Acquired predisposition to renal damage associated to tobacco consumption
Abstract
A relation between tobacco and renal damage has been described during the last years. Referring to early diagnosis of renal disease, our group has developed the acquired predisposition concept, which can be applied to the smoking patient context. So, our hypothesis is that tobacco may cause predisposition to acute kidney injury (AKI), which means smokers may suffer AKI after being exposed to any nephrotoxin, including under-toxicity-level doses. Our aim was to study the relationship between the predisposition biomarkers 1 (BM1), 2 (BM2) and 3 (BM3) (characterized in our laboratory) and tobacco consumption.
Urinary samples were taken from smokers and non-smokers volunteers with no renal damage nor exposure to risk factors of renal disease. The plasma creatinine of the patients was obtained from their medical history. The cotinine levels, which inform of the grade of smoking, were measured by ELISA. The urinary creatinine, used to correct urinary concentrations of biomarkers, was measured with a commercial kit based on Jaffé reaction, and the urinary biomarkers levels were measured by Western blot.
Only BM3 showed greater excretion in smoking patients than in non-smokers. However, that excretion is not related to cotinine levels. In any case, BM3 could be a good clinical biomarker of AKI predisposition which would help to prevent renal damage in smokers.
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