Contrast induced nephropathy definition
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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
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. However, other definitions have been used in clinical trials. The most commonly used definition uses a combination of 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:
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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[4]
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.
- ↑ 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.
- ↑ 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
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