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Revision as of 02:40, 30 September 2012

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: CIN

Overview

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]

Pathophysiology

Several mechanisims have been put forth to explain the development of nephropathy following contrast administration:

Renal medullary hypoxia secondary to renal vasoconstriction

It has been hypothesized that vasoconstriction occurs due to contrast induced release of adenosine and possibly endothelin as well as the high osmolality of the contrast medium [2] [3] [4]. Volume depletion and heart failure may also be associated with renal vasoconstriction as a result of stimulation of the renin-angiotensin cascade and impaired nitric oxide generation. Taken together, these factors potentiate renal medullary ischemia [5] [6]. Normally the metabolic rate and thereby oxygen consumption in the renal medulla is high as a result of active salt reabsorption by the thick ascending limbs of Henle's loop. Hence renal vasoconstriction, increased blood-contrast viscosity, and a leftward shift of the oxygen-hemoglobin dissociation curve may all contribute to intrarenal hypoxia, with an imbalance between oxygen demand and supply thereby playing a major role in radiocontrast-induced outer medullary hypoxic damage[7]

Cytotoxic effects of contrast

Contrast agents themselves can directly cause renal tubular injury [8]. Contast agents can also cause the generation of free oxygen radicals such as superoxide anions, hydrogen peroxide, hydroxyl radicals and hypochlorous acid. The endothelial dysfunction discussed above is also partly due to oxygen free-radical generation during post ischemic reperfusion as they decrease bioavailibility of nitric oxide leading to vasoconstriction. These reactive species also exerts their oxidative and nitrosative effects on the sulf hydrylic groups and aromatic rings of proteins, cellular membrane lipids and nucleic acids and contribute to vasoconstriction. This occurs through the nitrosation of tyrosine residues of enzymes, such as prostacycline synthase and nitric oxide synthase, which are involved in the synthesis of medulla vasodilators [9]. Mitochondrial injury/cytochrome-c release and plasma membrane damage may be other causes of renal injury as shown in animal experiments [10]. Reduction in creatinine clearence was also seen with increase in adenosine excreation on administration of low osmolality, non-ionic contrast and with use of theophylline the fall in creatinine clearance declined [3].

Predictors of 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)[13]:

Risk Factors:

  • 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%

Choice of contrast agent

The osmolality of the contrast agent has traditionally been believed to be of great importance in contrast-induced nephropathy. Ideally, the contrast agent should be iso-osmolar to blood. Modern iodinated contrast agents are non-ionic.

  • Hypo-osmolar, non-ionic contrast agents are beneficial if iso-osmolar, nonionic contrast media is not available due to costs.[15]

Prevention

Hydration with or without bicarbonate

Administration of sodium bicarbonate 3 mL/kg per hour for 1 hour before , followed by 1 mL/kg per hour for 6 hours after contrast was found superior to plain saline on one randomized controlled trial of patients with a creatinne of at least 1.1 mg/dL (97.2 µmol/L) .[16] To make the solution, the study used 154 mL of 1000 mEq/L sodium bicarbonate to 846 mL of 5% dextrose. This is approximately three 50 ml ampules of bicarbonate in 850 ml of water with 5% dextrose. This was subsequently corroborated by a multi-center randomized controlled trial, which also demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% normal saline[17]. The renoprotective effects of bicarbonate are thought to be due to urinary alkalinization, which creates an environment less amenable to the formation of harmful free radicals.[18].

Alternatively, one randomized controlled trial of patients with a creatinine over 1.6 mg per deciliter (140 µmol per liter) or creatinine clearance below 60 ml per minute used 1 ml/kg of 0.45 percent saline per per hour for 6-12 hours before and after the contrast.[19]

Methylxanthines

Adenosine antagonists such as the methylxanthines theophylline and aminophylline, may help although studies have conflicting results.[20] The best studied dose is 200 mg of theophylline given IV 30 minutes before contrast administration.[21][22]

N-acetylcysteine

N-acetylcysteine (NAC) 600 mg orally 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 nephropathy.[23]. A randomized controlled trial found higher doses of NAC (1200-mg IV bolus and 1200 mg orally twice daily for 2 days) benefited (relative risk reduction of 74%) patients receiving coronary angioplasty with higher volumes of contrast[24].

