Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 1.736
5-Year Impact Factor – 2.135
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MEiN – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
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Advances in Clinical and Experimental Medicine

2014, vol. 23, nr 5, September-October, p. 749–755

Publication type: original article

Language: English

Factors Related to Microalbuminuria in Patients with Chronic Obstructive Pulmonary Disease

Erdal Kaysoydu1,A,B,D, Sulhattin Arslan1,A,C,F,G, Gürsel Yıldız2,A,B,C, Ferhan Candan3,A,G

1 Department of Chest Disease, Faculty of Medicine, Cumhuriyet University, Turkey

2 Department of Nephrology, Atatürk State Hospital, Turkey

3 Department of Nephrology, Faculty of Medicine, Cumhuriyet University, Turkey

Abstract

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 a nd < 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).
Conclusion. 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.

Key words

COPD, arterial blood gas, inflammation, microalbuminuria, non-dipper.

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