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Renal Parenchymal Hypoxia, Hypoxia Adaptation, and the Pathogenesis of Radiocontrast Nephropathy

Samuel N. Heyman^*, Seymour Rosen, and Christian Rosenberger

^* Department of Medicine, Hadassah Hospital, Mt. Scopus and the Hebrew University Medical School, Jerusalem, Israel; Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts; and Critical Care and Hemodialysis Department, Charite University Clinic, Berlin, Germany

Correspondence: Dr. Samuel N. Heyman, Department of Medicine, Hadassah University Hospital, Mt. Scopus, P.O. Box 24035, Jerusalem 91240, Israel. Phone: 972-2-5844520; Fax: 972-2-5812754; E-mail: heyman{at}cc.huji.ac.il

Background and objectives: Renal parenchymal PO₂ declines after the administration of iodinated radiocontrast agents, reaching critically low levels of approximately 10 mmHg in medullary structures.

Design, setting, participants, & measurements: In this review, the causes of renal parenchymal hypoxia and its potential role in the pathogenesis of contrast nephropathy are appraised.

Results: Commonly associated predisposing factors are associated with a propensity to enhance renal hypoxia. Indeed, animal models of radiocontrast nephropathy require the induction of such predisposing factors, mimicking clinical scenarios that lead to contrast nephropathy in high-risk individuals. In these models, in association with medullary hypoxic damage, a transient local cellular hypoxia response is noted, initiated at least in part by hypoxia-inducible factors. Some predisposing conditions that are distinguished by chronically aggravated medullary hypoxia, such as tubulointerstitial disease and diabetes, are characterized by a priori upregulation of hypoxia-inducible factors, which seems to confer tolerance against radiocontrast-related hypoxic tubular damage. Renal dysfunction under such circumstances likely reflects to some extent altered intrarenal hemodynamics, rather than acute tubular injury.

Conclusions: Real-time, noninvasive novel methods may help to differentiate between evolving tubular damage and altered hemodynamics and in the design of appropriate preventive interventions.