Since publication of the meta-analyses, two small and underpowered negative studies, one of IV NAC[25] and one of 600 mg give four times around coronary angiography[26], found statistically insignificant trends towards benefit.

Some authors believe the benefit is not overwhelming.[27] The strongest results were from an unblinded randomized controlled trial that used NAC intravenously.[28] A systematic review by Clinical Evidence concluded that NAC is "likely to beneficial" but did not recommend a specific dose.[29] One study found that the apparent benefits of NAC may be due to its interference with the creatinine laboratory test itself.[30] This is supported by a lack of correlation between creatinine levels and cystatin C levels.

ACT Trial which is a randomized, placebo controlled trial randomized 2308 patients undergoing angiography with at least one risk factor for contrast induced nephropathy. Patients were randomized to receive either high dose of NAC or placebo on the day before and after the procedure. No difference was noted in rates of developing nephropathy between the two groups[31]. Therefore short-term use of NAC for the prevention of contrast induced nephropathy should be avoided[32].

In a series, 15% of patients receiving NAC intravenously had allergic reactions[28].

Prophylactic hemodialysis

Patients with chronic renal insufficiency and a creatinine over 309.4 µmol/L (3.5 mg.dl) who have elective coronary catheterization, a randomized controlled trial found benefit from prophylactic hemodialysis[33]

Other interventions

Other pharmacological agents, such as furosemide, mannitol, dopamine, and atrial natriuretic peptide have been tried, but have either not had beneficial effects, or had detrimental effects.[19][34]

REMEDIAL II Trial which is a randomized, multicenter, investigator-driven trial involving patients who are at high risk (GFR ≤30 mL · min−1 · 1.73 m−2 and/or a risk score ≥11) for contrast induced nephropathy tested the strategy of forced diuresis. These patients were randomized to receive either NAC + saline or NAC + saline + furosemide. Rates of developing nephropathy was lower among the group receiving diuretic as furosemide reduces the contrast exposure and renal reuptake while promoting accelerated elimination of contrast[35].

2011 ACCF/AHA/SCAI Guideline Recommendations: Pre-procedural Considerations [2]

Contrast-Induced Acute Kidney Injury

“

Class I

1. 1. Patients should be assessed for risk of contrast-induced acute kidney injury before PCI.[13][36] (Level of Evidence: C)

2. Patients undergoing cardiac catheterization with contrast media should receive adequate preparatory hydration.[37][18][19][38] (Level of Evidence: B)

3. In patients with chronic kidney disease (CKD) (creatinine clearance ≤60 mL/min), the volume of contrast media should be minimized.[39][11][40] (Level of Evidence: B)

Class III

1. Administration of N-acetyl-L-cysteine is not useful for the prevention of contrast-induced acute kidney injury.[41][42][43][44][31] (Level of Evidence: A)

”

