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INVITED REVIEW
1Servicio de Nefrología, Hospital Universitario, Universidad del Zulia, Instituto de Inmunobiología (Fundacite-Zulia), Maracaibo 400-A, Venezuela; 2Division of Nephrology and Hypertension, Department of Medicine, Physiology, and Biophysics, University of California, Irvine, California 92697; 3Departamento de Nefrología, Instituto Nacional de Cardiología "Ignacio Chávez," 14080 Mexico City, Mexico; and 4Renal Division, University of Florida, Gainesville, Florida 32610
Recent evidence indicates that interstitial infiltration of T cells and macrophages plays a role in the pathogenesis of salt-sensitive hypertension. The present review examines this evidence and summarizes the investigations linking the renal accumulation of immune cells and oxidative stress in the development of hypertension. The mechanisms involved in the hypertensive effects of oxidant stress and tubulointerstitial inflammation, in particular intrarenal ANG II activity, are discussed, focusing on their potential for sodium retention. The possibility of autoimmune reactivity in hypertension is raised in the light of the proinflammatory and immunogenic pathways stimulated by the interrelationship between oxidant stress and inflammatory response. Finally, we present some clinical considerations derived from the recognition of this interrelationship.
interstitial nephritis; autoimmunity; reactive oxygen species; angiotensin
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