Yoo Hugo Hyung Bok, Dos Reis Roberto, Telini Wagner Moneda, Telini Lidiane Rodrigues, Hueb João Carlos, Bazan Silmeia Garcia Zanati, Barretti Pasqual, Martin Luis Cuadrado, Queluz Thais Thomaz
Division of Pulmonology, Botucatu School of Medicine, Sao Paulo State University, Botucatu, Brazil.
Iran J Kidney Dis. 2017 Jul;11(4):303-308.
Pulmonary hypertension (PH) has been reported in hemodialysis patients, but data regarding its pathogenesis are scarce. This study aimed to evaluate the role of fluid overload in PH and its interrelationships with the usual biomarkers of micro-inflammatory state in hemodialysis patients.
In is a cross-sectional and prospective study, 119 consecutive hemodialysis patients at a Brazilian referral university hospital were evaluated between March 2007 and February 2013. Based on the presence of echocardiographic parameters of PH, patients were allocated to two groups of the PH group and the non-PH group. Clinical parameters, site and type of vascular access, bio-impedance, and laboratory findings were compared between the two groups and a logistic regression model was elaborated.
Pulmonary hypertension was found in 23 (19.0%) of 119 patients. The groups significantly differed in extracellular water, ventricular thickness, left atrium diameter, and ventricular filling. Additionally, laboratory data associated with PH were alpha-1-acid glycoprotein (140.0 ± 32.9 versus 116.0 ± 35.5; P < .001); C-reactive protein (median, 1.1 versus 1.6; P = .01) and B-type natriuretic peptide (median, 328 versus 77; P = .03). The adjusted logistic regression model, including alpha-1-acid glycoprotein and B-type natriuretic peptide, showed significant associations for both (odds ratio, 1.023; 95% confidence interval, 1.008 to 1.043; P = .004 and odds ratio, 3.074; 95% confidence interval, 1.49-6.35; P = .002, respectively).
Pulmonary hypertension, cardiac hypertrophy, fluid overload, and inflammation were associated to each other in hemodialysis patients, providing insight into its pathogenesis. Longitudinal studies are warranted.
血液透析患者中已报道存在肺动脉高压（PH），但其发病机制的数据却很匮乏。本研究旨在评估液体超负荷在血液透析患者肺动脉高压中的作用及其与微炎症状态常见生物标志物之间的相互关系。
这是一项横断面前瞻性研究，于2007年3月至2013年2月期间对巴西一所转诊大学医院的119例连续性血液透析患者进行了评估。根据超声心动图肺动脉高压参数的存在情况，将患者分为肺动脉高压组和非肺动脉高压组。比较了两组患者的临床参数、血管通路部位和类型、生物电阻抗以及实验室检查结果，并建立了逻辑回归模型。
119例患者中有23例（19.0%）发现有肺动脉高压。两组在细胞外液、心室厚度、左心房直径和心室充盈方面存在显著差异。此外，与肺动脉高压相关的实验室数据有α1酸性糖蛋白（140.0±32.9对116.0±35.5；P<.001）；C反应蛋白（中位数，1.1对1.6；P=.01）和B型利钠肽（中位数，328对77；P=.03）。纳入α1酸性糖蛋白和B型利钠肽的校正逻辑回归模型显示二者均有显著相关性（比值比分别为1.023；95%置信区间为1.008至1.043；P=.004以及比值比为3.074；95%置信区间为1.49 - 6.35；P=.002）。
血液透析患者的肺动脉高压、心脏肥大、液体超负荷和炎症相互关联，为其发病机制提供了见解。有必要进行纵向研究。
