Abstract

Microalbuminuria (MAB), a marker of endovascular dysfunction, is a predictor of cardiovascular events and all-cause mortality in the general population. There is evidence of vascular dysfunction in patients with chronic obstructive pulmonary disease (COPD). To assess the prevalence and relationship of MAB with clinical and physiological parameters in stable patients with COPD. We measured urinary albumin rate (urinary albumin to creatinine ratio: UACR), smoking history, arterial blood pressure, gas exchange, body mass index, lung function, BODE index (body mass index, airflow obstruction, dyspnea, exercise performance), and comorbidity index in 129 patients with stable COPD and 51 smokers with normal spirometry without known cardiovascular disease. MAB levels were compared between groups. A multivariate analysis was performed to determine the best determinants of MAB levels. MAB was higher in patients with COPD than in control smokers (8 [5th-95th percentile (P₅₋₉₅), 2.9-113] vs. 4.2 [P₅₋₉₅, 1.8-22.7] mg/g, P < 0.001]). The difference remained significant even after using the standard pathologic threshold (MAB, 30-299 mg/g in women and 20-299 mg/g in men; 24% in patients with COPD vs. 6% in control smokers; P = 0.005). In patients with COPD, there was a negative correlation between Pa(O₂) and MAB (r = -0.40, P < 0.001). Using multivariate analysis, MAB was only associated with the Pa(O₂) (relative risk, 0.934; 95% confidence interval, 0.880-0.992; P < 0.001) and with the systolic arterial blood pressure (relative risk, 1.034; 95% confidence interval, 1.011-1.057; P = 0.003). MAB is frequent in patients with COPD and is associated with hypoxemia independent of other cardiovascular risk factors. Further studies are necessary to investigate whether MAB could be an early simple biomarker of cardiovascular compromise in patients with COPD.

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