Contrast induced nephropathy overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamed Moubarak, M.D. [2]
Overview
Contrast media (CM) are widely used in diagnostic and interventional procedures with rising incidence of iatrogenic renal function impairment caused by the exposure to contrast media, a condition known as Contrast-induced nephropathy (CIN).
Historical Perspective
Most of data related to the contrast nephropathy come from animal models. Studies show evidence of acute tubular necrosis (ATN) but the mechanism by which ATN occurs is not well understood.
Pathophysiology
The exact mechanisms of nephrotoxicity have yet to be more illustrated, but are likely to involve several pathogenic factors. Intrinsic causes include increased vasoconstrictive forces, decreased local prostaglandin- and nitric oxide (NO)-mediated vasodilatation, a direct toxic effect on renal tubular cells with damage caused by oxygen free radicals, increased oxygen consumption, and increased intratubular pressure secondary to contrast-induced diuresis, increased urinary viscosity, and tubular obstruction, all of which leads to medullary ischemia.[1]
Contrast induced nephropathy differential diagnosis
The differential diagnosis includes, but not limited to, Atheroembolic renal failure, Acute renal failure, Acute interstitial nephritis, and Acute tubular necrosis.
Epidemiology and Demographics
An overall incidence of CIN in the general population is reported to be 0.6–2.3%.[2] CIN is the third most common cause of renal failure, the overall mortality rate was 19.4% and was similar among patients for all causes of renal insufficiency.[3]
Risk Factors
Many factors have been associated with an increased risk of contrast-induced nephropathy. Pre-existing renal insufficiency, pre-existing diabetes, age, volume of CM, and reduced intravascular volume are an example for these risk factor.[4][5] The total risk rises as the number of risk factors increase, it has been recommended that every known risk factor should be analyzed, to properly evaluate a total cumulative risk of developing contrast-induced nephropathy. A clinical prediction rule is available to estimate probability of nephropathy (increase ≥25% and/or ≥0.5 mg/dl in serum creatinine at 48 h)[6]
Natural history, Complications and Prognosis
The reported incidence of CIN varies widely depending on the presence or absence of risk factors, CIN associated with a significantly higher risk of in-hospital and 1-year mortality, even in patients who do not need dialysis.
History and Symptoms
Creatinine increase is the characteristic finding in CIN, kidney injury occure with in minutes of exposure to contrast agents, however clinical manifestations such as oliguria or elevation of serum creatinine are generally observed within 24 to 48 hours after contrast exposure.
Physical Examination
A physical examination is helpful to rule out other causes of acute nephropathy, such as cholesterol emboli (eg, blue toe, livedo reticularis), or drug-induced interstitial nephritis (eg, rash). Patients may have evidence of volume depletion or may be in decompensated CHF.
Laboratory Findings
Increase in the serum creatinine are generally observed within 24 to 48 hours after contrast exposure in most of patients, hyperkalemia, acidosis and hyperphosphatemia may be present.
Medical Therapy
Management of CIN routinely includes the avoidance of substances that are toxic to the kidneys. Dialysis is rarely required for AKI following contrast administration, but occasionally patients will require dialysis in the acute setting. The indications for dialysis are the same as in other forms of AKI.
Prevention
General measures should be followed to minimize the incidence CIN, include carefully considering whether the contrast examination is absolutely needed, especially in high-risk patients, using the minimal effective dose, and eliminating potentially nephrotoxic drugs at least 24 hr before the study. Encourage IV hydration and following protocols that allow clear liquids up to 2 hr before the procedure. Alternative diagnostic procedures should be considered in those at high-risk.
References
- ↑ Gleeson TG, Bulugahapitiya S (2004). "Contrast-induced nephropathy". AJR Am J Roentgenol. 183 (6): 1673–89. doi:10.2214/ajr.183.6.01831673. PMID 15547209.
- ↑ Lasser EC, Lyon SG, Berry CC (1997). "Reports on contrast media reactions: analysis of data from reports to the U.S. Food and Drug Administration". Radiology. 203 (3): 605–10. PMID 9169676.
- ↑ Nash K, Hafeez A, Hou S (2002). "Hospital-acquired renal insufficiency". Am J Kidney Dis. 39 (5): 930–6. doi:10.1053/ajkd.2002.32766. PMID 11979336.
- ↑ McCullough PA, Wolyn R, Rocher LL, Levin RN, O'Neill WW (1997). "Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality". Am J Med. 103 (5): 368–75. PMID 9375704.
- ↑ Scanlon PJ, Faxon DP, Audet AM, Carabello B, Dehmer GJ, Eagle KA, Legako RD, Leon DF, Murray JA, Nissen SE, Pepine CJ, Watson RM, Ritchie JL, Gibbons RJ, Cheitlin MD, Gardner TJ, Garson A Jr, Russell RO Jr, Ryan TJ, Smith SC Jr (1999). "ACC/AHA guidelines for coronary angiography. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Coronary Angiography). Developed in collaboration with the Society for Cardiac Angiography and Interventions". J Am Coll Cardiol. 33 (6): 1756–824. PMID 10334456.
- ↑ Mehran R, Aymong ED, Nikolsky E; et al. (2004). "A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation". J. Am. Coll. Cardiol. 44 (7): 1393–9. doi:10.1016/j.jacc.2004.06.068. PMID 15464318.