In addition, an accumulation of IS can cause degradation of the remaining renal nephrons, mainly in the proximal tubular cells, stimulating glomerular sclerosis, renal fibrosis and the progression of CKD contributing to increase the expression of the pro-α1 collagen, transforming growth factor β1 (TGF-β1) and tissue inhibitor of metalloproteinase 1 (TIMP-1) genes, resulting in greater loss of nephrons, which in turn increases the CKD progress (Niwa, 2010). The gene discussed is TIMP1; the disease is glomerulosclerosis.