¹Department of Medicine, Division of Nephrology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA

Correspondence: VM Campese, Department of Medicine, Division of Nephrology, Keck School of Medicine, USC, 1200 North State St, Los Angeles, California 90033, USA. E-mail: campese@usc.edu

Received 18 October 2005; Revised 18 October 2005; Accepted 24 October 2005; Published online 11 January 2006.

Abstract

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.