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Clin J Am Soc Nephrol. 2008 Jan;3(1):288-96. Epub 2007 Dec 5.

Renal parenchymal hypoxia, hypoxia adaptation, and the pathogenesis of radiocontrast nephropathy.

Author information

  • 1Department of Medicine, Hadassah University Hospital, Mt. Scopus, P.O. Box 24035, Jerusalem 91240, Israel. heyman@cc.huji.ac.il

Abstract

BACKGROUND AND OBJECTIVES:

Renal parenchymal Po(2) 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.

PMID:
18057308
[PubMed - indexed for MEDLINE]
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