For patients with chronic renal failure, peritoneal dialysis (PD) is a common, life sustaining form of renal replacement therapy that is used worldwide. Exposure to nonbiocompatible dialysate, inflammation, and uremia induces longitudinal changes in the peritoneal membrane. Application of molecular biology techniques has led to advances in our understanding of the mechanism of injury of the peritoneal membrane. This understanding will allow for the development of strategies to preserve the peritoneal membrane structure and function. This may decrease the occurrence of PD technique failure and improve patient outcomes of morbidity and mortality. 1. Introduction PD involves both diffusive and convective clearance driven mainly by glucose-based hyperosmolar PD fluid. The peritoneal membrane overlies the surface of all intra-abdominal organs, the diaphragm, and the parietal peritoneal wall. The peritoneal membrane is a fairly simple structure, with a superficial epithelial-like cell layer—the mesothelium—which is attached to a basement membrane (Figure 1). Beneath the basement membrane is a submesothelial layer consisting of connective tissue, fibroblasts, and blood vessels. Under optimal conditions, the peritoneum acts as an efficient, semipermeable dialysis membrane, enabling removal of metabolites, uremic toxins, salt, and water from the patient. Figure 1: Changes in the peritoneal membrane with dialysis treatment. (a) Normal peritoneal membrane consists of an intact mesothelium overlying a thin submesothelial compact zone containing extracellular matrix, blood vessels, and a few scattered cells—fibroblasts and peritoneal macrophages. (b) After time on dialysis, activated fibroblasts or myofibroblasts appear along with increased submesothelial extracellular matrix and angiogenesis. Mesothelial cells are injured and sometimes denuded from the peritoneal surface. The rate of removal of these products from the blood correlates with the vascular surface area in contact with PD fluids in the peritoneal cavity [1]. Peritoneal membrane solute transport is commonly quantified as a dialysate to plasma ratio of solute (i.e., d/p creatinine). Increased peritoneal membrane solute transport should confer benefit for the patient as blood clearance would be more efficient. However, many studies have demonstrated the opposite [2]. A meta-analysis of observational studies demonstrated that every 0.1 increase in d/p creatinine carries a 15% increased risk of mortality [3]. This risk may be modified by the use of nocturnal cycling PD and use of alternate fluids such as
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