It is now 25 years since the publication of the first clinical trial of icodextrin, a proof-of-principle study demonstrating its superiority over osmotically active glucose as an oncotic agent to drive ultrafiltration during long peritoneal dialysis exchanges.1 Since then, studies of icodextrin have demonstrated its efficacy as an agent for ultrafiltration, in particular by showing that it prevents fluid reabsorption in people with fast peritoneal transport and that this translates into improved fluid status.