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Renal parenchymal hypoxia, hypoxia adaptation, and the pathogenesis of radiocontrast nephropathy Heyman SN; Rosen S; Rosenberger CClin J Am Soc Nephrol 2008[Jan]; 3 (1): 288-96BACKGROUND 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.|*Acute Kidney Injury/chemically induced/etiology/physiopathology[MESH]|Adaptation, Physiological[MESH]|Animals[MESH]|Contrast Media/*adverse effects[MESH]|Humans[MESH]|Hypoxia/*complications/*physiopathology[MESH] |
