Abstract
BackgroundDespite epidemiological evidences of relationship between poor lung function and atherosclerosis, the relationship between poor lung function and microalbuminuria (MAU), an early surrogate marker of both kidney damage and atherosclerosis, is not well understood. Hence, we plan to investigate the relationship between poor lung function and MAU using multivariate models to adjust for other atherogenic risk factors.MethodsWe used data from the 5th Korean National Health and Nutrition Examination Survey. Poor lung function is determined by spirometric measurement, primarily through estimation of the forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1). Declines in the percent predicted FVC (<80%) and in the FEV1/FVC ratio (<0.7) are defined as restrictive and obstructive patterns, respectively. Urine albumin to urine creatinine levels ratio (UACR) were measured in spot urine samples. MAU was defined as UACR >30 mg/g.ResultsInverse relationship was observed between lung function and UACR. In an age-adjusted regression model, the regression coefficient (B) of 10% lower FVC was 11.09 in men (P = 0.002), which remained significant after adjustment for SBP, FBG, triglyceride level, BMI, smoking history, and heavy alcohol consumption (B = 7.52, P = 0.043). When the restrictive pattern was compared to the normal pattern, the odds ratios (OR) (95% confidence interval, 95%CI) for MAU were 1.90 (1.32–2.72) in men, after adjustment for age, hypertension, diabetes mellitus, triglyceride level, obesity, smoking history, physical activity, and heavy alcohol consumption.ConclusionsOur study, the first investigation in Asia, demonstrated that the restrictive pattern is related to MAU in men. Furthermore, there was linear relationship between lower FVC and UACR. Thus, our current study suggests that poor lung function, particularly the restrictive pattern, is related to kidney damage as well as atherosclerosis.
Highlights
Microalbuminuria (MAU), as indicated by the urine albuminto-creatinine ratio (UACR), occurs when blood albumin leaks from the kidneys into the urine [1]
In an age-adjusted regression model, the regression coefficient (B) of 10% lower in predicted forced vital capacity (FVC) was 11.09 in men (P = 0.002), which remained significant after adjustment for systolic blood pressure (SBP), fasting blood glucose (FBG), triglyceride level, Body mass index (BMI), smoking history, and heavy alcohol consumption (B = 7.52, P = 0.043)
When the restrictive pattern was compared to the normal pattern, the crude odds ratios (OR) (95%CI) for MAU were 2.60 (1.87–3.62) in men and 1.55 (1.07–2.25) in women
Summary
Microalbuminuria (MAU), as indicated by the urine albuminto-creatinine ratio (UACR), occurs when blood albumin leaks from the kidneys into the urine [1] This leakage represents underlying problems in blood vessels and endothelial dysfunction, a key mechanism of atherosclerosis [2]. The strong predictive power of MAU for the risk of atherosclerosis is independent of conventional cardiovascular risk factors, even in diabetes mellitus and hypertension patients [4]. Multiple pathological steps such as retention, modification, and accumulation of lipids in the endothelium occur prior to vascular damage or atherosclerosis, all of which are negatively influenced by systemic inflammation [5]. We plan to investigate the relationship between poor lung function and MAU using multivariate models to adjust for other atherogenic risk factors
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