4.6 Article

Baseline peritoneal solute transport rate is not associated with markers of systemic inflammation or comorbidity in incident Korean peritoneal dialysis patients

Journal

NEPHROLOGY DIALYSIS TRANSPLANTATION
Volume 23, Issue 7, Pages 2356-2364

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/ndt/gfm921

Keywords

comorbidity; inflammation; interleukin-6; peritoneal solute transport

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Background. It is controversial whether comorbid status or systemic inflammation has an influence on the peritoneal solute transport rate (PSTR). Our aim is to elucidate whether baseline PSTR is associated with markers of systemic inflammation or degree of comorbidity in incident peritoneal dialysis (PD) patients. Methods. One hundred and ninety-five incident PD patients were prospectively included. Results of their baseline peritoneal equilibration test (PET) using 3.86% glucose PD fluid were analysed. Clinical and laboratory parameters of inflammation, comorbidity, nutritional status, dialysis adequacy and residual renal function (RRF) were assessed at the time of PET. Results. Mean dialysate-to-plasma ratio for creatinine at 4 h (D/Pcr(4)) of our patients was 0.72 +/- 0.11. High-sensitivity C-reactive protein (hsCRP), serum interleukin-6 (IL-6) and serum albumin concentrations were closely interrelated to one another and these markers of systemic inflammation were also related to the Davies comorbidity score. No differences in age, sex ratio, body mass index, body surface area and presence of diabetes were found among four transport groups. RRF, total Kt/N, haemoglobin, nitrogen appearance and the Davies comorbidity score were not different either. High-sensitivity CRP, serum IL-6 and albumin concentrations were not associated with the baseline PSTR. By multiple linear regression analysis, only the serum albumin concentration measured at the time of PET (beta = -0.081 +/- 0.020, P < 0.001) remained significantly associated with D/Pcr(4). Conclusion. In our study with incident Korean PD patients, the baseline PSTR was not influenced by markers of systemic inflammation or comorbidity. For a subgroup of PD patients without serious comorbidity, other mechanisms of high baseline PSTR need to be elucidated.

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