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Am J Physiol Renal Physiol 283: F1132-F1141, 2002. First published July 24, 2002; doi:10.1152/ajprenal.00199.2002
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Vol. 283, Issue 5, F1132-F1141, November 2002

Overload proteinuria is followed by salt-sensitive hypertension caused by renal infiltration of immune cells

Violeta Alvarez, Yasmir Quiroz, Mayerly Nava, Héctor Pons, and Bernardo Rodríguez-Iturbe

Renal Service and Laboratory and Instituto de Investigaciones Biomédicas, Fundacite-Zulia, Hospital Universitario, Universidad del Zulia, Maracaibo 4001-A, Venezuela

Recent evidence suggests that salt-sensitive hypertension develops as a consequence of renal infiltration with immunocompetent cells. We investigated whether proteinuria, which is known to induce interstitial nephritis, causes salt-sensitive hypertension. Female Lewis rats received 2 g of BSA intraperitoneally daily for 2 wk. After protein overload (PO), 6 wk of a high-salt diet induced hypertension [systolic blood pressure (SBP) = 156 ± 11.8 mmHg], whereas rats that remained on a normal-salt diet and control rats (without PO) on a high-salt diet were normotensive. Administration of mycophenolate mofetil (20 mg · kg-1 · day-1) during PO resulted in prevention of proteinuria-related interstitial nephritis, reduction of renal angiotensin II-positive cells and oxidative stress (superoxide-positive cells and renal malondialdehyde content), and resistance to the hypertensive effect of the high-salt diet (SBP = 129 ± 12.2 mmHg). The present studies support the participation of renal inflammatory infiltrate in the pathogenesis of salt-sensitive hypertension and provide a direct link between two risk factors of progressive renal damage: proteinuria and hypertension.

interstitial nephritis; oxidative stress


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