Malnutrition-inflammation syndrome is associated with endothelial dysfunction in peritoneal dialysis patients.

Endothelial dysfunction with atherosclerosis is a recognized complication of uremic patients. The hypoalbuminemia of peritoneal dialysis (PD) patients can induce a hypercoagulable and atherogenic state. In this study, we investigated the role played by malnutrition-inflammation syndrome on endothelial function markers in PD patients. We measured markers of nutrition [normalized protein catabolic rate (nPCR), albumin, prealbumin, insulin-like growth factor 1 (IGF-1), transferrin, and cholesterol], markers of endothelial damage and/ unction [tissue-type plasminogen activator (tPA), thrombomodulin (TM), von Willebrand factor (vWF), and NO 3 (representing NO)], markers of a coagulable state [fibrinogen and plasminogen activator inhibitor I (PAI-1)], markers of inflammation [tumor necrosis factor a (TNFa) and C-reactive protein (CRP)], and other endothelial injury factors {lipoprotein(a) [Lp(a)] and homocysteine}. We also performed an endothelial stimulation test consisting of right-arm venous occlusion (VO) for 10 minutes. The patients were divided into four groups according to their clinical atherosclerotic score (CAS). We studied 45 clinically stable PD patients. At baseline, statistically significant negative linear correlations were found between albumin and age (r = -0.54, p 4 g/dL [tPA ratio: 2.1 ′ 1.56 (n = 29) vs. 2.6 ′ 2.3 (n = 16), p < 0.05; NO 3 : 47 ′ 27 μg/mL vs. 69 ′ 33 μg/mL, p < 0.05; CRP: 1.8 ′ 3 mg/dL vs. 1.1 ′ 1.6 mg/dL, p < 0.05; TNFa: 44.4 ′ 16 pg/mL vs. 36.6 ′ 21.4 pg/mL, p < 0.05; Lp(a): 55 ′ 39 mg/dL vs. 33 ′ 21 mg/dL, p < 0.05]. Patients with a worse CAS showed higher homocysteine levels and lower albumin values. Those relationships were maintained in both periods of the study. We found no relationships between dialysis dose and endothelial function markers. In conclusion, malnutrition-inflammation syndrome may contribute to endothelial dysfunction and, consequently, to prothrombotic and proatherogenic processes in PD patients.