Peritoneal Dialysis Solution Biocompatibility: Inhibitory Mechanisms and Recent Studies with Bicarbonate-Buffered Solutions

O understanding of the inflammatory processes that occur in the peritoneal cavity of patients being treated for end-stage renal failure with peritoneal dialysis (PD) and the relationship of this to peritoneal membrane longevity, have increased considerably over the past decade (1). These investigations have confirmed that the peritoneal membrane, and the mesothelium in particular, rather than being a passive organ allowing solute transfer, plays a pivotal role in the peritoneum's response to inflammation (2,3). In this respect, both the mesothelial cells which line the parietal and visceral peritoneum and the peritoneal fibroblasts which reside within the submesothelial interstitium secrete mediators important in the activation and control of inflammation (2-5) Whilst it is apparent that severe or recurrent peritonitis is associated with subsequent membrane dysfunction (1), it is also clear that structural and functional changes in the peritoneal membrane occur in patients without a significant history of infection, suggesting that continuous exposure to unphysiological dialysis solutions may play a major role (6,7). This line of argument suggests that dialysis fluids, which each patient is continuously exposed to for years, contribute to the loss of membrane function in two ways: 1) by compromising peritoneal host defense mediated by resident and infiltrating leukocytes and the resident cells of the peritoneal membrane, and 2) by directly contributing to structural or "fibrotic" changes in the peritoneal membrane. Over the past 15 years, since Duwe, Vas and Weatherhead (8) made the original observations on