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==Definition== | ==Definition== | ||
There are three necessary components for the definition of CIN:<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> | There are three necessary components for the definition of CIN:<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> | ||
* Elevated serum creatinine compared to the baseline values. | * Elevated serum creatinine compared to the baseline values. | ||
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Contrast-induced nephropathy is defined as either a greater than 25% increase of serum creatinine or an absolute increase in serum creatinine of 0.5 mg/dL that occur 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> According to a study that aimed to describe the course of creatinine rise and its determinants after exposure to contrast media, the first 24 hours post-exposure appear to be crucial in the development of CIN.<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="pmid12440177">{{cite journal| author=Guitterez NV, Diaz A, Timmis GC, O'Neill WW, Stevens MA, Sandberg KR et al.| title=Determinants of serum creatinine trajectory in acute contrast nephropathy. | journal=J Interv Cardiol | year= 2002 |volume= 15 | issue= 5 | pages= 349-54 | pmid=12440177 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12440177 }} </ref> The same study showed that patients with less than 0.5 mg/dl rise in serum creatinine within the first 24 h were unlikely to have any clinically meaningful form of CIN. | Contrast-induced nephropathy is defined as either a greater than 25% increase of serum creatinine or an absolute increase in serum creatinine of 0.5 mg/dL that occur 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> According to a study that aimed to describe the course of creatinine rise and its determinants after exposure to contrast media, the first 24 hours post-exposure appear to be crucial in the development of CIN.<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="pmid12440177">{{cite journal| author=Guitterez NV, Diaz A, Timmis GC, O'Neill WW, Stevens MA, Sandberg KR et al.| title=Determinants of serum creatinine trajectory in acute contrast nephropathy. | journal=J Interv Cardiol | year= 2002 |volume= 15 | issue= 5 | pages= 349-54 | pmid=12440177 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12440177 }} </ref> The same study showed that patients with less than 0.5 mg/dl rise in serum creatinine within the first 24 h were unlikely to have any clinically meaningful form of CIN. | ||
==2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury== | |||
===Definition and staging of AKI=== | |||
{|class="wikitable" style="width:80%" | |||
|- | |||
|colspan="1" style="text-align:center; background:LightCoral"|[[KDIGO guidelines classification scheme|Not Graded]] | |||
|- | |||
|bgcolor="LightCoral"|<nowiki>"</nowiki>'''1.''' AKI is defined as any of the following: | |||
:'''a.''' Increase in SCr by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or | |||
:'''b.''' Increase in SCr to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or | |||
:'''c.''' Urine volume <0.5 ml/kg/h for 6 hours. ([[KDIGO guidelines classification scheme|Level of Evidence: Not Graded]])''<nowiki>"</nowiki> | |||
|- | |||
|bgcolor="LightCoral"|<nowiki>"</nowiki>'''2.''' AKI is staged for severity according to the following criteria (Table 2). ([[KDIGO guidelines classification scheme|Level of Evidence: Not Graded]])''<nowiki>"</nowiki> | |||
|- | |||
|} | |||
====Table 2: Staging of AKI==== | |||
{| {{table}} | |||
| align="center" style="background:#f0f0f0;"|'''Stage''' | |||
| align="center" style="background:#f0f0f0;"|'''Serum creatinine''' | |||
| align="center" style="background:#f0f0f0;"|'''Urine output''' | |||
|- | |||
| 1||1.5–1.9 times baseline OR ≥0.3 mg/dl (≥26.5 μmol/l) increase||<0.5 ml/kg/h for 6–12 hours | |||
|- | |||
| 2||2.0–2.9 times baseline||<0.5 ml/kg/h for ≥12 hours | |||
|- | |||
| 3||3.0 times baseline OR Increase in serum creatinine to ≥4.0 mg/dl (≥353.6 μmol/l) OR Initiation of renal replacement therapy OR In patients <18 years, decrease in eGFR to <35 ml/min per 1.73 m<sup>2</sup>||<0.3 ml/kg/h for ≥24 hours OR Anuria for ≥12 hours | |||
|} | |||
===Definition and staging of CI-AKI=== | |||
{|class="wikitable" style="width:80%" | |||
|- | |||
|colspan="1" style="text-align:center; background:LightCoral"|[[KDIGO guidelines classification scheme|Not Graded]] | |||
|- | |||
|bgcolor="LightCoral"|<nowiki>"</nowiki>'''1.''' Define and stage AKI after administration of intravascular contrast media as per Recommendations 2.1.1–2.1.2. ([[KDIGO guidelines classification scheme|Level of Evidence: Not Graded]])''<nowiki>"</nowiki> | |||
|- | |||
|bgcolor="LightCoral"|<nowiki>"</nowiki>'''2.''' In individuals who develop changes in kidney function after administration of intravascular contrast media, evaluate for CI-AKI as well as for other possible causes of AKI. ([[KDIGO guidelines classification scheme|Level of Evidence: Not Graded]])''<nowiki>"</nowiki> | |||
|- | |||
|} | |||
==References== | ==References== | ||
Revision as of 22:36, 11 September 2013
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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
Definition
There are three necessary components for the definition of CIN:[1]
- Elevated serum creatinine compared to the baseline values.
- Temporal relationship between the rise in serum creatinine and exposure to a contrast agent.
- Exclusion of alternative explanations for renal impairment.
Contrast-induced nephropathy is defined as either a greater than 25% increase of serum creatinine or an absolute increase in serum creatinine of 0.5 mg/dL that occur 48–72 hours following the exposure to CM.[1][2] According to a study that aimed to describe the course of creatinine rise and its determinants after exposure to contrast media, the first 24 hours post-exposure appear to be crucial in the development of CIN.[1][3] The same study showed that patients with less than 0.5 mg/dl rise in serum creatinine within the first 24 h were unlikely to have any clinically meaningful form of CIN.
2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury
Definition and staging of AKI
| Not Graded |
"1. AKI is defined as any of the following:
|
| "2. AKI is staged for severity according to the following criteria (Table 2). (Level of Evidence: Not Graded)" |
Table 2: Staging of AKI
| Stage | Serum creatinine | Urine output |
| 1 | 1.5–1.9 times baseline OR ≥0.3 mg/dl (≥26.5 μmol/l) increase | <0.5 ml/kg/h for 6–12 hours |
| 2 | 2.0–2.9 times baseline | <0.5 ml/kg/h for ≥12 hours |
| 3 | 3.0 times baseline OR Increase in serum creatinine to ≥4.0 mg/dl (≥353.6 μmol/l) OR Initiation of renal replacement therapy OR In patients <18 years, decrease in eGFR to <35 ml/min per 1.73 m2 | <0.3 ml/kg/h for ≥24 hours OR Anuria for ≥12 hours |
Definition and staging of CI-AKI
| Not Graded |
| "1. Define and stage AKI after administration of intravascular contrast media as per Recommendations 2.1.1–2.1.2. (Level of Evidence: Not Graded)" |
| "2. In individuals who develop changes in kidney function after administration of intravascular contrast media, evaluate for CI-AKI as well as for other possible causes of AKI. (Level of Evidence: Not Graded)" |
References
- ↑ 1.0 1.1 1.2 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.
- ↑ Guitterez NV, Diaz A, Timmis GC, O'Neill WW, Stevens MA, Sandberg KR; et al. (2002). "Determinants of serum creatinine trajectory in acute contrast nephropathy". J Interv Cardiol. 15 (5): 349–54. PMID 12440177.