Hypertensive nephrosclerosis.
OBJECTIVE
Hypertensive nephrosclerosis is the second most common cause of end-stage renal disease, however morphologic evidence on the subject is poorly understood. A perennial and vexing problem in understanding kidney hypertension is that correlations between hypertension and vascular and glomerular lesions are only moderate, in part because all of these lesions are present to a greater or lesser degree in the normotensive, aging kidney, with racial differences in severity further compounding the problem. This review looks at newer data on this topic.


RESULTS
Recent data suggest that there are two different processes leading to glomerulosclerosis, and the combination of the two begins to explain why global correlations between hypertension and morphologic lesions are destined to remain poor. Arterial stiffening with increased pulse pressure down as far as the afferent arteriolar level likely plays an important role in the progression of glomerular lesions. Loss of renal autoregulation with glomerular hypertrophy, hyperfiltration, and focal segmental glomerulosclerosis is now recognized to contribute significantly to nephrosclerosis, particularly in the black population. Ischemic glomerulosclerosis, however, may ultimately be the most important lesion, with consequent hypoxia in the parenchyma beyond, leading to tubular atrophy and interstitial fibrosis.


CONCLUSIONS
Hypertensive nephrosclerosis should be seen as a process with two principal modes of glomerular sclerosis, ischemic and hypertrophic, with consequent focal segmental glomerulosclerosis, contributing variably to renal failure according to race and level of hypertension.
Hill
Gary S
GS
European Hospital Georges Pompidou, Paris, France. garyhillparis@aol.com
D000818:Animals; D001284:Atrophy; D001794:Blood Pressure; D015687:Cell Hypoxia; D004195:Disease Models, Animal; D004548:Elasticity; D005355:Fibrosis; D005919:Glomerular Filtration Rate; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D006984:Hypertrophy; D018836:Inflammation Mediators / Q000378:metabolism; D007511:Ischemia / Q000150:complications / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology*; D009400:Nephrosclerosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D012077:Renal Artery / Q000503:physiopathology; D012079:Renal Circulation; D016212:Transforming Growth Factor beta / Q000378:metabolism
D018836:Inflammation Mediators; D016212:Transforming Growth Factor beta