Fig 2: Evaluation of the progression of tobacco-associated subclinical kidney damage after two years of consumption through a panel of urinary biomarkers. Data are presented as absolute increase in box plots. ** p < 0.01 vs. NS-NRF. NS-NRF: non-smokers, no risk factors; S-NRF: smokers, no risk factors. AU, arbitrary units; Cru, urinary creatinine; GM2AP, GM2 ganglioside activating protein; KIM-1, kidney injury molecule 1; NAG, N-acetyl-β-D-glucosaminidase; NGAL, neutrophil gelatinase-associated lipocalin.

Fig 3: Effect of tobacco cessation on renal function through a panel of urinary biomarkers. Data are presented in box plot ** p < 0.01; *** p < 0.001 vs. NS-NRF. ## p < 0.01, ### p < 0.001 vs. FS-NRF. NS-NRF: non-smokers, no risk factors; S-NRF: smokers, no risk factors; FS-NRF former smokers, no risk factors; Cru, urinary creatinine; GM2AP, GM2 ganglioside activating protein; KIM-1, kidney injury molecule 1; NAG, N-acetyl-β-D-glucosaminidase; NGAL, neutrophil gelatinase-associated lipocalin.

Fig 4: Comparison of cytotoxicity between COP-MPS and PDMS-MPS. (a) Phase-contrast images of RPTEC layers; (b) Time course of KIM-1 secretion; (c) Time course of LDH release. Data are presented as mean ± SD (technical replicates, n = 3). * p < 0.05.

Fig 5: Association of tobacco consumption with kidney damage through a panel of urinary biomarkers. Data are presented in box plots. * p < 0.05; ** p < 0.01; *** p < 0.001 vs. NS-NRF. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. NS-RF. NS-NRF: non-smokers, no risk factors; NS-RF: non-smokers with risk factors; S-NRF: smokers, no risk factors; S-RF: smokers with risk factors; AU, arbitrary units; Cru, urinary creatinine; GM2AP, ganglioside GM2 activator protein; KIM-1, kidney injury molecule 1; NAG, N-acetyl-β-D-glucosaminidase; NGAL, neutrophil gelatinase-associated lipocalin.