and iron deposition (4). Elevated hepatic vein hydrostatic pressure (7), fluid retention, increased peritoneal membrane permeability (8), and impaired lymphatic drainage have also been cited as possible contributing factors (2). Although fluid retention occurs in more than 70% of the reported cases, the role of fluid retention is not completely clear as dialysis patients are commonly fluid overloaded yet do not develop ascites. Perhaps, other factors (noted above) serve as a ‘‘second hit’’ in the presence of fluid overload (5). Hypoalbuminemia (5), which was present in 75%of uremic patients with ascites in one series, may contribute to ascites formation (4). While some authors have found an association between duration of HD and ascites development (8), others have not (5). Prior therapy with peritoneal dialysis (PD) may play a role in either altering peritoneal membrane permeability or inducing inflammation. However, the low incidence of prior peritoneal dialysis in patients with dialysis-associated ascitesmakes this unlikely (4). Treatment of patients with refractory dialysis-associated ascites initially requires appropriate fluid management and salt restriction. A recent study (9) on six patients with this condition showed that severe salt restriction and frequent ultrafiltration (UF) andHD significantly improved the ascites. Intensive daily isolated UFmay prove beneficial. DailyHDwas effective in controlling ascites in 78% of the patients in 1–2 weeks (4). However, volume reduction may not be well tolerated especially if simultaneous cardiac dysfunction is present. Intradialytic hypotension and noncompliance with strict salt restriction (large interdialytic fluid gains) contribute to intolerance of aggressive UF. Thus, it is essential that excessive interdialytic weight gain is prevented. Interventions such as hyperalimentation and repeated paracentesis are often undertaken to control ascites (5). Reinfusion of ultrafiltered ascitic fluid and extracorpeal ascites dialysis has improved hemodynamic stability and reduced ascites in some patients (10,11). Unfortunately, CAPD is complicated by decreased serum protein concentration, because of repeated removal of protein-rich ascitic fluid (12). However, resolution of abdominal distention ultimately leads to an improvement in appetite and increased protein intake, which may improve serum albumin levels. Because peritoneal hemosiderosis has been implicated as a cause of this entity, desferrioxamine therapy along with phlebotomy has improved ascites in some cases (4). Intraperitoneal administration of steroids and parathyroidectomy has proved successful in some cases (13,14). Table 1 summarizes medical and surgical therapies attempted in this entity. Surgical placement of peritoneovenous shunts has been reported to be effective in some patients; however, they are critically dependent on shunt longevity (15). This approach should be considered only after medical options have been tried, particularly because it limits future employment of peritoneal dialysis. Another surgical option that has been attempted is bilateral nephrectomy (6). In a series of 10 patients, seven who did not undergo nephrectomy died of cachexia, uncontrolled hypertension, and ascites. In contrast, the three who underwent bilateral nephrectomy gained lean body mass with prompt resolution of ascites. The use of an ACEI was evaluated in one patient with ascites (16). Seminars in Dialysis—Vol 24, No ** (***–***) 2011 pp. ***–*** DOI: 10.1111/j.1525-139X.2011.00893.x a 2011 Wiley Periodicals, Inc.