Pathophysiology of Nephrosclerosis?
The term hypertensive nephrosclerosis has traditionally been used to describe a clinical syndrome characterized by long-term essential hypertension, hypertensive retinopathy, left ventricular hypertrophy, minimal proteinuria, and progressive kidney failure. Most cases are diagnosed based solely on clinical findings. In fact, most of the literature dedicated to hypertensive nephrosclerosis is based on the assumption that progressive kidney failure in a patient with long-standing hypertension, moderate proteinuria, and no evidence suggesting an alternative diagnosis characterizes hypertensive nephrosclerosis.
@sreejon Two pathophysiologic mechanisms have been proposed for the development of hypertensive nephrosclerosis. One mechanism suggests that glomerular ischemia causes hypertensive nephrosclerosis. This occurs as a consequence of chronic hypertension resulting in narrowing of preglomerular arteries and arterioles, with a consequent reduction in glomerular blood flow. Alternatively, glomerulosclerosis may occur because of glomerular hypertension and glomerular hyperfiltration. According to this theory, hypertension causes some glomeruli to become sclerotic. As an attempt to compensate for the loss of kidney function, the remaining nephrons undergo vasodilation of the preglomerular arterioles and experience an increase in renal blood flow and glomerular filtration. The result is glomerular hypertension, glomerular hyperfiltration, and progressive glomerular sclerosis. These mechanisms are not mutually exclusive, and they may operate simultaneously in the kidney.