Abstract
Contrast-induced nephropathy (CIN) is the third leading cause of acute kidney injury in hospitalized patients and is associated with significant patient morbidity. The pathogenesis of CIN is complex and not fully understood, but iodinated contrast agents induce intense and prolonged vasoconstriction at the corticomedullary junction of the kidney. Moreover, high-osmolar dyes directly impair the autoregulatory capacity of the kidney through a loss of nitric oxide production. These effects, coupled with direct tubular toxicity of contrast media, lead to overt acute tubular necrosis and the syndrome of CIN.
MeSH terms
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Acute Kidney Injury / chemically induced*
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Acute Kidney Injury / physiopathology*
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Adenosine / blood
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Biomarkers / urine
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Consensus Development Conferences as Topic
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Contrast Media / adverse effects*
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Embolism, Cholesterol / physiopathology
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Endothelins / blood
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Humans
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Kidney Tubules / drug effects
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Kidney Tubules / physiopathology
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Nitric Oxide / metabolism
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Reactive Oxygen Species / metabolism
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Renal Circulation / drug effects
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Renal Circulation / physiology
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Reperfusion
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Sodium / urine
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Vasoconstriction / drug effects
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Vasoconstriction / physiology
Substances
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Biomarkers
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Contrast Media
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Endothelins
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Reactive Oxygen Species
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Nitric Oxide
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Sodium
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Adenosine