MO406: Evolution of Kidney Damage Associated With Tobacco Consumption

Abstract

Abstract BACKGROUND AND AIMS Tobacco consumption is associated with cancer, cardiovascular and respiratory diseases. Although new research relates tobacco use with the development of kidney damage, classic biomarkers, such as plasma creatinine, are not useful to detect this kidney injury [1]. In this sense, innovative diagnostic methods have been developed, such as early biomarkers capable of detecting subclinical kidney damage in the initial stages of the disease [2, 3]. In fact, studies carried out in our laboratory have shown that smoking patients suffer subclinical kidney damage evidenced by the excretion of these urinary biomarkers [4]. The aim of this work was to study the evolution of kidney damage associated with tobacco consumption using these biomarkers after monitoring smoking patients for 2 years. METHOD A longitudinal study was carried out that included 150 smokers and 150 non-smokers, without previous kidney damage and risk factors for kidney disease, from a Salamanca Health Centre (Spain). Urine samples were collected at the time of inclusion and after 2 years, and the biomarkers of subclinical kidney damage N-acetyl-β-D-glucosaminidase (NAG), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1) and total proteins, were quantified using ELISA and colorimetric techniques. The data obtained were analyzed with the statistical software SPSS®. RESULTS The results showed a higher excretion of NAG, NGAL, KIM-1 and total proteins in smoker patients with respect to non-smoker ones, measured at baseline, which was maintained after 2 years. CONCLUSION Our research suggests that subclinical kidney damage associated with tobacco consumption would remain stable in the 2 years studied and could become chronic and it could constitute the basis for the development of chronic kidney failure.