Pathophysiology of contrast-induced nephropathy.
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.
Tumlin
James
J
Southeast Renal Research Institute (SERRI), Charlotte, North Carolina 28028, USA. jtumlin@emory.edu
Stacul
Fulvio
F
Adam
Andy
A
Becker
Christoph R
CR
Davidson
Charles
C
Lameire
Norbert
N
McCullough
Peter A
PA
D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000503:physiopathology*; D000241:Adenosine / Q000097:blood; D015415:Biomarkers / Q000652:urine; D003245:Consensus Statements as Topic; D003287:Contrast Media / Q000009:adverse effects*; D017700:Embolism, Cholesterol / Q000503:physiopathology; D016232:Endothelins / Q000097:blood; D006801:Humans; D007684:Kidney Tubules / Q000187:drug effects / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology; D015424:Reperfusion; D012964:Sodium / Q000652:urine; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology
D015415:Biomarkers; D003287:Contrast Media; D016232:Endothelins; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D012964:Sodium; D000241:Adenosine