Contrast induced nephropathy overview: Difference between revisions
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==Definition== | ==Definition== | ||
In 2012, a new definiton for contrast induced nephropathy was put forth by the KDIGO-AKI guidelines. CIN was to be considered a new form of AKI caused by contrast media, and definition criteria for AKI would also apply for CIN now called contrast-induced acute kidney injury (CI-AKI).<ref name="doi10.1038/kisup.2011.34">{{cite journal|author=Kidney Disease Improving Global Outcomes Work Group| title=2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury| journal=Kidey Int Supp |year= 2012 | volume= 2 | pages= 69-88 | doi=10.1038/kisup.2011.34 | pmc=|url=http://www.nature.com/kisup/journal/v2/n1/full/kisup201134a.html }} </ref> However, the most commonly used definition in clinical trails is acute renal insufficiency marked by an increase in baseline serum creatinine of >25% or an absolute increase in serum creatinine of 0.5 mg/dL that occurs 48-72 hours following the exposure to CM.<ref name="pmid16612394">{{cite journal| author=Mehran R, Nikolsky E| title=Contrast-induced nephropathy: definition, epidemiology, and patients at risk. | journal=Kidney Int Suppl | year= 2006 | volume= | issue= 100 | pages= S11-5 | pmid=16612394 | doi=10.1038/sj.ki.5000368 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16612394 }} </ref><ref name="pmid16436769">{{cite journal |author=Barrett BJ, Parfrey PS |title=Clinical practice. Preventing nephropathy induced by contrast medium |journal=N. Engl. J. Med.|volume=354 |issue=4 |pages=379–86 |year=2006 |pmid=16436769 |doi=10.1056/NEJMcp050801}}</ref> | In 2012, a new definiton for contrast induced nephropathy was put forth by the KDIGO-AKI guidelines. CIN was to be considered a new form of AKI caused by contrast media, and definition criteria for AKI would also apply for CIN now called contrast-induced acute kidney injury (CI-AKI).<ref name="doi10.1038/kisup.2011.34">{{cite journal|author=Kidney Disease Improving Global Outcomes Work Group| title=2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury| journal=Kidey Int Supp |year= 2012 | volume= 2 | pages= 69-88 | doi=10.1038/kisup.2011.34 | pmc=|url=http://www.nature.com/kisup/journal/v2/n1/full/kisup201134a.html }} </ref> However, the most commonly used definition in clinical trails is acute renal insufficiency marked by an increase in baseline serum creatinine of >25% or an absolute increase in serum creatinine of 0.5 mg/dL that occurs 48-72 hours following the exposure to CM.<ref name="pmid16612394">{{cite journal| author=Mehran R, Nikolsky E| title=Contrast-induced nephropathy: definition, epidemiology, and patients at risk. | journal=Kidney Int Suppl | year= 2006 | volume= | issue= 100 | pages= S11-5 | pmid=16612394 | doi=10.1038/sj.ki.5000368 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16612394 }} </ref><ref name="pmid16436769">{{cite journal |author=Barrett BJ, Parfrey PS |title=Clinical practice. Preventing nephropathy induced by contrast medium |journal=N. Engl. J. Med.|volume=354 |issue=4 |pages=379–86 |year=2006 |pmid=16436769 |doi=10.1056/NEJMcp050801}}</ref> The new definition shifted the 0.5 mg/dL cutoff to 0.3 mg/dL an the 25% increase in baseline to 1.5 times. | ||
==Historical Perspective== | ==Historical Perspective== | ||
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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).
Definition
In 2012, a new definiton for contrast induced nephropathy was put forth by the KDIGO-AKI guidelines. CIN was to be considered a new form of AKI caused by contrast media, and definition criteria for AKI would also apply for CIN now called contrast-induced acute kidney injury (CI-AKI).[1] However, the most commonly used definition in clinical trails is acute renal insufficiency marked by an increase in baseline serum creatinine of >25% or an absolute increase in serum creatinine of 0.5 mg/dL that occurs 48-72 hours following the exposure to CM.[2][3] The new definition shifted the 0.5 mg/dL cutoff to 0.3 mg/dL an the 25% increase in baseline to 1.5 times.
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 pathophysiology of CIN is not clearly understood; however, several attempts have been made to explain the underlying mechanism. It is generally agreed that CIN is due to a combination of several influences brought on by contrast-media infusion rather than a single process. The most important mechanism thought to be involved in CIN is a reduction in renal perfusion and subsequent hypoxia. This has been attributed to several alterations in the renal microenvironment including activation of the tubuloglomerular feeback, local vasoactive metabolites including adenosine, prostaglandin, NO, and endothelin as well as increased interstitial pressure.[4] Although sometimes considered controversial, studies have also proposed injury to renal tubular cells as another contributor both via a direct cytotoxic effect and via reactive oxygen species production.[5]
Contrast induced nephropathy differential diagnosis
The differential diagnosis includes atheroembolic renal failure, acute renal failure, acute interstitial nephritis, and acute tubular necrosis.
Epidemiology and Demographics
Incidence of CIN in the general population have been reported to be 0.6–2.3%.[6] Considered to be the third most common cause of renal failure with overall mortality rate 19.4%, which is similar for all causes of renal insufficiency.[7]
Risk Factors
Many factors have been associated with an increased risk of nephropathy in patients exposed to contrast media. Pre-existing renal insufficiency, pre-existing diabetes, age, volume of CM, and reduced intravascular volume are examples for these risk factor.[8][9] 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)[10]
Natural history, Complications and Prognosis
The reported incidence varies widely according to the presence or absence of risk factors, and usually 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 occur 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
Physical examination is helpful to differentiate other causes of acute nephropathy, examples for different presentations include rash in drug-induced interstitial nephritis, blue toe and livedo reticularis in case of embolism. Some risk factors can be detected as evidence of volume depletion, and decompensated CHF, and correcting these factors help improving the outcome.
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 of 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
- ↑ Kidney Disease Improving Global Outcomes Work Group (2012). "2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury". Kidey Int Supp. 2: 69–88. doi:10.1038/kisup.2011.34.
- ↑ Mehran R, Nikolsky E (2006). "Contrast-induced nephropathy: definition, epidemiology, and patients at risk". Kidney Int Suppl (100): S11–5. doi:10.1038/sj.ki.5000368. PMID 16612394.
- ↑ Barrett BJ, Parfrey PS (2006). "Clinical practice. Preventing nephropathy induced by contrast medium". N. Engl. J. Med. 354 (4): 379–86. doi:10.1056/NEJMcp050801. PMID 16436769.
- ↑ Wong PC, Li Z, Guo J, Zhang A (2012). "Pathophysiology of contrast-induced nephropathy". Int J Cardiol. 158 (2): 186–92. doi:10.1016/j.ijcard.2011.06.115. PMID 21784541.
- ↑ Persson PB, Hansell P, Liss P (2005). "Pathophysiology of contrast medium-induced nephropathy". Kidney Int. 68 (1): 14–22. doi:10.1111/j.1523-1755.2005.00377.x. PMID 15954892.
- ↑ 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.