Iodinated Contrast-Induced Acute Kidney Injury. Pathophysiology and Prevention

Abstract

The term acute renal failure (ARF) secondary to ischemic/nephrotoxic injury should no longer be used and be replaced by acute kidney injury (AKI), indicating an abrupt (within 24–48 hours) increase in serum creatinine by 0.5 mg/dL or by 25% above baseline. Replacing “failure” with “injury” served to include the entire range of renal impairment from small changes in serum creatinine to complete loss of renal function. The term ARF should be limited to a decrease in renal function so severe as to require dialysis. When AKI is due to radiographic contrast agents, it is called contrast-induced (CI) AKI. The pathogenesis of CI-AKI is complex and not well known. Many factors are involved, including hemodynamic changes such as renal vasoconstriction, particularly in the outer medulla where tubular segments devoted to active sodium reabsorption are located; the vasoconstriction may be due to direct action of the contrast agent but may also be mediated by stimulation of angiotensin II and adenosine, or by a decrease in the local production of prostaglandins and nitric oxide, all leading to medullary hypoxia. Other factors are osmotic diuresis (with increased tubular reabsorption of sodium and tubular epithelium injury, both worsening medullary hypoxia) and production of reactive oxygen species that will cause endothelial and epithelial damage, likewise worsening medullary hypoxia. The fall in renal blood flow and tubular obstruction will decrease the glomerular filtration rate. Treatment and prevention of CI-AKI are based on opposing these factors by adequate hydration; administration of furosemide along with fluid replacement; theophylline and aminophylline; PGE1 and PGI2; N-acetylcysteine, ascorbic acid and vitamin E; nebivolol and statins.