NDT Advance Access originally published online on December 6, 2005
Nephrology Dialysis Transplantation 2006 21(3):763-769; doi:10.1093/ndt/gfi245
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Original Articles: Dialysis and Transplantation
Peritoneal fast transport in incident peritoneal dialysis patients is not consistently associated with systemic inflammation
1 Nephrology Department, 2 Neurology Department and 3 Clinical Pathology Department, Hospital Geral de Santo António, Porto, Portugal
Correspondence and offprint requests to: Anabela S. Rodrigues, Largo Abel Salazar, Hospital Geral Santo António, Serviço de Nefrologia, Porto, Portugal. Email: ar.cbs{at}mail.telepac.pt
Background. The determinants of peritoneal fast transport status at the beginning of peritoneal dialysis (PD) are still under debate. The relationship between fast transport status and inflammation or co-morbidity, and its impact on patient survival are not fully elucidated. Our objective was to investigate if fast transport status in incident patients is associated with markers of inflammation and atherosclerosis, and its relationship to patient survival.
Methods. Seventy-three incident patients on PD performed a 3.86% peritoneal equilibrium test (PET) at 4.7±2.7 months after starting PD. Doppler carotid wall intima-media thickness (IMT) and the presence of carotid plaque were used as markers of atherosclerosis. C-reactive protein (CRP) and serum interleukin-6 (IL-6) were evaluated as markers of systemic inflammation. Baseline plasma levels of albumin, homocysteine, lipoprotein (a) [Lp(a)] and other lipid parameters were measured. Body mass index and residual renal function (RRF) were calculated. Patients were classified with the Davies co-morbidity score.
Results. The dialysate–plasma creatinine ratio (D/P creatinine) was 0.75±0.10; 26% were fast transporters (D/P 
0.85). In comparison with other transport categories, these had similar age, body mass index and RRF, and did not present a higher co-morbidity score than non-fast transporters. IMT did not significantly differ between groups. By multiple regression analysis, baseline peritoneal small solute transport was not related to systemic inflammation biomarkers. Fast transporters did not present higher levels of CRP or serum IL-6. Plasma levels of lipids, Lp(a), calcium x phosphorus product and albumin also did not differ between groups. Similar results were obtained when patients were grouped according to mass transfer area coefficient for creatinine. Patients with more than two co-morbidities had lower levels of plasma albumin (3.6±0.58 vs 3.9±0.9 g/dl, P = 0.054), significantly higher median levels of serum IL-6 (19.3 vs 9.2 pg/ml, P = 0.003) and wider IMT (0.90±0.36 vs 0.65±0.28 mm, P = 0.017). Multivariate analysis confirmed that baseline peritoneal transport was not a significant determinant of patient survival (P = 0.848), while the co-morbidity score remained significant (hazard ratio = 3.48, 95% confidence interval = 1.29–9.38, P = 0.014).
Conclusion. Initial fast transport was not associated with systemic inflammation and atherosclerosis. In a population with preserved RRF and absence of baseline serious co-morbidity, it was not predictive of worse prognosis. Other determinants of early peritoneal fast transport deserve investigation.
Keywords: inflammation; peritoneal transport; survival
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