The first hypothesis derives primarily from studies that show how ACE inhibitors diminish proteinuria, the renal filtration fraction, and the intraglomerular pressure in various experimental models of renal disease.[24, 25] Since angiotensin II increases the tone of the efferent arteriole, the intraglomerular pressure, and the proteinuria, it is conceivable that ACE inhibitors can reduce the proteinuria by inhibiting the effect of angiotensin II in renal microcirculation. Here, AGT is linked to kidney disorder.