Histomorphological and functional changes of the peritoneal membrane during long-term peritoneal dialysis.

In long-term peritoneal dialysis (PD) morphological and functional changes of the peritoneal membrane are common. Sub-mesothelial fibrosis, angiogenesis and vasculopathy are typical histomorphological alterations of the peritoneal membrane, which, to a certain degree, are induced by uremia and recurrent peritonitis. The most important causative factor, however, represents the chronic exposure to PD solutions. Glucose, glucose degradation products and advanced glycation end-products (AGEs) via different pathways induce inflammation, fibrosis and angiogenesis. As a functional consequence ultrafiltration failure due to peritoneal hyperpermeability and an increased effective peritoneal surface area represents a major clinical problem. An insufficient function of the water-selective aquaporin 1 (AQP-1) channel may also be causative for inadequate ultrafiltration. A rare but life-threatening complication of long-term PD is encapsulating peritoneal sclerosis (EPS). For both impaired AQP-1 function and EPS, the long-term effects of PD fluids are believed to be responsible, even though the mechanisms are not yet understood. The avoidance of glucose and modern PD fluids with fewer glucose degradation products, as well as first pharmacological attempts may help to preserve the peritoneal membrane in the long term.