Stephen C Textor

Hypertension and parenchymal disease of the kidney are closely interrelated. Most primary renal diseases eventually disturb sodium and volume control sufficiently to produce clinical hypertension. Both on theoretical and practical grounds, many authors argue that any sustained elevation of blood pressure depends ultimately on disturbed renal sodium excretion, ie, altered pressure natriuresis. Hence, some investigators argue that a clinical state of hypertension represents de facto evidence of disturbed (or "reset") renal function even before changes in glomerular filtration can be measured.

Many renal insults further induce inappropriate activation of vasoactive systems such as the renin-angiotensin system, adrenergic sympathetic nerve traffic, and endothelin. These mechanisms may both enhance vasoconstriction and act as mediators of additional tissue injury by altering the activity of inflammatory cytokines and promoters of interstitial fibrosis.

Arterial hypertension itself accelerates many forms of renal disease and hastens the progression to advanced renal failure. Recent studies have firmly established the importance of blood pressure reduction as a means to slow the progression of many forms of renal parenchymal injury, particularly those characterized by massive proteinuria. Over the long term, damage to the heart and cardiovascular system resulting from hypertension represents the major causes of morbidity and mortality for patients with end-stage renal disease.

Here are illustrated the roles of renal parenchymal disease in sustaining hypertension and of arterial pressure reduction in slowing the progression of renal injury. As discussed, parenchymal renal disease may refer to either unilateral (uncommon) or bilateral conditions.

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