Chronic renal oxidative stress and inflammation subsequently trigger apoptosis through TGF-β-mediated activation of Casp-3 [17,18], with glomerulopathy and tubular damage that are manifested by albuminuria and decreased GFR [38,39], and by increasing renal expression of NGAL and KIM-1 [4,40]. Here, CASP3 is linked to lipoprotein glomerulopathy.