Contrast induced nephropathy definition: Difference between revisions

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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>
The definition of CIN requires 3 criteria:<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.
* An absolute elevation in serum creatinine of 0.5 mg/dL or and increase of >25% of the baseline creatinine
* Temporal relationship between the rise in serum creatinine and exposure to a contrast agent.
* Rise of serum creatinine within 72 hours of exposure to contrast media
* Exclusion of alternative explanations for renal impairment.
* Exclusion of other diagnoses to explain the 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.<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 after exposure to contrast media, the first 24 hours post-exposure are very critical 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.
The PRINCE trial (Prevention of Radiocontrast Induced Nephropathy Clinical Evaluation) showed that the first 24 hours after exposure to CM are the most essential in determining outcome. In 80% of patients with CIN, serum creatinine increase became apparent in the first 24 hours. Virtually all patients with complicated CIN defined as serious renal impairment requiring either acute dialysis or nephrology consultation had a rise in creatinine within that time frame.<ref name="pmid9973020">{{cite journal| author=Stevens MA, McCullough PA, Tobin KJ, Speck JP, Westveer DC, Guido-Allen DA et al.| title=A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy: results of the P.R.I.N.C.E. Study. Prevention of Radiocontrast Induced Nephropathy Clinical Evaluation. | journal=J Am Coll Cardiol | year= 1999 | volume= 33 | issue= 2 | pages= 403-11 | pmid=9973020 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9973020 }} </ref>


==2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury (DO NOT EDIT)==
==2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury (DO NOT EDIT)==

Revision as of 19:00, 1 October 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

Contrast-induced nephropathy is defined as 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.[1][2]

Definition

The definition of CIN requires 3 criteria:[1]

  • An absolute elevation in serum creatinine of 0.5 mg/dL or and increase of >25% of the baseline creatinine
  • Rise of serum creatinine within 72 hours of exposure to contrast media
  • Exclusion of other diagnoses to explain the renal impairment

The PRINCE trial (Prevention of Radiocontrast Induced Nephropathy Clinical Evaluation) showed that the first 24 hours after exposure to CM are the most essential in determining outcome. In 80% of patients with CIN, serum creatinine increase became apparent in the first 24 hours. Virtually all patients with complicated CIN defined as serious renal impairment requiring either acute dialysis or nephrology consultation had a rise in creatinine within that time frame.[3]

2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury (DO NOT EDIT)

Definition and staging of AKI

Not Graded
"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. (Level of Evidence: Not Graded)"
"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)"

Guideline Resource

KDIGO Clinical Practice Guideline for Acute Kidney Injury[4]

References

  1. 1.0 1.1 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.
  2. 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.
  3. Stevens MA, McCullough PA, Tobin KJ, Speck JP, Westveer DC, Guido-Allen DA; et al. (1999). "A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy: results of the P.R.I.N.C.E. Study. Prevention of Radiocontrast Induced Nephropathy Clinical Evaluation". J Am Coll Cardiol. 33 (2): 403–11. PMID 9973020.
  4. Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID doi:10.1038/kisup.2011.34 Check |pmid= value (help).


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