ACEI is an angiotensinase inhibitor and ARB is an angiotensin receptor antagonist, both of which are classified as antihypertensive agents. ACEI and ARB have similar target organ protective effects, and in addition to their clear antihypertensive effects, they can protect the kidney. ACEI and ARB can exert renoprotective effects through two pathways: hemodynamic and non-hemodynamic effects. The hemodynamic effect refers to the renoprotective effect of improving the “three highs” (high pressure, high perfusion and high filtration) in the glomerulus. ACEI and ARB can adjust the systemic hemodynamic effect and Adjustment of local hemodynamic effects: ① In chronic kidney disease, the small glomerular arteries are often in a dilated state, and if clinical hypertension exists (measured blood pressure ≥ 140/90 mmHg), then systemic hypertension can easily be transmitted to the glomerulus, resulting in “three highs” in the glomerulus. (2) ACEI and ARB can dilate the small glomerular arteries, and the effect of dilating the small glomerular arteries is stronger than that of dilating the small glomerular arteries, so even if there are no clinical hypertension symptoms, ACEI/ARB can be applied to directly reduce the “three highs” in the glomerulus. Therefore, even in the absence of clinical hypertension, ACEI/ARB can be applied to directly reduce the “triple high” in the glomerulus and provide renal protection. Another non-hemodynamic effect of nephroprotective function, mainly including: ① improve glomerular filtration membrane selective permeability, angiotensin II can make small pores on glomerular filtration membrane bigger, resulting in poor filtration membrane selective permeability, ACEI and ARB blocked the effect of angiotensin II, which can reduce urinary protein excretion; ② protect glomerular foot cells, angiotensin II can damage foot cell function. ACEI and ARB blocked the effect of angiotensin II, thus protecting the podocytes; (3) reduce the accumulation of extracellular matrix in the glomerulus, angiotensin II can stimulate glomerular cells to increase the synthesis of extracellular matrix (moderate to severe accumulation of extracellular matrix forms glomerulosclerosis), ACEI and ARB blocked the effect of angiotensin II, thus reducing the accumulation of extracellular matrix in the glomerulus, thus delaying the progression of glomerulosclerosis. progression of sclerosis.