What is the best chronic dialysis modality for ESRD patients with end-stage liver disease?

Patients with end-stage renal disease (ESRD) and concomitant end-stage liver disease with ascites pose unique management problems. Hemodynamic instability combined with bleeding and metabolic derangements make delivery of renal replacement therapy (RRT), a challenging proposition for the nephrologist. The earliest problem is the accurate measurement of GFR; serum creatinine-based formulas such as Cockroft–Gault and modification of diet in renal diseases often overestimate the GFR, and it has been shown that cystatin C measurements predict the GFR better than serum creatinine-based equations (1). The optimal time to initiate RRT in these patients can be difficult to determine as symptoms such as poor appetite, weight loss, and feeling of being unwell could be attributed to uremia or the underlying liver disease. Although the choices for RRT in these patients are several, there have been no clinical trials evaluating the impact of one dialysis modality over another. Hemodialysis (HD) as a RRT in these patients is often difficult to deliver, owing to problems with intradialytic hypotension and complications associated with bleeding. Intradialytic hypotension can limit ultrafiltration and result in sustained or worsening ascites. Patients with cirrhosis have high circulating levels of nitric oxide (NO), and HD exacerbates the high NO levels resulting in a further decrease in peripheral vascular resistance and hypotension (2,3). The risk of bleeding is increased in patients with arteriovenous access, andminimal use of anticoagulation should be the goal. Hemodialysis performed through a catheter can decrease this problem but with an inherent risk of infection and malfunction. Patients with cirrhosis are also at risk of hepatic encephalopathy and cerebral edema which may be exacerbated with hemodialysis because of rapid changes in extracellular osmolality (4,5). Hemodialysis adequacy measurements may overestimate the true dialysis dose, as ascites is a large pool of urea-rich fluid that is not cleared as rapidly as other bodily fluids, and thus, this disequilibration can cause postdialysis plasma urea levels that overestimate total body urea removal if drawn too soon after the completion of the treatment. Thus, it might be prudent to wait (1 hour or more) before drawing the sample, a practice that may be unfeasible for aHD center. Peritoneal dialysis (PD) offers certain advantages over HD, in patients (6) [Table 1]. PD is hemodynamically better tolerated than HD in patients with cirrhosis and ascites, especially in those patients who are unable to tolerate HD (7). There has been some concern of a higher peritonitis rates in these patients (8,9), though, not all studies support this notion (10,11). In a study of eight patients, the peritonitis rates in patients with cirrhosis were 2.5 times greater than that of noncirrhotics (1 episode ⁄9 months vs. 1 episode ⁄22 months) (8). In a larger series of 21 cirrhotic patients undergoing PD, when compared with 41 patients with PD without liver disease, the authors found slightly lower peritonitis rates in patients with cirrhosis: 1 episode ⁄39 months vs. 1 episode ⁄22 months in controls. In another study of 25 patients with hepatitis B and cirrhosis, the authors found no difference in peritonitis rates—1 in 19.2 patient months vs. 1 in 20.5 patient months in noncirrhotic patients (11). No prophylaxis for spontaneous bacterial peritonitis (SBP) was administered. There have been recent reports that treatment of hepatic encephalopathy with lactulose may reduce peritonitis rates (12). The breakdown of lactulose by the intestinal bacteria produces lactate and pyruvate, which might reduce intestinal bacterial load resulting in fewer episodes of peritonitis. Increased protein loss in the dialysate is another concern in patients with ascites receiving PD. In the previously mentioned study by Selgas et al. (8), the initial high protein losses decreased over time, an observation seen in two other studies (9,10). It is thought that an increase in intra-abdominal pressure opposes the portal pressure and leads to decreased ascites formation and subsequent protein loss over time (13). The increase in serum albumin could also be attributed to the improvement of appetite as uremia resolves. The decreased formation of ascites because of a reduction in portal pressuremay also decrease protein losses, and indirect evidence such as decreased portal vein diameter and decrease in splenomegaly with PD support this hypothesis (14). The survival of patients with cirrhosis receiving PD when compared with noncirrhotic patients on the same modality is comparable. In De Vecchi’s series, of the 21 patients with cirrhosis, 11 stayed on PD for >1 year and 8 for >2 years; the 5-year technique and patient survival were also similar as compared with controls. In another series, six of the nine patients survived >18 months, and one patient developed encapsulating peritoneal sclerosis after 8 years on PD (7). It is difficult to determine whether a given episode of peritonitis is PD related or spontaneous (SBP). One advantage of PD is the early noninvasive diagnosis of peritonitis because of