Mitigating Contrast-Induced Acute Kidney Injury Associated With Cardiac Catheterization

Abstract

Contrast-induced nephropathy, also referred to as contrast-induced acute kidney injury (CIAKI), is among the most common causes of AKI, especially in patients with underlying chronic kidney disease. In addition to the increased cost engendered by the development of CIAKI, several studies have suggested the occurrence of AKI after cardiac procedures is associated with an increase in both morbidity and mortality. This increase in morbidity and mortality occurs after both intravenous and intra-arterial studies. This review focuses on relevant proposed pathophysiological mechanisms, risk factors, and current prophylactic strategies, which may reduce the incidence of CIAKI during cardiac angiographic imaging studies.

Contrast-Induced Nephropathy: Pathophysiology and Preventive Strategies

“…Two deleterious effects: Interstitial inflammation 17 Decreased production of vasodilatory prostaglandins, thereby potentiating the effect of adenosine, increasing vasoconstriction 17,20 Vasoconstriction of afferent arterioles, resulting in irreversible damage; glomerular sclerosis 29 Risk of volume depletion before procedure 17 After procedure, forced euvolemic diuresis associated with increase in risk for contrastinduced nephropathy 2,3,6,16 Intracellular accumulation of medication in proximal tubule cells thought to interfere with cellular function, eventually leading to cell death and decreased glomerular filtration rate 9,20 Binds to tubular epithelial cells, alters cell permeability, and causes vasoconstriction of intrarenal arteries and arterioles angiography and contrast-enhanced computed tomography. Patients who undergo coronary angiography are at highest risk for CIN.…”

“…Patients who undergo coronary angiography are at highest risk for CIN. 17,24 Often the procedure is done under emergent conditions, and patients may be volume depleted, and their hemodynamic status may be less than optimal. 17,24 An increased incidence of CIN is predicted because of more frequent use of contrast media in radiology departments, an increase in the incidence of chronic kidney disease, and an aging population.…”

“…[2][3][4]7,9,10,[12][13][14] A lack of risk factors for renal disease effectively eliminates the likelihood that a patient will have renal impairment associated with infusion of contrast media. 1 Kelly et al, 6 Nunag et al, 17 and Benko et al…”

“…Diagnosis of CIN is most often based on an increase in the serum level of creatinine after exposure to a contrast agent 17 (Table 2). A baseline assessment before administration of contrast material is required so that renal insufficiency can be detected before the procedure with contrast material and the diagnosis of CIN after the procedure.…”

Role of nephrotoxic drugs in contrast-induced nephropathy

“…Aminoglycosides cause the release of lysosomal acid hydrolases thus resulting in mitochondrial degeneration and cellular death. 10 The toxicity results from accumulation and retention of an aminoglycoside in the proximal tubular cells. The initial manifestation of damage at this site is the excretion of enzymes of the renal tubular brush border.…”