Contrast induced nephropathy risk factors

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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

Many factors have been associated with an increased risk of nephropathy in patients exposed to contrast media. Pre-existing renal insufficiency, pre-existing diabetes, age, volume of CM, and reduced intravascular volume are examples for these risk factor.[1][2] The total risk rises as the number of risk factors increase, it has been recommended that every known risk factor should be analyzed, to properly evaluate a total cumulative risk of developing contrast-induced nephropathy. A clinical prediction rule is available to estimate probability of nephropathy (increase ≥25% and/or ≥0.5 mg/dl in serum creatinine at 48 h)[3]

Risk Factors

Pre-existing Renal Disease

Studies have shown that it ts the most critical risk factor, particularly if associated with elevated level of serum creatinine, with a reported high incidence ranging from 14.8 to 55%[4] [1] [5] Pre-procedure hydration and the use of non-ionic CM could not prevent the occurrence of CIN in one-third of 439 consecutive patients who underwent PCI .[5]

Although baseline creatinine is not reliable enough for identification of patients at risk for CIN, this is because serum creatinine value varies with age, muscle mass, and gender, one of the studies shown that the higher the baseline creatinine value, the greater is the risk of CIN.

Baseline plasma creatinine level is less than or equal to 1.2 mg/dl, the risk of CIN is only 2%
Values of creatinine in the range of 1.4–1.9 mg/dl, the risk of CIN compared with that in the previous group increases fivefold (10.4%)
Patients with baseline creatinine level more than 2.0 mg/dl, more than half of them (62%) subsequently develop CIN.[6]

Diabetes Mellitus

Due to complications caused by diabetes, especially cardiovascular diseases that require radiological procedures and exposure to CM, and the fact that Diabetes mellitus has a wide prevalence in general population, diabetic patients represent a significant proportion of those undergoing contrast exposure with incidence of CIN varies from 5.7 to 29.4%.[7][8]

Diabetes mellitus with associated renal insufficiency has been identified as an independent risk factor for contrast nephropathy, with as many as 56% of those who develop the condition progressing to irreversible renal failure. In addition, diabetic patients who have advanced chronic renal failure (serum creatinine levels > 3.5 mg/dL) due to causes other than diabetic nephropathy are significantly at higher risk of developing CIN.[9]

Age

Elderly have a higher risk to develop CIN compared to other population, the reasons of this elevated risk were not studied specifically, authors suggested that it is probably multifactorial. Theories explain this elevated risk by age-related changes in renal function, diminished glomerular filtration rate, tubular secretion, and concentrating ability. Several studies proved that older age is an independent predictor of CIN.[10] [11]

Volume of Contrast Media

The association between the amount of CM and the risk of CIN is well documented,[1][11][12][13][14][15] The higher volume of CM, the greater the damaging effect in the presence of other risk factors, even a low dose of CM can induce permanent renal failure and the need for dialysis in patients with chronic kidney disease.

Previous Contrast Media Administration

Multiple injections of contrast media within 72 hour increase the risk of the patient's developing contrast-induced nephropathy.[16][17][18]

Osmolarity of the contrast media

Large clinical studies and meta-analyses indicated that the use of an low osmolarity CM reduces the risk of nephropathy in high-risk patients compared with the use of High osmolarity CM.[19] [20]

Anemia and procedure-related blood loss

Anemia might be one of the factors contributing to renal ischemia, in a study based on interventional cardiology database analysis, it showed a steadily increased rates of CIN as pre-procedure hematocrit decreased.[21]

Reduction of Effective Intravascular Volume

Reduction of effective intravascular volume can lead to reduction in renal perfusion, thus enhancing the ischemic insult of contrast media. Congestive heart failure, liver cirrhosis, abnormal fluid losses, dehydration, and prolonged hypotension (especially when induced by intensive antihypertensive treatment combined with angiotensin-converting enzyme inhibitors and diuretics), all of which contribute to reduce the intravascular volume.[22] [23] [24] [17]

