Seminars in Nephrology
Volume 25, Issue 1 , Pages 61-66, January 2005

Uric acid in chronic heart failure

  • Wolfram Doehner

      Affiliations

    • Division of Applied Cachexia Research, Department of Cardiology, Campus Virchow-Klinikum, Charite Medical School, Humboldt University, Berlin, Germany.
    • Corresponding Author InformationAddress reprint requests to Wolfram Doehner, MD, PhD, Department of Cardiology, Charité Campus Virchow-Klinikum, Augustenburger Platz 1, D-13353 Berlin, Germany.
    • ,
  • Stefan D. Anker

      Affiliations

    • Division of Applied Cachexia Research, Department of Cardiology, Campus Virchow-Klinikum, Charite Medical School, Humboldt University, Berlin, Germany.
    • Department of Clinical Cardiology, National Heart & Lung Institute, Imperial College School of Medicine, London, UK.

The pathophysiologic understanding of chronic heart failure (CHF) has shifted from a mere hemodynamic disorder to a much more complex approach including changes and imbalances in neurohormonal, immune, and metabolic functions. Among metabolic abnormalities, hyperuricemia is a constant finding in CHF. The xanthine oxidase metabolic pathway increasingly is appreciated as an important contributor to both symptoms of CHF as well as progression of the disease. Recent data suggest hyperuricemia to be an independent marker of impaired prognosis in CHF. In this article, the significance of the xanthine oxidase metabolic pathway in CHF is discussed. Data on xanthine oxidase inhibition are reviewed, which suggest a beneficial effect of therapeutically targeting this enzymatic pathway.

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 Supported by the Verein der Freunde und Förderer der Berliner Charité, Germany; and the NHLI London (W.D.); and by the Vandervell Fellowship, London, UK, and a grant for Applied Cachexia Research by the Charite Medical School, Berlin, Germany (S.D.A.).

PII: S0270-9295(04)00153-6

doi:10.1016/j.semnephrol.2004.09.010

Seminars in Nephrology
Volume 25, Issue 1 , Pages 61-66, January 2005

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