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
In 2012, a new definiton for contrast induced nephropathy was put forth by the KDIGO-AKI guidelines. CIN was to be considered a new form of AKI caused by contrast media, and definition criteria for AKI would also apply for CIN now called contrast-induced acute kidney injury (CI-AKI).[1] However, the most commonly used definition in clinical trails is acute renal insufficiency marked by 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.[2][3] The new definition shifted the 0.5 mg/dL cut-off to 0.3 mg/dL and the 25% increase in baseline to 1.5 times the original serum creatinine.
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.[1] A new combined definition was introduced in 2012 to define AKI which included any of the following:
- Increase in serum creatinine by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or
- Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
- Urine volume <0.5 ml/kg/h for 6 hours
However, the above definition and cut-offs used have not been thoroughly studied and associated with clinical outcome in CIN specifically. They have been better substantiated in other forms of AKI. 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 defined 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.[1]
Following the trend of clinical outcomes after contrast exposure, a more common definition for CIN was recognized that combined 3 criteria:[2][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 this 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]
Serum Creatinine Variability
The use of serum creatinine as a marker of glomerular filtration and kidney injury relies on certain convenience assumptions. Those assumptions include that creatinine is only filtered by the kidney, its excretion rate shows little variability among individuals and over time, and measurement is accurate and reproducible. In fact, none of the previous assumptions are true.[10] Creatinine is actually filtered and secreted and has been shown to have significant variability with age, sex, ethnicity, and diet.[11] For that, the trend of following renal function based on previously set reference intervals for the general population has largely been replaced by following changes in serum creatinine or creatinine clearance in an individual compared to their baseline. However, to detect pathological changes in serum creatinine one must first consider the existing variance in measurements related to biological and analytical influences.
Rosano and Brown were among the first to examine intra-individual day-to-day creatinine variability by following two individuals for the period of two months. They showed a combined analytical and biological variability of 0.18 – 0.2 mg/dL with analytical variances accounting for the most significant difference.[12] The intra-individual variance for creatinine has been discussed in many studies with values ranging from 4.7 to 6.1% in healthy individuals.[13][14][15] Reinhard et al showed that in patients with pre-existing renal function the variance in serum creatinine can almost reach 8.9%.[13]
The inter-individual variance in creatinine is not as well established, although Reinhard also showed a variance of 14.4% in healthy individuals.[13] Many laboratory factors can have a noted effect on serum creatinine measurements including calibration which can account for changes of up to 0.23 mg/dL,[16] unexplained variance among labs (0.07 mg/dl) and unexplained variance with time (0.053 mg/dL).[17]
2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury (DO NOT EDIT)
Definition and staging of AKI
| Not Graded |
"1. Two similar definitions based on SCr and urine output (RIFLE and AKIN) have been proposed and validated. A single definition for practice, research, and public health was proposed as 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)" |
Guideline Resource
KDIGO Clinical Practice Guideline for Acute Kidney Injury[18]
References
- ↑ 1.0 1.1 1.2 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.
- ↑ 2.0 2.1 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.
- ↑ 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.
- ↑ National Kidney Foundation (2002). "K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification". Am J Kidney Dis. 39 (2 Suppl 1): S1–266. PMID 11904577.
- ↑ Perrone RD, Madias NE, Levey AS (1992). "Serum creatinine as an index of renal function: new insights into old concepts". Clin Chem. 38 (10): 1933–53. PMID 1394976.
- ↑ Rosano TG, Brown HH (1982). "Analytical and biological variability of serum creatinine and creatinine clearance: implications for clinical interpretation". Clin Chem. 28 (11): 2330–1. PMID 7127791.
- ↑ 13.0 13.1 13.2 Reinhard M, Erlandsen EJ, Randers E (2009). "Biological variation of cystatin C and creatinine". Scand J Clin Lab Invest. 69 (8): 831–6. doi:10.3109/00365510903307947. PMID 19929276.
- ↑ Toffaletti JG, McDonnell EH (2008). "Variation of serum creatinine, cystatin C, and creatinine clearance tests in persons with normal renal function". Clin Chim Acta. 395 (1–2): 115–9. doi:10.1016/j.cca.2008.05.020. PMID 18573244.
- ↑ Bandaranayake N, Ankrah-Tetteh T, Wijeratne S, Swaminathan R (2007). "Intra-individual variation in creatinine and cystatin C." Clin Chem Lab Med. 45 (9): 1237–9. doi:10.1515/CCLM.2007.256. PMID 17848122.
- ↑ Coresh J, Astor BC, McQuillan G, Kusek J, Greene T, Van Lente F; et al. (2002). "Calibration and random variation of the serum creatinine assay as critical elements of using equations to estimate glomerular filtration rate". Am J Kidney Dis. 39 (5): 920–9. doi:10.1053/ajkd.2002.32765. PMID 11979335.
- ↑ Joffe M, Hsu CY, Feldman HI, Weir M, Landis JR, Hamm LL; et al. (2010). "Variability of creatinine measurements in clinical laboratories: results from the CRIC study". Am J Nephrol. 31 (5): 426–34. doi:10.1159/000296250. PMC 2883847. PMID 20389058.
- ↑ 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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