Nephrotoxic Drugs

Some drugs have been reported to render the kidney more vulnerable to the nephrotoxic effect of the contrast, directly nephrotoxic drugs (e.g., cyclosporin A, aminoglycosides, amphotericin, and cisplatin) and those that inhibit the local vasodilatory effects of prostaglandins (e.g., nonsteroidal antiinflammatory drugs NSAIDs)[25]

Others

Sepsis has been reported as being a risk factor through direct damage by bacterial toxins to renal tubules. Hypertension, multiple myeloma, peripheral vascular disease, and atopic allergy also have been reported as risk factors.[26] [16]

2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury (DO NOT EDIT)

Assessment of the population at risk for CI-AKI

Not Graded
"1. Assess the risk for CI-AKI and, in particular, screen for pre-existing impairment of kidney function in all patients who are considered for a procedure that requires intravascular (i.v. or i.a.) administration of iodinated contrast medium. (Level of Evidence: Not Graded)"
"2. Consider alternative imaging methods in patients at increased risk for CI-AKI. (Level of Evidence: Not Graded)"

Guideline Resource

KDIGO Clinical Practice Guideline for Acute Kidney Injury[27]

References

  1. ↑ 1.0 1.1 1.2 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.
  2. ↑ Scanlon PJ, Faxon DP, Audet AM, Carabello B, Dehmer GJ, Eagle KA, Legako RD, Leon DF, Murray JA, Nissen SE, Pepine CJ, Watson RM, Ritchie JL, Gibbons RJ, Cheitlin MD, Gardner TJ, Garson A Jr, Russell RO Jr, Ryan TJ, Smith SC Jr (1999). "ACC/AHA guidelines for coronary angiography. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Coronary Angiography). Developed in collaboration with the Society for Cardiac Angiography and Interventions". J Am Coll Cardiol. 33 (6): 1756–824. PMID 10334456.
  3. ↑ Mehran R, Aymong ED, Nikolsky E; et al. (2004). "A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation". J. Am. Coll. Cardiol. 44 (7): 1393–9. doi:10.1016/j.jacc.2004.06.068. PMID 15464318.
  4. ↑ Rihal CS, Textor SC, Grill DE, Berger PB, Ting HH, Best PJ; et al. (2002). "Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention". Circulation. 105 (19): 2259–64. PMID 12010907.
  5. ↑ 5.0 5.1 Gruberg L, Mehran R, Dangas G, Mintz GS, Waksman R, Kent KM; et al. (2001). "Acute renal failure requiring dialysis after percutaneous coronary interventions". Catheter Cardiovasc Interv. 52 (4): 409–16. doi:10.1002/ccd.1093. PMID 11285590.
  6. ↑ Hall KA, Wong RW, Hunter GC, Camazine BM, Rappaport WA, Smyth SH; et al. (1992). "Contrast-induced nephrotoxicity: the effects of vasodilator therapy". J Surg Res. 53 (4): 317–20. PMID 1405611.
  7. ↑ Nikolsky E, Mehran R, Turcot D, Aymong ED, Mintz GS, Lasic Z; et al. (2004). "Impact of chronic kidney disease on prognosis of patients with diabetes mellitus treated with percutaneous coronary intervention". Am J Cardiol. 94 (3): 300–5. doi:10.1016/j.amjcard.2004.04.023. PMID 15276092.
  8. ↑ Lasser EC, Lyon SG, Berry CC (1997). "Reports on contrast media reactions: analysis of data from reports to the U.S. Food and Drug Administration". Radiology. 203 (3): 605–10. PMID 9169676.
  9. ↑ Manske CL, Sprafka JM, Strony JT, Wang Y (1990). "Contrast nephropathy in azotemic diabetic patients undergoing coronary angiography". Am J Med. 89 (5): 615–20. PMID 2239981.
  10. ↑ Gussenhoven MJ, Ravensbergen J, van Bockel JH, Feuth JD, Aarts JC (1991). "Renal dysfunction after angiography; a risk factor analysis in patients with peripheral vascular disease". J Cardiovasc Surg (Torino). 32 (1): 81–6. PMID 2010458.
