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Clinical features, diagnosis, and treatment of hypertensive nephrosclerosis

INTRODUCTION

Hypertensive nephrosclerosis is a disorder that is usually associated with chronic hypertension. In addition to the level of blood pressure, it is clear that individual factors are involved. As an example, black patients have an approximate eight-fold elevation in the risk of hypertension-induced end-stage renal disease [1]; this increase in risk may persist even with "adequate" blood pressure control. Although low birth weight and bias in diagnosis based upon the patient's race may be involved, the recent recognition of an association between two independent sequence variants in the APOL1 gene on chromosome 22 and renal disease in African-Americans, including focal segmental glomerular sclerosis and hypertension-related end-stage renal disease, provides a much more likely pathophysiologic mechanism [2], and suggests that hypertensive nephrosclerosis in blacks and whites may be distinct diseases. (See "Epidemiology, classification, and pathogenesis of focal segmental glomerulosclerosis", section on 'FSGS in African Americans'.)

PATHOLOGY

Hypertensive nephrosclerosis is characterized histologically by vascular, glomerular, and tubulointerstitial involvement (picture 1) [3]. The histologic pattern of renal injury in patients with malignant hypertension (ie, malignant nephrosclerosis) is different, and is discussed separately. (See "Moderate to severe hypertensive retinopathy and hypertensive encephalopathy in adults", section on 'Clinical manifestations and diagnosis'.)

Vascular disease — The vascular disease consists of intimal thickening and luminal narrowing of the large and small renal arteries and the glomerular arterioles. Two different processes appear to contribute to the development of the vascular lesions:

A hypertrophic response to chronic hypertension that is manifested by medial hypertrophy and fibroblastic intimal thickening, leading to narrowing of the vascular lumen [4,5]. This response is initially adaptive by minimizing the degree to which the rise in systemic pressure is transmitted to the arterioles and capillaries [5].

The deposition of hyaline-like material (plasma protein constituents, such as inactive C3b, part of the third component of complement) into the damaged, more permeable arteriolar wall [5].

             

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Literature review current through: Aug 2014. | This topic last updated: Jul 1, 2013.
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