PT - JOURNAL ARTICLE AU - Francesca Polverino AU - Maria Laucho-Conttreras AU - Vanesa Bijol AU - Victor Pinto-Plata AU - Miguel Divo AU - Mary Choi AU - Lynette Sholl AU - Hans Petersen AU - Yohannes Tesfaigzi AU - Bartolome Celli AU - Caroline Owen TI - Evidence of renal and pulmonary endothelial dysfunction in chronic obstructive pulmonary disease (COPD) AID - 10.1183/13993003.congress-2016.PA4016 DP - 2016 Sep 01 TA - European Respiratory Journal PG - PA4016 VI - 48 IP - suppl 60 4099 - http://erj.ersjournals.com/content/48/suppl_60/PA4016.short 4100 - http://erj.ersjournals.com/content/48/suppl_60/PA4016.full SO - Eur Respir J2016 Sep 01; 48 AB - Background: About 25% of COPD patients have microalbuminuria (MAB; which is a marker of endothelial dysfunction [ED]) associated with increased mortality, but it is unknown whether COPD have underlying renal lesions. ED is linked to increased oxidative stress which induces advanced end glycation products (AGE) and their receptor (RAGE) in endothelial cells (EC) in patients with diabetes mellitus and cardiovascular diseases. We hypothesize that: 1) COPD patients have renal injury; and 2) the oxidative stress-AGE-RAGE axis in EC contributes to pulmonary and renal injury in COPD.Methods: Urinary albumin:creatinine ratios (UACRs) were measured in smoker controls (SC) and wild type mice exposed to air or CS for 1-6 months. In these groups we also examined: 1) ultrastructural (evidence of renal injury using electron microscopy); 2) lung and kidney oxidative stress levels; 3) lung and kidney EC apoptosis and AGEs and RAGE levels.Results: SC had increased UACRs which correlated directly with rate of lung function decline. COPD kidneys had greater subcapsular scarring, glomerulo-sclerosis, interstitial fibrosis, tubular atrophy, arterial sclerosis, and mesangial expansion than kidneys from SC. CS-exposed mice had increased UACRs and shrunken glomeruli. COPD patients and/or CS-exposed mice also had increased oxidative stress levels in lungs and kidneys, and staining for AGES, RAGE, and apoptosis in pulmonary and renal EC.Conclusions: COPD patients, SC, and CS-exposed mice develop generalized ED and kidney injury with MAB and increased UACRs that may be linked to the oxidative stress-AGE-RAGE axis in EC. Thus, COPD patients with MAB may benefit from therapies targeting ED.