(Circulation. 2006;113:1799-1806.)
© 2006 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
From the Department of Nephrology, Medizinische Klinik IV, Charité Campus Benjamin Franklin, Berlin, Germany (M.T.); Division of Radiology, Department of Clinical Science, Intervention, and Technology, Karolinska Institutet, Stockholm, Sweden (P.A.); and the Renal Division, Department of Medicine, University Hospital Ghent, Ghent, Belgium (N.L.).
Correspondence to Dr Martin Tepel, Medizinische Klinik IV Nephrologie, Charité Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. E-mail Martin.Tepel@charite.de
Key Words: nephropathy kidney mortality
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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| Clinical Relevance |
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Although the exact mechanisms of CIN have yet to be fully elucidated, several causes have been described. Increased adenosine-, endothelin-, and free radicalinduced vasoconstriction and reduced nitric oxide and prostaglandin-induced vasodilatation have been observed. These mechanisms
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