Coexisting CKD in COPD patients was associated with higher systemic inflammation, oxidative stress, and endothelial dysfunction, with disease duration >10 years predicting CKD (OR 2.01; 95% CI 1.42-2.87).
Observational (n=150)
Does the presence of CKD in COPD patients increase systemic inflammation, oxidative stress, and endothelial dysfunction?
Coexisting CKD in COPD is associated with amplified systemic inflammation, oxidative stress, and endothelial dysfunction, highlighting the need for early renal risk assessment.
Effect estimate: OR 2.01 (95% CI 1.42-2.87)
Abstract Background Chronic kidney disease (CKD) frequently coexists with COPD and may amplify systemic inflammation and vascular injury, worsening clinical outcomes. Objective To evaluate inflammatory, oxidative stress, and endothelial dysfunction markers in COPD depending on the presence of CKD, and to identify predictors of renal impairment. Materials and Methods A total of 130 COPD patients (87 without CKD; 43 with CKD) and 20 healthy controls were examined. Spirometry, inflammatory markers (TNF-α, CRP), oxidative stress markers (MDA, SOD, catalase), and endothelial function indicators (ET-1, NO metabolites) were measured. Correlation and logistic regression analyses were applied. Results Early renal dysfunction was detected in 49.2% of COPD patients by cystatin C-eGFR vs 34.6% by creatinine-eGFR, indicating earlier sensitivity of cystatin C. Albuminuria and ACR increased progressively with COPD severity. COPD+CKD patients demonstrated higher systemic inflammation (TNF-α 14.25±1.5 pg/mL, CRP 11.6±1.2 mg/L, both p 0.01), increased oxidative stress (MDA 3.35±0.12 nmol/mL, p 0.001), reduced antioxidant activity (SOD 1035.7±45.8 U/g Hb, catalase 6.68±0.27 U/g Hb), and marked endothelial dysfunction (ET-1 1.18±0.04 fmol/mL, NO metabolites 16.65±1.06 μmol/L, p 0.001). MDA negatively correlated with eGFR (r = −0.66, p 0.01) and FEV1 (r = −0.62), while ET-1 correlated with ACR (r = 0.55). Independent predictors of CKD in COPD included: disease duration 10 years (OR 2.01, 95% CI 1.42-2.87), ≥2 exacerbations/year (OR 1.52, p 0.05), smoking history 35 pack-years (OR 1.63, p 0.05), CRP 15 mg/L (OR 1.81, p 0.01), MDA 2.5 nmol/mL (OR 1.94, p 0.01). These findings indicate that renal dysfunction in COPD amplifies the systemic inflammatory cascade and promotes vascular endothelial injury, potentially accelerating both pulmonary function decline and microvascular remodeling. Conclusion Coexisting CKD in COPD is accompanied by increased systemic inflammation, oxidative stress, and endothelial dysfunction. TNF-α, CRP, MDA, and ET-1 may help identify early renal impairment and support timely preventive treatment. These results highlight the importance of early risk assessment in COPD patients to prevent progression of kidney damage. This abstract is funded by: none
Muminov et al. (Fri,) conducted a observational in COPD with coexisting Chronic Kidney Disease (n=150). Coexisting Chronic Kidney Disease vs. COPD without CKD and healthy controls was evaluated on Predictors of CKD in COPD (disease duration >10 years) (OR 2.01, 95% CI 1.42-2.87). Coexisting CKD in COPD patients was associated with higher systemic inflammation, oxidative stress, and endothelial dysfunction, with disease duration >10 years predicting CKD (OR 2.01; 95% CI 1.42-2.87).