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Nephrosclerosis from childhood to old age, a viewpoint

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Geriatric Nephrology and Urology

Abstract

Cortical arteries of the kidney in benign nephrosclerosis are characterized by arterial intimal fibroplasia whereas arterioles are affected by hyalinization; these features overlap in the tiniest terminal arteries. In malignant nephrosclerosis, the characteristic lesions are mucoid edema and fibrinoid necrosis respectively. A fifth kind of vasculopathy is marked by reduced calibre and increased wall thickness to diameter ratio; although this is often called “hypertrophy”, wall mass may not be increased, and the name “structural autoregulation” has been proposed in its place. Fibroplasia is found to some degree in every elderly person, even those who never experienced high blood pressure; blood pressure is elevated in those who manifest more than what is usual for the age. A review of reports concerning hypertension in subjects who lack evidence of nephrosclerosis suggests that such subjects may be statistical outliers who are likely to demonstrate regression to the mean in blood pressure rather than subsequent progression of renovasculopathies. It is proposed that uneven sclerosis of arteries may cause heterogeneity of nephrons so that some nephrons are sufficiently ischemic to evoke elevation of blood pressure by Goldblatt mechanisms, while other nephrons have structural autoregulation. A kidney with a small population of ischemic nephrons may show normal overall average function by available clinical methods. The etiology of arterial intimal fibroplasia in aging normotensives is unknown. That unknown etiology could, in theory, explain hypertension as merely the consequence of the more extreme degrees of benign renovasculopathies. A novel kind of epidemiological approach is proposed for pursuing clues to the unknown etiology.

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Tracy, R.E. Nephrosclerosis from childhood to old age, a viewpoint. Geriatric Nephrol Urol 1, 201–211 (1992). https://doi.org/10.1007/BF00636328

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