Peritoneal glucose exposure and changes in membrane solute transport with time on peritoneal dialysis

Citation
Sj. Davies et al., Peritoneal glucose exposure and changes in membrane solute transport with time on peritoneal dialysis, J AM S NEPH, 12(5), 2001, pp. 1046-1051
Citations number
24
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
ISSN journal
10466673 → ACNP
Volume
12
Issue
5
Year of publication
2001
Pages
1046 - 1051
Database
ISI
SICI code
1046-6673(200105)12:5<1046:PGEACI>2.0.ZU;2-N
Abstract
Peritoneal solute transport increases with time on treatment in a proportio n of peritoneal dialysis (PD) patients, contributing to ultrafiltration fai lure. Continuous exposure of the peritoneum to hypertonic glucose solutions results in morphologic damage that may have a causative role in changes in peritoneal function. The purpose of this analysis was to establish whether increased exposure to glucose preceded changes in solute transport in a se lected group of long-term PD patients. Peritoneal solute transport, residua l renal function, peritonitis rate, and peritoneal exposure to glucose were recorded prospectively in a cohort of 303 patients at a single dialysis ce nter. A subgroup of individuals, treated continuously for 5 yr, were identi fied and defined retrospectively as having either stable or increasing tran sport status. Of the 22 patients who were treated continuously for 5 yr, 13 had stable solute transport (solute transport at start, 0.67 [+/-0.1]: at 5 yr, 0.67 [+/-0.1]), whereas 9 had a sustained increase (solute transport at start, 0.56 [+/-0.08]; at 5 yr, 0.77 [+/-0.09]). Compared with the stabl e patients, those with increasing transport had earlier loss in residual re nal function and were exposed to significantly more hypertonic glucose duri ng the first 2 yr of treatment that preceded the increase in solute transpo rt. This was associated with greater achieved ultrafiltration compensating for the reduced urinary volumes in these patients. Further increases in glu cose exposure were observed as solute transport continued to rise. Peritoni tis, including severity of infection and causative organism, was similar in both groups. In this selected group of long-term survivors on PD, an incre ase in solute transport with time was preceded by increased peritoneal expo sure to hypertonic glucose. This is supportive evidence that hypertonic glu cose may play a causative role in alterations in peritoneal membrane functi on.