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Kidney transplantation (KT) potentially reduces pulmonary damage associated with chronic kidney disease. This study explored this assumption by comparing pulmonary functionality and endothelial function between dialysis and KT patients.
Cross-sectional study including 23 patients on dialysis for ≥24 months and 23 patients transplanted for ≥12 months, with glomerular filtration rate ≥ 40 mL/min/1.73m2, matched by gender and age. Pulmonary functionality was analyzed by maximal inspiratory and expiratory pressure (MIP and MEP), forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and Tiffeneau index. Endothelial damage was assessed using syndecan-1, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM 1), and angiopoietin-2 (Ang-2).
style="font-size: 1rem; font-weight: var(--bs-body-font-weight); text-align: var(--bs-body-text-align);">Both groups had poor performance in pulmonary functionality tests. The percentage of patients reaching the predicted MIP, MEP, FEV1, and FCV was low and similar between groups (43.5%, 4.3%, 0%, and 17.4%, respectively). There were no differences in the observed/predicted MEP (66 ± 17%), FEV1 (60±18%), and FCV (76 ± 22%) ratios, and in the Tiffeneau index (0.8 [IQR 0.6-0.9] %). KT patients showed lower MIP% (82±19 vs. 94±12%, p=0.019). In KT group, endothelial damage was significantly inversely correlated with pulmonary functionality parameters, and this group presented lower levels of VCAM-1 (1,589 [IQR 1,009-1827] vs 2,302 [IQR 1,642–3,540] ng/mL, p=0.001), Ang-2 (0.17 [IQR 0.01-1.14] vs 0.75 [IQR 0.30-1.29] ng/mL, p=0.040), and Syndecan-1 (47.9 [IQR 33.1-67.8] vs 195.8 [IQR 126.9-286.8] ng/mL, p<0.001).
Despite better endothelial function, KT was not associated with superior pulmonary functionality, suggesting multifactorial pathophysiology for lung impairment.