title: Poor outcomes for fast transporters on PD: the rise and fall of a clinical concern.
abstract: A rapid peritoneal solute transport rate (PSTR), generally termed a "high" PSTR, may in fact be associated with low small solute transport due to the low ultrafiltration rates with which it is associated; the term "fast" PSTR has, therefore, been proposed as a more accurate descriptive term. During the 1990s several studies showed that fast PSTR was associated with high mortality-presumably because it may lead to fluid overload, nutritional and metabolic alterations but also because it may be associated with other risk factors such as cardiovascular disease, other comorbid diseases, and inflammation. However, the consensus of today is that a fast PSTR is not as critical for patient survival as previously thought but that the prognosis depend on the type of fast PSTR: Type 1-an early inherent type which is associated with increased mortality mainly because it is associated with comorbidity and inflammation; these patients would have a poor prognosis also if they were treated by hemodialysis. Type 2-an early inherent type with a large peritoneal surface area; and Type 3-a late acquired type with peritoneal membrane changes which develop with time on peritoneal dialysis (PD); these two types have a good prognosis provided that fluid balance is controlled using automated peritoneal dialysis (APD) and icodextrin-based PD solution. Thus, with the increased use of APD and icodextrin, the prognosis of fast transporters now looks less bleak. Perhaps, it will be possible in the future to even demonstrate improved survival in the Type 2 and Type 3 fast transporters using APD and icodextrin. In addition, there is hope that the new PD solutions may prevent the development of fast PSTR as well as have a favorable impact on its complications.
authors.forename: Sung Hee
authors.initials: SH
authors.lastname: Chung
authors.forename: Olof
authors.initials: O
authors.lastname: Heimbürger
authors.forename: Bengt
authors.initials: B
authors.lastname: Lindholm
mesh_terms: D000042:Absorption / Q000502:physiology; D001692:Biological Transport / Q000502:physiology; D015314:Dialysis Solutions / Q000493:pharmacokinetics*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism / Q000628:therapy*; D010530:Peritoneal Dialysis / Q000379:methods*; D010537:Peritoneum / Q000378:metabolism*
chemical_list: D015314:Dialysis Solutions