Contrast-induced nephropathy

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Contrast-induced nephropathy
Classification and external resources
ICD-10 N99.0
ICD-9-CM 586

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[1] after using iodine contrast agent without another clear cause for kidney injury.[2] Despite extensive speculation, the actual occurrence of contrast-induced nephropathy in other patient populations has not been demonstrated in the literature.[3]

Risk factors[edit]

To minimize the risk for contrast-induced nephropathy, various actions can be taken if the patient has predisposing conditions. These have been reviewed in a meta-analysis.[4] A separate meta-analysis addresses interventions for emergency patients with baseline insufficient kidney function.[5]

Individuals with chronic kidney disease, diabetes mellitus, high blood pressure, reduced intravascular volume, or who are elderly are at increased risk of developing CIN after exposure to iodinated contrast.[2]

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):[6]

Risk Factors:

  • Systolic blood pressure <80 mm Hg - 5 points
  • Intraarterial balloon pump - 5 points
  • Congestive heart failure (Class III-IV or history of pulmonary edema) - 5 points
  • Age >75 y - 4 points
  • Hematocrit level <39% for men and <35% for women - 3 points
  • Diabetes mellitus- 3 points
  • Contrast media volume - 1 point for each 100 mL
  • Decreased kidney function:
    • Serum creatinine level >1.5 g/dL - 4 points
or
    • 2 for 40–60 mL/min/1.73 m2
    • 4 for 20–40 mL/min/1.73 m2
    • 6 for < 20 mL/min/1.73 m2

Scoring:
5 or less points

  • Risk of CIN - 7.5
  • Risk of Dialysis - 0.04%

6–10 points

  • Risk of CIN - 14.0
  • Risk of Dialysis - 0.12%

11–16 points

  • Risk of CIN - 26.1*
  • Risk of Dialysis - 1.09%

>16 points

  • Risk of CIN - 57.3
  • Risk of Dialysis - 12.8%

Contrast agent[edit]

The osmolality of the contrast agent was previously believed to be an important factor in contrast-induced nephropathy. Today it has become increasingly clear that other physicochemical properties play a greater role, such as viscosity. Attention should be paid to use contrast agents of low viscosity. Moreover, sufficient fluids should be supplied to limit fluid viscosity of urine. Modern iodinated contrast agents are non-ionic, the older ionic types caused more adverse effects and are not used much anymore.

Prevention[edit]

Evidence supports the use of N-acetylcysteine with intravenous saline among those getting low molecular weight contrast. The use of statins with N-acetylcysteine and intravenous saline is also supported.[7]

Methylxanthines[edit]

Adenosine antagonists such as the methylxanthines theophylline and aminophylline, may help[5] although studies have conflicting results.[8]

N-acetylcysteine[edit]

N-acetylcysteine (NAC) by mouth twice a day, on the day before and of the procedure if creatinine clearance is estimated to be less than 60 mL/min [1.00 mL/s]) may reduce risk.[medical citation needed] Some authors believe the benefit is not overwhelming.[9] A systematic review concluded that NAC is "likely to be beneficial" but did not recommend a specific dose.[10]

Ascorbic acid[edit]

Ascorbic acid may help according to a systematic review of randomized controlled trials.[11]

Research[edit]

While there are currently no FDA-approved therapies for contrast-induced nephropathy, two therapies are currently being investigated. CorMedix is currently in the latter part of phase II clinical trials with approved phase III Special Protocol Assessment for CRMD001 (unique formulation Deferiprone) to prevent contrast-induced acute kidney injury and to slow progression of chronic kidney disease. Dosing trials began in June 2010 in the sixty patient trial.[12][13]

There is also a phase III clinical trial of RenalGuard Therapy to prevent contrast-induced nephropathy.[14] The therapy utilizes the RenalGuard System, which measures the patient's urine output and infuses an equal volume of normal saline in real-time. The therapy involves connecting the patient to the RenalGuard System, then injecting a small dosage of furosemide to induce high urine rates.[15]

References[edit]

  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. 
  2. ^ a b Subramaniam, RM; Suarez-Cuervo, C; Wilson, RF; Turban, S; Zhang, A; Sherrod, C; Aboagye, J; Eng, J; Choi, MJ; Hutfless, S; Bass, EB (February 2016). "Effectiveness of Prevention Strategies for Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis". Annals of Internal Medicine. doi:10.7326/M15-1456. PMID 26830221. 
  3. ^ McDonald, Robert; McDonald, Jennifer S.; Carter, Rickey E.; Hartman, Robert P.; Katzberg, Richard W.; Kallmes, David F.; Williamson, Eric E. (December 2014). "Intravenous Contrast Material Exposure Is Not an Independent Risk Factor for Dialysis or Mortality". Radiology 273 (3): 714–725. doi:10.1148/radiol.14132418. PMID 25203000. 
  4. ^ Pannu N, Wiebe N, Tonelli M (2006). "Prophylaxis strategies for contrast-induced nephropathy". JAMA 295 (23): 2765–79. doi:10.1001/jama.295.23.2765. PMID 16788132. 
  5. ^ a b Sinert R, Doty CI (2007). "Evidence-based emergency medicine review. Prevention of contrast-induced nephropathy in the emergency department". Annals of Emergency Medicine 50 (3): 335–45, 345.e1–2. doi:10.1016/j.annemergmed.2007.01.023. PMID 17512638. 
  6. ^ 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. 
  7. ^ Subramaniam, RM; Suarez-Cuervo, C; Wilson, RF; Turban, S; Zhang, A; Sherrod, C; Aboagye, J; Eng, J; Choi, MJ; Hutfless, S; Bass, EB (15 March 2016). "Effectiveness of Prevention Strategies for Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis.". Annals of internal medicine 164 (6): 406–16. PMID 26830221. 
  8. ^ Bagshaw SM, Ghali WA (2005). "Theophylline for prevention of contrast-induced nephropathy: a systematic review and meta-analysis". Arch. Intern. Med. 165 (10): 1087–93. doi:10.1001/archinte.165.10.1087. PMID 15911721. 
  9. ^ Gleeson TG, Bulugahapitiya S (2004). "Contrast-induced nephropathy". AJR Am J Roentgenol 183 (6): 1673–89. doi:10.2214/ajr.183.6.01831673. PMID 15547209. 
  10. ^ Kellum J, Leblanc M, Venkataraman R (2006). "Renal failure (acute)". Clinical evidence (15): 1191–212. PMID 16973048. 
  11. ^ Sadat U, Usman A, Gillard JH, Boyle JR (2013). "Does ascorbic acid protect against contrast-induced acute kidney injury in patients undergoing coronary angiography: a systematic review with meta-analysis of randomized, controlled trials.". J Am Coll Cardiol 62 (23): 2167–75. doi:10.1016/j.jacc.2013.07.065. PMID 23994417. 
  12. ^ [1], CorMedix June 25, 2010 Press Release, "CorMedix Doses First Patient in Phase II Clinical Trial of CRMD-001"
  13. ^ [2], ClinicalTrials.gov, "Deferiprone for the Prevention of Contrast-Induced Acute Kidney Injury"
  14. ^ [3], ClinicalTrials.gov,"Evaluation of RenalGuard® System to Reduce the Incidence of Contrast Induced Nephropathy in At-Risk Patients (CIN-RG)"
  15. ^ Marenzi, Giancarlo; Bartorelli,A (2012). "Prevention of Contrast Nephropathy by Furosemide With Matched Hydration". J Am Coll Cardiol Intv 5 (1): 90–97. doi:10.1016/j.jcin.2011.08.017. PMID 22230154.