Guideline Resource

2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions

References

  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. ↑ Cantley LG, Spokes K, Clark B, McMahon EG, Carter J, Epstein FH (1993). "Role of endothelin and prostaglandins in radiocontrast-induced renal artery constriction". Kidney International. 44 (6): 1217–23. PMID 8301922. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  3. ↑ 3.0 3.1 Katholi RE, Taylor GJ, McCann WP, Woods WT, Womack KA, McCoy CD, Katholi CR, Moses HW, Mishkel GJ, Lucore CL (1995). "Nephrotoxicity from contrast media: attenuation with theophylline". Radiology. 195 (1): 17–22. PMID 7892462. Retrieved 2011-03-06. Unknown parameter |month= ignored (help)
  4. ↑ Pflueger A, Larson TS, Nath KA, King BF, Gross JM, Knox FG (2000). "Role of adenosine in contrast media-induced acute renal failure in diabetes mellitus". Mayo Clinic Proceedings. Mayo Clinic. 75 (12): 1275–83. PMID 11126837. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  5. ↑ Rosenstock JL, Gilles E, Geller AB, Panagopoulos G, Mathew S, Malieckal D, DeVita MV, Michelis MF (2010). "Impact of heart failure on the incidence of contrast-induced nephropathy in patients with chronic kidney disease". International Urology and Nephrology. 42 (4): 1049–54. doi:10.1007/s11255-010-9798-. PMID 20602168. Retrieved 2011-03-06. Unknown parameter |month= ignored (help)
  6. ↑ Agmon Y, Peleg H, Greenfeld Z, Rosen S, Brezis M (1994). "Nitric oxide and prostanoids protect the renal outer medulla from radiocontrast toxicity in the rat". The Journal of Clinical Investigation. 94 (3): 1069–75. doi:10.1172/JCI117421. PMC 295165. PMID 8083347. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  7. ↑ Heyman SN, Reichman J, Brezis M (1999). "Pathophysiology of radiocontrast nephropathy: a role for medullary hypoxia". Investigative Radiology. 34 (11): 685–91. PMID 10548380. Retrieved 2011-03-06. Unknown parameter |month= ignored (help)
  8. ↑ Heinrich MC, Kuhlmann MK, Grgic A, Heckmann M, Kramann B, Uder M (2005). "Cytotoxic effects of ionic high-osmolar, nonionic monomeric, and nonionic iso-osmolar dimeric iodinated contrast media on renal tubular cells in vitro". Radiology. 235 (3): 843–9. doi:10.1148/radiol.2353040726. PMID 15845795. Retrieved 2011-03-08. Unknown parameter |month= ignored (help)
  9. ↑ Detrenis S, Meschi M, Musini S, Savazzi G (2005). "Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art". Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 20 (8): 1542–50. doi:10.1093/ndt/gfh868. PMID 16033768. Retrieved 2011-03-08. Unknown parameter |month= ignored (help)
  10. ↑ Zager RA, Johnson AC, Hanson SY (2003). "Radiographic contrast media-induced tubular injury: evaluation of oxidant stress and plasma membrane integrity". Kidney International. 64 (1): 128–39. doi:10.1046/j.1523-1755.2003.00059.x. PMID 12787403. Retrieved 2011-03-08. Unknown parameter |month= ignored (help)
  11. ↑ 11.0 11.1 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.
  12. ↑ 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.
  13. ↑ 13.0 13.1 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.
  14. ↑ Aspelin P, Aubry P, Fransson S, Strasser R, Willenbrock R, Berg K (2003). "Nephrotoxic effects in high-risk patients undergoing angiography". N Engl J Med. 348 (6): 491–9. PMID 12571256.
  15. ↑ Schwab S, Hlatky M, Pieper K, Davidson C, Morris K, Skelton T, Bashore T (1989). "Contrast nephrotoxicity: a randomized controlled trial of a nonionic and an ionic radiographic contrast agent". N Engl J Med. 320 (3): 149–53. PMID 2643042.
  16. ↑ Merten G, Burgess W, Gray L, Holleman J, Roush T, Kowalchuk G, Bersin R, Van Moore A, Simonton C, Rittase R, Norton H, Kennedy T (2004). "Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial". JAMA. 291 (19): 2328–34. PMID 15150204.
