Journal of the American Society of Nephrology
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J Am Soc Nephrol 17: 218-225, 2006
© 2006 American Society of Nephrology
doi: 10.1681/ASN.2006080918

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Supplement Articles

Mycophenolate Mofetil Treatment Improves Hypertension in Patients with Psoriasis and Rheumatoid Arthritis

Jose Herrera*, Atilio Ferrebuz*, Ernesto García MacGregor{dagger} and Bernardo Rodriguez-Iturbe*

* Renal Service, Hospital Universitario, and {dagger} Hospital Central, Centro de Medicina y Cirugía Experimental, Universidad del Zulia and Instituto de Investigaciones Biomédicas, FUNDACITE-Zulia, Maracaibo, Venezuela

Address correspondence to: Dr. Bernardo Rodríguez-Iturbe, Apartado Postal 1430, Maracaibo, Estado Zulia, Venezuela. Phone: +58-261-7519610; Fax: +58-261-7524838; E-mail: bernardori{at}telcel.net.ve

Evidence that was obtained in several experimental models and in strains of hypertensive rats indicates that infiltration of inflammatory cells and oxidative stress in the kidney play a role in the induction and maintenance of hypertension. Similar evidence is lacking in human hypertension, at least in part, because immunosuppressive treatment is unjustified in patients with hypertension. For addressing this issue, patients who were prescribed by their private physicians mycophenolate mofetil (MMF) for the treatment of psoriasis or rheumatoid arthritis and had, in addition, grade I essential hypertension and normal renal function were studied. Eight patients were studied before MMF was started, during MMF treatment, and 1 mo after MMF treatment had been discontinued. Other treatments and diet were unchanged in the three phases of the study. MMF therapy was associated with a significant reduction in systolic, diastolic, and mean BP. Urinary excretion of TNF-{alpha} was reduced progressively by MMF treatment and increased after MMF was discontinued. Reduction of urinary malondialdehyde, TNF-{alpha}, and RANTES excretion during MMF administration did not reach statistical significance but had a direct positive correlation with the BP levels. These data are consistent with the hypothesis that renal immune cell infiltration and oxidative stress play a role in human hypertension.




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