Contrast induced nephropathy definition: Difference between revisions
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#'''Exclusion of other diagnoses to explain the renal impairment''' | #'''Exclusion of other diagnoses to explain the renal impairment''' | ||
To note, Recent data have challenged the new definition, showing that the traditional rationale requiring >0.5 mg/dL increase in serum creatinine is better predictive of serious adverse events (dialysis and all-cause mortality) when compared to the >25% increase in serum creatinine baseline.<ref name="pmid22607861">{{cite journal| author=Slocum NK, Grossman PM, Moscucci M, Smith DE, Aronow HD, Dixon SR et al.| title=The changing definition of contrast-induced nephropathy and its clinical implications: insights from the Blue Cross Blue Shield of Michigan Cardiovascular Consortium (BMC2). | journal=Am Heart J | year= 2012 | volume= 163 |issue= 5 | pages= 829-34 | pmid=22607861 | doi=10.1016/j.ahj.2012.02.011 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22607861 }} </ref> | |||
Recent data have challenged the new definition, showing that the traditional rationale requiring >0.5 mg/dL increase in serum creatinine is better predictive of serious adverse events (dialysis and all-cause mortality) when compared to the >25% increase in serum creatinine baseline.<ref name="pmid22607861">{{cite journal| author=Slocum NK, Grossman PM, Moscucci M, Smith DE, Aronow HD, Dixon SR et al.| title=The changing definition of contrast-induced nephropathy and its clinical implications: insights from the Blue Cross Blue Shield of Michigan Cardiovascular Consortium (BMC2). | journal=Am Heart J | year= 2012 | volume= 163 |issue= 5 | pages= 829-34 | pmid=22607861 | doi=10.1016/j.ahj.2012.02.011 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22607861 }} </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 20:30, 1 October 2013
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Contrast Induced Nephropathy Microchapters |
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Differentiating Contrast induced nephropathy from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Contrast induced nephropathy definition On the Web |
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American Roentgen Ray Society Images of Contrast induced nephropathy definition |
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Directions to Hospitals Treating Contrast induced nephropathy |
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Risk calculators and risk factors for Contrast induced nephropathy definition |
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
CIN, defined simply, is acute kidney injury (AKI) that occurs within a time frame after the administration of intravenous contrast agents. According to the 2012 KDIGO AKI guidelines, CIN can be considered as a subtype of AKI related to contrast media, and the term contrast-induced acute kidney injury (CI-AKI) was proposed instead of CIN. The Work Group even advocated the use of the RIFLE/AKIN criteria to define CI-AKI.[3] However, several other definitions have been used in clinical trials. Before 2007, four different definitons were used to define CIN especially post-PCI. Increases in serum creatinine of >0.5 mg/dL, >1.0 mg/dL, and >25% of baseline were used.[4] The American College of Cardiology National Cardiovascular Data Registry proposed a fourth definition that required a doubling in serum creatinine to a value >2.0mg/dL or the need for dialysis following PCI.[5] In 2007, Harjai et al showed that only 2 of the four definitions proposed (>0.5 mg/dL increase [P<0.0018] or >25% increase in baseline [P<0.002]) predicted adverse events within the first 6 months following PCI. The authors also proposed a prognostic nephropathy grading system to predict 6 months major adverse cardiovascular events and all-cause mortality. The timing of serum creatinine measurement was 24-48 hours (mean=1.6 days) after the PCI procedure.[6]
The time frame for serum creatinine rise after PCI has also been debated. 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.[7] However, some patients develop renal impairment after the 24-48 hour time frame. The European Society of Urogenital Radiology guidelines used a cut-off of 72 hours after exposure for the rise in serum creatinine.[8] It is also important to mention that the peak in serum creatinine can occur up to 5 days after exposure in a minority of patients.[3]
Following the trend of clinical outcomes after contrast exposure, a more common definition for CIN was recognized that combined 3 criteria:[1][6]
- 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
To note, Recent data have challenged the new definition, showing that the traditional rationale requiring >0.5 mg/dL increase in serum creatinine is better predictive of serious adverse events (dialysis and all-cause mortality) when compared to the >25% increase in serum creatinine baseline.[9]
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:
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| "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[10]
References
- ↑ 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.
- ↑ 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.
- ↑ 3.0 3.1 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.
- ↑ Shoukat S, Gowani SA, Jafferani A, Dhakam SH (2010). "Contrast-induced nephropathy in patients undergoing percutaneous coronary intervention". Cardiol Res Pract. 2010. doi:10.4061/2010/649164. PMC 2945641. PMID 20886058.
- ↑ Brindis RG, Fitzgerald S, Anderson HV, Shaw RE, Weintraub WS, Williams JF (2001). "The American College of Cardiology-National Cardiovascular Data Registry (ACC-NCDR): building a national clinical data repository". J Am Coll Cardiol. 37 (8): 2240–5. PMID 11419906.
- ↑ 6.0 6.1 Harjai KJ, Raizada A, Shenoy C, Sattur S, Orshaw P, Yaeger K; et al. (2008). "A comparison of contemporary definitions of contrast nephropathy in patients undergoing percutaneous coronary intervention and a proposal for a novel nephropathy grading system". Am J Cardiol. 101 (6): 812–9. doi:10.1016/j.amjcard.2007.10.051. PMID 18328846.
- ↑ 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.
- ↑ Thomsen HS, Morcos SK (2003). "Contrast media and the kidney: European Society of Urogenital Radiology (ESUR) guidelines". Br J Radiol. 76 (908): 513–8. PMID 12893691.
- ↑ Slocum NK, Grossman PM, Moscucci M, Smith DE, Aronow HD, Dixon SR; et al. (2012). "The changing definition of contrast-induced nephropathy and its clinical implications: insights from the Blue Cross Blue Shield of Michigan Cardiovascular Consortium (BMC2)". Am Heart J. 163 (5): 829–34. doi:10.1016/j.ahj.2012.02.011. PMID 22607861.
- ↑ 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).