Abstract
For patients undergoing long-term peritoneal dialysis (PD), exposure to biologically incompatible PD solutions and the consequent peritoneal structure change can lead to progressive angiogenesis and fibrosis, and ultimately result in ultrafiltration failure (UFF). Peritoneal transport studies in aquaporin 1 (AQP1) knockout mice indicate that water transport across the peritoneum is mediated by AQP1, which accounts for up to 50% of ultrafiltration. Another recent study on a large cohort of PD patients with kidney failure further substantiated the impact of AQP1 genotype variation on water channel expression in the peritoneal membrane, influencing water transport, ultrafiltration, and patient prognosis. High-dose corticosteroid therapy in both patients and mice seems to be effective in regulating AQP1 to improve ultrafiltration. At present, increasing evidence suggests that AQP1 is relevant for the process of PD water osmotic transport and ultrafiltration. Despite a great deal of research having been done on the structure and function of aquaporin proteins, many fundamental issues remain unresolved.