Pulmonary function and endothelial damage in patients undergoing renal replacement therapy: a cross-sectional study.

Authors

Italo Caldas Silva, Gdayllon Cavalcante Meneses, Alice Maria Costa Martins, Alexandre Braga Libório, Elizabeth De Francesco Daher, Ronaldo de Matos Esmeraldo, Nataly Gurgel Campos, Tainá Veras de Sandes-Freitas

Published in

Jornal brasileiro de nefrologia. Volume 48. Issue 4. Pages e20250222.

Abstract

To compare pulmonary function and biomarkers of endothelial injury between hemodialysis patients with end-stage renal disease (ESRD) and kidney transplant (KT) recipients.
Cross-sectional study including 23 patients on dialysis for ≥ 24 months and 23 patients transplanted for ≥ 12 months, with a glomerular filtration rate ≥ 40 mL/min/1.73 m2, matched by sex and age. Pulmonary function was analyzed by maximal inspiratory and expiratory pressure (MIP and MEP), forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and the 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).
Both groups had poor performance in pulmonary function tests. The percentage of patients reaching the predicted MIP, MEP, FEV1, and FVC values was low and similar between groups (43.5%, 4.3%, 0%, and 17.4%, respectively). There were no differences in the observed/predicted ratios for MEP (66 ± 17%), FEV1 (60 ± 18%), and FVC (76 ± 22%), or in the Tiffeneau index (0.8 [IQR 0.6-0.9]). KT patients showed lower MIP percentages (82 ± 19 vs. 94 ± 12%; p = 0.019). In the KT group, endothelial damage was significantly inversely correlated with pulmonary function parameters, and this group had 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 function, suggesting a multifactorial pathophysiology for lung impairment.

PMID:
42636346
Bibliographic data and abstract were imported from PubMed on 25 Aug 2026.

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