The renal mechanisms of hypertension were reviewed, and new way to classify hypertension based on renal mechanisms was proposed. Theoretically, the pressurenatriuresis relationship can be affected in two different ways; either a parallel shift along the blood pressure axis toward a higher blood pressure level or a depression in the slope. The parallel shift of the pressure-natriuresis relationship induces non-sodium sensitive hypertension, while the depressed slope induces sodium sensitive hypertension. Since the degree of the shift of the pressure-natriuresis relationship is determined by the preglomerular vascular resistance from heart to glomeruli, non-sodium sensitive hypertension should be based on the increased preglomerular vascular resistance. On the other hand, the slope of the pressure-natriuresis relationship is determined by glomerulo-tubular balance of sodium, which is mainly controlled by the difference between the whole kidney ultrafiltration coefficient and the rate of tubule sodium reabsorption. Therefore, sodium sensitivity of blood pressure is based on a decrease in the whole kidney ultrafiltration coefficient (due to a decrease in either filtration surface area per glomerulus, hydraulic permeability of glomerular filtration barrier or the number of glomeruli) and/or an increase in tubule sodium reabsorption. In sodium sensitive states, whether whole kidney ultrafiltration coefficient is reduced or tubule sodium reabsorption is enhanced, the glomerular capillary hydraulic pressure rises to compensate for the impairments in sodium excretory capability. If there is a linkage between sodium sensitivity of blood pressure and glomerular hypertension as proposed, renal failure may be expected to be more common in sodium sensitive types of hypertension than in non-sodium sensitive types. Thus, new classification of hypertension based on renal mechanisms may provide an important key to understand pathophysiology of hypertensive diseases as well as nature of their renal lesions.