  11. ↑ 11.0 11.1 Kini AS, Mitre CA, Kim M, Kamran M, Reich D, Sharma SK (2002). "A protocol for prevention of radiographic contrast nephropathy during percutaneous coronary intervention: effect of selective dopamine receptor agonist fenoldopam". Catheter Cardiovasc Interv. 55 (2): 169–73. PMID 11835641.
  12. ↑ Diaz-Sandoval LJ, Kosowsky BD, Losordo DW (2002). "Acetylcysteine to prevent angiography-related renal tissue injury (the APART trial)". Am J Cardiol. 89 (3): 356–8. PMID 11809444.
  13. ↑ Albert SG, Shapiro MJ, Brown WW, Goodgold H, Zuckerman D, Durham R; et al. (1994). "Analysis of radiocontrast-induced nephropathy by dual-labeled radionuclide clearance". Invest Radiol. 29 (6): 618–23. PMID 8088970.
  14. ↑ Rosovsky MA, Rusinek H, Berenstein A, Basak S, Setton A, Nelson PK (1996). "High-dose administration of nonionic contrast media: a retrospective review". Radiology. 200 (1): 119–22. PMID 8657898.
  15. ↑ Kahn JK, Rutherford BD, McConahay DR, Johnson WL, Giorgi LV, Shimshak TM; et al. (1990). "High-dose contrast agent administration during complex coronary angioplasty". Am Heart J. 120 (3): 533–6. PMID 2389689.
  16. ↑ 16.0 16.1 Cochran ST, Wong WS, Roe DJ (1983). "Predicting angiography-induced acute renal function impairment: clinical risk model". AJR Am J Roentgenol. 141 (5): 1027–33. doi:10.2214/ajr.141.5.1027. PMID 6605043.
  17. ↑ 17.0 17.1 Byrd L, Sherman RL (1979). "Radiocontrast-induced acute renal failure: a clinical and pathophysiologic review". Medicine (Baltimore). 58 (3): 270–9. PMID 449662.
  18. ↑ Oliveira DB (1999). "Prophylaxis against contrast-induced nephropathy". Lancet. 353 (9165): 1638–9. doi:10.1016/S0140-6736(98)90076-9. PMID 10335780.
  19. ↑ Taliercio CP, Vlietstra RE, Ilstrup DM, Burnett JC, Menke KK, Stensrud SL; et al. (1991). "A randomized comparison of the nephrotoxicity of iopamidol and diatrizoate in high risk patients undergoing cardiac angiography". J Am Coll Cardiol. 17 (2): 384–90. PMID 1991894.
  20. ↑ Barrett BJ, Carlisle EJ (1993). "Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media". Radiology. 188 (1): 171–8. PMID 8511292.
  21. ↑ Nikolsky E, Mehran R, Lasic Z, Mintz GS, Lansky AJ, Na Y; et al. (2005). "Low hematocrit predicts contrast-induced nephropathy after percutaneous coronary interventions". Kidney Int. 67 (2): 706–13. doi:10.1111/j.1523-1755.2005.67131.x. PMID 15673320.
  22. ↑ Barrett BJ, Parfrey PS (1994). "Prevention of nephrotoxicity induced by radiocontrast agents". N Engl J Med. 331 (21): 1449–50. doi:10.1056/NEJM199411243312111. PMID 7969286.
  23. ↑ Rudnick MR, Berns JS, Cohen RM, Goldfarb S (1994). "Nephrotoxic risks of renal angiography: contrast media-associated nephrotoxicity and atheroembolism--a critical review". Am J Kidney Dis. 24 (4): 713–27. PMID 7942832.
  24. ↑ Lang EK, Foreman J, Schlegel JU, Leslie C, List A, McCormick P (1981). "The incidence of contrast medium induced acute tubular necrosis following arteriography". Radiology. 138 (1): 203–6. PMID 7455084.
  25. ↑ Morcos SK (1998). "Contrast media-induced nephrotoxicity--questions and answers". Br J Radiol. 71 (844): 357–65. PMID 9659127.
  26. ↑ Kolonko A, Kokot F, Wiecek A (1998). "Contrast-associated nephropathy--old clinical problem and new therapeutic perspectives". Nephrol Dial Transplant. 13 (3): 803–6. PMID 9550679.
  27. ↑ 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).

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