Inflammation and myocardial damage markers influence loss of residual renal function in peritoneal dialysis patients

Silvia Palomo-Piñón, Carmen Josefina Mora-Villalpando, Ma Del Carmen Prado-Uribe, Guillermo Manuel Ceballos-Reyes, Ma De Jesús Ventura-García, Marcela Ávila-Díaz, Oscar Orihuela Rodríguez, José Ramón Paniagua-Sierra

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

23 Citas (Scopus)

Resumen

Background: Residual renal function (RRF) has been identified as the most important component in dialysis adequacy and has a strong effect on clinical outcomes. This justifies any effort in understanding the mechanism behind the preservation or decline in RRF. The aim of this study was to analyze the possible association of components of cardio-renal syndrome with the rate of decline in RRF. Methods: A retrospective cohort study was performed in a group of prevalent adult patients on continuous ambulatory peritoneal dialysis (CAPD). Patients were analyzed at baseline and after a 30-month follow-up. Evaluations included measurements of residual renal function, dialysis adequacy parameters, cardiovascular comorbidity, and measurements of biochemical markers of cardiovascular disease (CVD) and inflammation, as well as resting electrocardiography. Results: We included 129 patients in the study who were divided into groups according to loss of RRF, considering the cut-off point as 100 mL/day of 24 h urine volume. At baseline, there were no differences between groups: patients who lost RRF showed low values of 24 h urine volume, higher levels of systolic blood pressure, N-terminal pro-brain natriuretic peptide (NT-proBNP), C-reactive protein (CRP), IL-6, and low values of serum albumin. In the multivariate analysis, age, albumin, CRP, and NT-proBNP were significant risk factors for the loss of RRF. Conclusions: Data indicate a close relationship between heart and kidney function where chronic kidney disease (CKD) affects and is an effect of, heart function, indicative of a bi-directional influence that leads to a vicious cycle, promoting deleterious effects on both systems.

Idioma originalInglés
Páginas (desde-hasta)484-488
Número de páginas5
PublicaciónArchives of Medical Research
Volumen45
N.º6
DOI
EstadoPublicada - 1 ago. 2014

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