Hypertension in renal parenchymal disease: Why is it so resistant to treatment?
Author(s) -
V. M. Campese,
Noémi Mitra,
Duanpen Sandee
Publication year - 2006
Publication title -
kidney international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.499
H-Index - 276
eISSN - 1523-1755
pISSN - 0085-2538
DOI - 10.1038/sj.ki.5000177
Subject(s) - medicine , pathophysiology of hypertension , kidney disease , renin–angiotensin system , pathogenesis , cardiology , sympathetic nervous system , kidney , obstructive sleep apnea , vasodilation , angiotensin ii , endothelial dysfunction , ischemia , endothelin receptor , endocrinology , blood pressure , receptor
The association between hypertension and chronic renal disease is well known. The pathogenesis of hypertension in patients with chronic kidney disease (CKD) is complex and multifactorial, which may explain why it is resistant to treatment. The traditional paradigm is that hypertension in CKD is due either to an excess of intravascular volume (volume dependent) or to excessive activation of the renin-angiotensin system in relation to the state of sodium/volume balance (renin-dependent hypertension). This review focuses on the importance of less established mechanisms, such as increased activity of the sympathetic nervous system, increased endothelin production, decreased availability of endothelium-derived vasodilators and structural changes of the arteries, renal ischemia, and sleep apnea.
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