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
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 after exposure to contrast media, the first 24 hours post-exposure are very critical 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 (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 1.2 1.3 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.
- ↑ 2.0 2.1 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.
- ↑ 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).