[PP.09.08] SMOKING ACCELERATES ALBUMIN EXCRETION IN HYPERTENSIVE PATIENTS WITH METABOLIC SYNDROME. (September 2016)

• Record Type: Journal Article
• Authors: Pietri, P.; Vlachopoulos, C.; Ioakeimidis, N.; Terentes-Printzios, D.; Abdelrasoul, M.; Gourgouli, I.; Tousoulis, D.; Stefanadis, C.
• Is Part Of: Journal of hypertension. Volume 34:(2016) Supplement 2
• Publication Date: 2016-09
• Subjects: Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/01.hjh.0000491796.14402.5b
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Objective: Microalbuminuria is a marker of kidney organ damage and has independent prognostic value for future cardiovascular events. Metabolic syndrome (MS) is prognostic of cardiovascular disease, either as a distinct entity or through its clustering cardiometabolic abnormalities. Whether smoking may accelerate microalbuminuria in patients with MS, is not well clarified. Design and method: We studied 524 patients with never-treated arterial hypertension and metabolic syndrome, defined by the ATP III criteria. Smoking status was assessed by recording the current habit of smoking. Albumin excretion was evaluated in all patients after 24 h urine collection, using immunonephelometry, and albumin to creatinine ratio (ACR) was calculated. High-sensitivity C-reactive protein (hsCRP) was measured as an inflammatory biomarker. All participants were free from overt cardiovascular disease. Results: Smokers (n = 274) were younger compared to non-smokers (mean age: 51 vs 56 years old, p < 0.001), had increased levels of hsCRP (1.9 ± 1.2 vs 1.7 ± 1.1 mg/L, p < 0.01) but, marginally, lower mean arterial pressure (MAP) levels compared to non-smokers (111.3 ± 11.8 vs 113.2 ± 12.8 mmHg, p = 0.06). No difference in glucose, total cholesterol and triglycerides was observed between the two groups (p = NS). Albumin excretion was significantly higher in smokers compared to non-smokers (mean ACR: 40.4 vs 32.9 mg/g, p = 0.04). In linear regression analysis, ACR was independently associated with smoking (b = 0.10, p = 0.01) after adjustment for age, gender, BMI, plasma glucose, MAP and hsCRP. Conclusions: Smoking accelerates microalbuminuria in hypertensive patients with MS, independently of other classic or novel risk factors. Given the prognostic significance of microalbuminuria, it might be suggested that smoking may further enhance the cardiovascular risk associated with MS through the adverse effect on albumin excretion. Whether quitting smoking may result in regression of microalbumiuria, thus with a more favorable cardiovascular risk profile, is a question that warrants further investigation. Until then, microalbuminuria should be assesed in all smokers with MS and arterial hypertension in order to improve risk stratification and guide therapy.