Myths in Peritoneal Dialysis

Martin B. Lee; Joanne M. Bargman


Curr Opin Nephrol Hypertens. 2016;25(6):602-608. 

In This Article

Myth 6: Chronic use of Hypertonic Glucose Dialysate Leads to Peritoneal Membrane Failure

It is widely believed that chronic use of hypertonic glucose dialysate causes peritoneal membrane failure. The concern is that the consequent avoidance of hypertonic glucose dialysate might result in inadequate ultrafiltration and chronic fluid overload with adverse cardiovascular outcomes. This was suggested in the IMPENDIA-EDEN trial where the low-glucose group had a higher incidence of serious adverse events related to volume expansion such as heart failure, hypertensive crises and death, despite better metabolic parameters.[35]

In studies of the role of glucose in membrane failure, it has been difficult to isolate the effect of peritoneal glucose exposure on the membrane, because membrane failure itself results in poor ultrafiltration, which leads to the use of more hypertonic glucose. Davies et al.[36] observed in a retrospective cohort study that greater peritoneal glucose exposure in the first 2 years of peritoneal dialysis preceded the development of higher transport status in nine patients, in contrast to 13 patients with stable transport status in whom glucose exposure had been significantly lower. This temporal association has been interpreted as evidence that peritoneal glucose exposure results in membrane failure. However, the high glucose exposure group started dialysis with only half the RRF of the low glucose exposure group, and therefore needed higher glucose dialysate from the outset to maintain ultrafiltration.

An alternative hypothesis for the findings by Davies et al. is that factors covariately associated with low RRF, such as systemic inflammation, may have been the cause of membrane failure. Consistent with this inflammation hypothesis, Chung et al.[37] observed in 76 incident peritoneal dialysis patients that lower RRF and higher serum C-reactive protein were predictive of a rise in transport status over the first year of peritoneal dialysis. Of note, low glucose and low GDP dialysate have been associated with elevated markers of peritoneal inflammation, neoangiogenesis and mesothelial proliferation in the peritoneal dialysis effluent, such as leucocytes, CA125, interleukins, VEGF and the development of a higher transport status.[38,39]

Accumulated evidence and our clinical experience with patients on glucose dialysate would suggest that membrane failure is an incompletely understood multifactorial process requiring synergy between genetic,[40] and clinical characteristics,[41,42] falling RRF, inflammatory mediators[39,40,43] and the dialysate.[44,45–47] Indeed, the effects of systemically derived glucose, advanced glycation end-products and inflammation have not been adequately controlled for in studies of glucose dialysate and membrane failure. The avoidance of hypertonic glucose exchanges in an attempt to prevent membrane failure and metabolic complications needs to be balanced against the adverse consequences of volume overload and cardiovascular events.