title: Higher daily peritoneal protein clearance when initiating peritoneal dialysis is independently associated with peripheral arterial disease (PAD): a possible new marker of systemic endothelial dysfunction?
abstract: BACKGROUND
  Patients starting peritoneal dialysis (PD) with active cardiovascular disease (CVD) show higher protein and albumin levels in peritoneal effluent. Peripheral arterial disease (PAD) is increasingly recognized as an entity particularly associated with higher mortality.
  
  
  METHODS
  To explore whether higher daily peritoneal protein clearance (PrC) on starting PD is a cardiovascular risk marker, we have formulated the hypothesis that PAD, as an expression of the highest CVD grade, is specifically related to the amount of PrC.
  
  
  RESULTS
  The average of 24-h effluent peritoneal protein losses (PPL) was 6.88 +/- 3.31 g. The median of PrC was 94.43 ml/day and quartiles 1 and 4 were delimited by 56.25 and 114.18 ml/day, respectively. A significant positive correlation between PrC and peritoneal small solute transport was detected. Patients in the highest quintile of Cr-MTAC (>14.04 ml/min) demonstrated significantly greater PrC than the remainder. An inverse significant correlation with plasma albumin levels was also demonstrated (r = -0.52, P = 0.0001). Eighteen patients with PAD showed significantly higher PrC than patients with no PAD (130.62 +/- 74.89 versus 88.77 +/- 47.56 ml/day; P = 0.033). Other CVDs were not significantly associated with greater PrC. In the univariable logistic regression analysis, PAD was directly and significantly related to PrC, Charlson's index, gender, diabetes and age. Multivariable analysis confirmed that PAD was significantly related to PrC, independent of age (RR: 1.07, IC: 1.02-1.12, P = 0.006) and diabetes (RR: 11.29, IC: 2.9-42.60, P = 0.000).
  
  
  CONCLUSIONS
  Our study shows that daily peritoneal PrC on initiating PD is significantly and independently related to the presence of PAD. Peritoneal PrC appears to be a possible new marker of systemic endothelial dysfunction.
authors.affiliation: Servicio de Nefrologia, Hospital Universitario La Paz, Madrid, Spain. rjsanchez.hulp@salud.madrid.org
authors.forename: Rafael
authors.initials: R
authors.lastname: Sánchez-Villanueva
authors.forename: Auxiliadora
authors.initials: A
authors.lastname: Bajo
authors.forename: Gloria
authors.initials: G
authors.lastname: Del Peso
authors.forename: M-Jose
authors.initials: MJ
authors.lastname: Fernandez-Reyes
authors.forename: Elena
authors.initials: E
authors.lastname: González
authors.forename: Sara
authors.initials: S
authors.lastname: Romero
authors.forename: Patricia
authors.initials: P
authors.lastname: Estrada
authors.forename: Rafael
authors.initials: R
authors.lastname: Selgas
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism* / Q000401:mortality; D008297:Male; D008875:Middle Aged; D016491:Peripheral Vascular Diseases / Q000175:diagnosis / Q000453:epidemiology / Q000378:metabolism*; D010530:Peritoneal Dialysis; D010537:Peritoneum / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism*; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D011506:Proteins