Contrast induced nephropathy natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
CIN is often characterized by a transient increase in serum creatinine that peaks at 3 to 6 days after exposure to radiocontrast. Rarely, CIN leads to ESRD in patients with baseline kidney disease. CIN is also associated with increased risk for adverse cardiovascular events and a higher all-cause mortality. Prognosis is especially poor in patients that require hemodialysis after CIN.
Natural history, Complications and Prognosis
Natural History
Usually, CIN causes a form of transient acute kidney injury with bridging hemodialysis only needed in a few cases until renal function returns to normal. Serum creatinine usually peaks between 3 to 6 days following contrast exposure and slowly decreases afterwards.[1] The most important determinant of the peak serum creatinine and the creatinine trajectory is the baseline creatinine clearance. The PRINCE trial (Prevention of Radiocontrast Induced Nephropathy Clinical Evaluation) showed that the first 24 hours after exposure to contrast media 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.[2] However, a minority of patients develop renal impairment after the 24-72 hour time frame taking up to 5 days after exposure.[3]
The association between early creatinine rise following contrast administration and the occurrence of CIN is not very clear, particularly regarding the cut off value of the variation of the serum creatinine from baseline as well as the time frame of the variation. According to a study of 98 patients undergoing cardiac catheterization, an increment in serum creatinine concentration of 0.5 mg/L or less within the first 24 hours following contrast administration is associated with good outcomes. Moreover, it has been demonstrated that the change in serum creatinine between baseline and 12 hours after the administration of the contrast media is the best predictor of CIN. The sensitivity and specificity of the change in serum creatinine for the subsequent occurrence of CIN are 75% and 72% respectively for a creatinine change of > 5%, and 43% and 93% for a creatinine change of > 15%.
Complications and Prognosis
Studies have substantiated greater all-cause and cardiovascular mortality,[4] prolonged duration of hospitalization,[5] and late cardiovascular events[6] associated with CIN. The evidence is seen mostly in patients undergoing PCI.[7][8] Weisbord et al showed that an absolute increase in serum creatinine of 0.25 to 0.5 mg/dL within 72 hours after coronary angiography was associated with significantly greater odds for in-hospital mortality in the 30 day period following the procedure.[8] The need for dialysis following CIN is also a separate prognostic indicator. Dialysis requirement has been associated with a fivefold increase in all-cause mortality when compared to patients with CIN not requiring renal replacement. Furthermore, mortality in the former group was as high as 81% at 2 years.[9] Several of the studies targeting prognosis following CIN have been limited by the confounding factors mostly because high risk patients for CIN are naturally at higher risk for cardiovascular complications.
Harjai et al proposed a nephropathy grading system in 2008 to predict prognosis in patients with CIN after PCI. The classification system included 3 separate nephropathy grades:
- Grade 0 = no nephropathy (increase in Cr<25% and <0.5mg/dl)
- Grade 1 = mild nephropathy (increase in Cr>25% but <0.5mg/dl)
- Grade 2 = significant nephropathy (increase in Cr>25% and >0.5mg/dl)
They compared the classification system to the incidence of major adverse cardiovascular events (MACE) after 6 months. The grading system showed significant correlation with adverse outcomes (G0=12.4% / G1=19.4% / G2=28.6% [P= 0.003]) and all-cause mortality (G0=10.2% / G1=10.45% / G2=40.9%, [P<0.0001]).[10]
Shown below is a table summarizing the suggested classification system, incidence of MACE after 6 months and all-cause mortality.
| Grade | Description | Creatinine Change | MACE | All-Cause Mortality |
| Grade 0 | No nephropathy | Increase in Cr<25% and <0.5mg/dl | 12.4% (P= 0.003) | 10.2% (P<0.0001) |
| Grade 1 | Mild nephropathy | Increase in Cr>25% but <0.5mg/dl | 19.4% (P= 0.003) | 10.45% (P<0.0001) |
| Grade 2 | Significant nephropathy | Increase in Cr>25% and >0.5mg/dl | 28.6% (P= 0.003) | 40.9% (P<0.0001) |
End stage renal disease requiring chronic dialysis following CIN occurs in a small proportion of patients[11], although data is still scarce. Usually patients that require chronic dialysis have some form of advanced kidney disease prior to exposure to contrast media.
References
- ↑ Rudnick MR, Goldfarb S, Wexler L, Ludbrook PA, Murphy MJ, Halpern EF; et al. (1995). "Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: a randomized trial. The Iohexol Cooperative Study". Kidney Int. 47 (1): 254–61. PMID 7731155.
- ↑ 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.
- ↑ 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.
- ↑ Marenzi G, Lauri G, Assanelli E, Campodonico J, De Metrio M, Marana I; et al. (2004). "Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction". J Am Coll Cardiol. 44 (9): 1780–5. doi:10.1016/j.jacc.2004.07.043. PMID 15519007.
- ↑ McCullough PA, Sandberg KR (2003). "Epidemiology of contrast-induced nephropathy". Rev Cardiovasc Med. 4 Suppl 5: S3–9. PMID 14668704.
- ↑ McCullough PA, Adam A, Becker CR, Davidson C, Lameire N, Stacul F; et al. (2006). "Epidemiology and prognostic implications of contrast-induced nephropathy". Am J Cardiol. 98 (6A): 5K–13K. doi:10.1016/j.amjcard.2006.01.019. PMID 16949375.
- ↑ McCullough PA (2008). "Radiocontrast-induced acute kidney injury". Nephron Physiol. 109 (4): p61–72. doi:10.1159/000142938. PMID 18802377.
- ↑ 8.0 8.1 Weisbord SD, Chen H, Stone RA, Kip KE, Fine MJ, Saul MI; et al. (2006). "Associations of increases in serum creatinine with mortality and length of hospital stay after coronary angiography". J Am Soc Nephrol. 17 (10): 2871–7. doi:10.1681/ASN.2006030301. PMID 16928802.
- ↑ McCullough PA, Wolyn R, Rocher LL, Levin RN, O'Neill WW (1997). "Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality". Am J Med. 103 (5): 368–75. PMID 9375704.
- ↑ 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.
- ↑ Freeman RV, O'Donnell M, Share D, Meengs WL, Kline-Rogers E, Clark VL; et al. (2002). "Nephropathy requiring dialysis after percutaneous coronary intervention and the critical role of an adjusted contrast dose". Am J Cardiol. 90 (10): 1068–73. PMID 12423705.