Recent studies revealed the association between the expression of TLR-4 in glomeruli, tubules, or monocytes and proteinuria in patients with type 2 diabetic nephropathy or IgA nephropathy.[36–38] Ang II infusion induced proteinuria in rats.[39] Glomerular filtration and endocytic uptake of pro-renin and angiotensinogen in the kidney and vasculature in diabetic rats also contributed to increased tissue RAAS.[40] Furthermore, proteinuria, an established risk factor in the progression of renal disease, increases Ang II levels in tubular cells in a NFκB-dependent manner.[41]. This evidence concerns the gene NFKB1 and IgA glomerulonephritis.