Key result
Patients with COPD had a significantly higher urinary albumin to creatinine ratio compared to healthy controls (64.8 vs 10.6 mg/g, p < 0.001), with microalbuminuria linked to higher CRP and nocturnal heart rate.
Why the study?
Is microalbuminuria associated with systemic inflammation and ambulatory blood pressure alterations in patients with COPD?
Observational (n=110)
No
Is microalbuminuria associated with systemic inflammation and ambulatory blood pressure alterations in patients with COPD?
Absolute Event Rate: 64.8% vs 10.6%
p-value: p=<0.001
Microalbuminuria is significantly more prevalent in patients with severe COPD and is associated with increased systemic inflammation (CRP) and higher nocturnal heart rates, suggesting a link between inflammation and endothelial dysfunction in this population.
Microalbuminuria was associated with inflammation in COPD; hypothesis-generating and requires prospective validation before clinical use.
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterized by inhaled particles and gases inducing chronic inflammation of the airways accompanied by a not fully reversible airflow limitation. Systemic inflammation has an important role in the pathogenesis of COPD. In parallel, several comorbidites can be observed. Microalbuminuria is related to endothelial dysfunction. Microalbuminuria was increased in exacerbation periods of COPD. OBJECTIVES: The aim of the study was evaluate to the presence of microalbuminuria (MA) in patients with chronic obstructive pulmonary disease (COPD) and its relationship to inflammation, arterial blood gas parameters and 24-hour ambulatory blood pressure alterations. MATERIAL AND METHODS: Seventy COPD patients and 40 healthy volunteers were enrolled in the study. 24-h ambulatory blood pressure monitoring (ABPM) results, including pressure and pulse rates of the subjects were recorded and the cases were classified as "dipper" if a normal fall of more than 10% in blood pressure was observed at night and "non-dipper" if not. Routine renal function tests were performed, C-reactive protein (CRP) values were examined and urine samples were obtained to scrutinize the presence of MA. Patients were allocated into two groups, those with and without MA. The spirometry and arterial blood gas results of the patients were recorded. RESULTS: The urinary albumin creatinin ratio (64.8 ± 91.8), CRP (21 ± 14.8), nocturnal systolic and diastolic blood pressure (118 ± 14 and 72 ± 10), nocturnal and diurnal pulse (87 ± 17 and 90 ± 14), nocturnal pulse pressure (49 ± 11), mean pulse (89 ± 15), mean pulse pressure (48 ± 10) and the number of non-dipper subjects (65) were found significantly higher in the COPD group than in the control group (10.6 ± 6, 5.4 ± 2.4, 105 ± 6 and 68 ± 7, 70 ± 10 and 78 ± 11, 42 ± 1, 75± 11, 42 ± 7 and 5, respectively); (p < 0.001, < 0.001, < 0.001 and 0.041, < 0.001 and < 0.001, < 0.001, < 0.001, < 0.001 and < 0.001, respectively). Nocturnal pulse (89 ± 17) and CRP (23.5 ± 14.8) were found to be significantly higher in COPD patients with MA than in COPD patients without MA (78 ± 8 and 8.8 ± 6.3, respectively); (p = 0.021 and < 0.001, respectively). CONCLUSIONS: The facts that CRP, a systemic inflammation marker, and mean nocturnal pulse pressure values were significantly higher in the group with MA among COPD patients, and that ambulatory blood pressure values did not differ between COPD patients with and without MA, suggest both a possible role of inflammation in MA development in COPD patients and a relationship between MA and increased heart rate.
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Kaysoydu et al. (2014) conducted an observational in Chronic Obstructive Pulmonary Disease (COPD) (n=110). Chronic Obstructive Pulmonary Disease (COPD) vs. Healthy volunteers was evaluated on Urinary albumin to creatinine ratio (UACR) (p=<0.001). Patients with COPD had a significantly higher urinary albumin to creatinine ratio compared to healthy controls (64.8 vs 10.6 mg/g, p < 0.001), with microalbuminuria linked to higher CRP and nocturnal heart rate.
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