Impaired water and sodium excretion is a central aspect of the pathogenesis of hypertension, and if the tendency for renal water and sodium retention is not corrected, then an increase in blood pressure is inevitable. The normalization of blood pressure depends mainly on the blood displacement of the heart, the resistance of the peripheral vessels, and the blood volume. Normal kidneys play an important role in regulating intravascular blood volume. Assuming that certain factors, such as intravenous infusions, cause an increase in blood volume, the blood perfusion pressure in the kidneys increases, leading to an increase in water and sodium excretion, an increase in urination, and a consequent decrease in intravascular volume, blood pressure may stabilize at normal levels. In patients with hypertension, the kidneys have a tendency to retain sodium and water, and require high perfusion pressure to produce the same sodium- and water-reducing effects, so that blood pressure needs to be maintained at a high level. The significance of this mechanism is that elevated blood pressure is used as a way to compensate for the normal water-sodium balance in the body, and if the tendency of the kidneys to retain water and sodium is not corrected, then elevated blood pressure is inevitable and necessary for the body. If a kidney in this condition is transplanted into a person with normal blood pressure, the recipient will also become hypertensive, and therefore, impaired water-sodium excretion is a central aspect of the pathological mechanism of hypertension. In addition, kidneys that have been under high perfusion pressure for a long time will undergo structural changes, resulting in renal vascular degeneration, lumen narrowing or even occlusion, leading to renal parenchymal ischemia, glomerular fibrosis, and tubular atrophy until renal failure.