Pathophysiology of hypertension in renal failure

Hypertension (HTN) is ubiquitous in the renal failure patient. It has long been thought that renal disease interferes with salt excretion, leading to volume overload and consequent hypertension. This theory gives prominence to the kidney in long-term regulation of blood pressure (BP). It is assumed that the excess salt and water retention increases the blood flow to the tissues, which sets in motion the phenomenon of autoregulation. The tissue arterioles vasoconstrict to decrease the excessive blood flow. The resulting vasoconstriction raises the peripheral vascular resistance, which is the cardinal most consistent findings in HTN (whether essential or renal in origin). Recently, more light has been shed on the multitude of factors and pathophysiologic mechanisms that lead to HTN in the renal disease patient. The level of BP is most likely determined by the level of the peripheral vascular resistance and volume status in combination. If the peripheral vascular resistance is not appropriately lowered in the face of hypervolemia, HTN results. This primary role of the blood vessel in HTN is consistent with the close correlation of vascular disease to HTN (because HTN is a manifestation of vessel disease). In this review, evidence for and against the different pathophysiologic mechanisms that have been postulated to explain renal HTN is presented.