  17. ↑ Briguori C, Airoldi F, D'Andrea D, Bonizzoni E, Morici N, Focaccio A, Michev I, Montorfano M, Carlino M, Cosgrave J, Ricciardelli B, Colombo A (2007). "Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies". Circulation. 115 (10): 1211–7. PMID 17309916.
  18. ↑ 18.0 18.1 Mueller C, Buerkle G, Buettner H, Petersen J, Perruchoud A, Eriksson U, Marsch S, Roskamm H (2002). "Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty". Arch Intern Med. 162 (3): 329–36. PMID 11822926.
  19. ↑ 19.0 19.1 19.2 Solomon R, Werner C, Mann D, D'Elia J, Silva P (1994). "Effects of saline, mannitol, and furosemide to prevent acute decreases in renal function induced by radiocontrast agents". N. Engl. J. Med. 331 (21): 1416–20. PMID 7969280.
  20. ↑ 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.
  21. ↑ Huber W, Schipek C, Ilgmann K; et al. (2003). "Effectiveness of theophylline prophylaxis of renal impairment after coronary angiography in patients with chronic renal insufficiency". Am. J. Cardiol. 91 (10): 1157–62. doi:10.1016/S0002-9149(03)00259-5. PMID 12745095.
  22. ↑ Huber W, Ilgmann K, Page M; et al. (2002). "Effect of theophylline on contrast material-nephropathy in patients with chronic renal insufficiency: controlled, randomized, double-blinded study". Radiology. 223 (3): 772–9. PMID 12034949.
  23. ↑ Kay J, Chow W, Chan T, Lo S, Kwok O, Yip A, Fan K, Lee C, Lam W (2003). "Acetylcysteine for prevention of acute deterioration of renal function following elective coronary angiography and intervention: a randomized controlled trial". JAMA. 289 (5): 553–8. PMID 12578487.
  24. ↑ Marenzi G, Assanelli E, Marana I, Lauri G, Campodonico J, Grazi M, De Metrio M, Galli S, Fabbiocchi F, Montorsi P, Veglia F, Bartorelli A (2006). "N-acetylcysteine and contrast-induced nephropathy in primary angioplasty". N Engl J Med. 354 (26): 2773–82. PMID 16807414.
  25. ↑ Haase M, Haase-Fielitz A, Bagshaw SM; et al. (2007). "Phase II, randomized, controlled trial of high-dose N-acetylcysteine in high-risk cardiac surgery patients". Crit. Care Med. 35 (5): 1324–31. doi:10.1097/01.CCM.0000261887.69976.12. PMID 17414730.
  26. ↑ Seyon RA, Jensen LA, Ferguson IA, Williams RG (2007). "Efficacy of N-acetylcysteine and hydration versus placebo and hydration in decreasing contrast-induced renal dysfunction in patients undergoing coronary angiography with or without concomitant percutaneous coronary intervention". Heart & lung : the journal of critical care. 36 (3): 195–204. doi:10.1016/j.hrtlng.2006.08.004. PMID 17509426.
  27. ↑ Gleeson TG, Bulugahapitiya S (2004). "Contrast-induced nephropathy". AJR Am J Roentgenol. 183 (6): 1673–89. PMID 15547209.
  28. ↑ 28.0 28.1 Baker CS, Wragg A, Kumar S, De Palma R, Baker LR, Knight CJ (2003). "A rapid protocol for the prevention of contrast-induced renal dysfunction: the RAPPID study". J. Am. Coll. Cardiol. 41 (12): 2114–8. PMID 12821233.
  29. ↑ Kellum J, Leblanc M, Venkataraman R (2006). "Renal failure (acute)". Clinical evidence (15): 1191–212. PMID 16973048.
  30. ↑ Hoffmann U, Fischereder M, Kruger B, Drobnik W, Kramer BK (2004). "The value of N-acetylcysteine in the prevention of radiocontrast agent-induced nephropathy seems questionable". J Am Soc Nephrol. 15 (2): 407–10. PMID 14747387.
  31. ↑ 31.0 31.1 ACT Investigators (2011). "Acetylcysteine for Prevention of Renal Outcomes in Patients Undergoing Coronary and Peripheral Vascular Angiography: Main Results From the Randomized Acetylcysteine for Contrast-Induced Nephropathy Trial (ACT)". Circulation. doi:10.1161/CIRCULATIONAHA.111.038943. PMID 21859972.
  32. ↑ http://circ.ahajournals.org/content/124/11/1210.full
  33. ↑ Hart RG, Pearce LA, McBride R, Rothbart RM, Asinger RW (1999). "Factors associated with ischemic stroke during aspirin therapy in atrial fibrillation: analysis of 2012 participants in the SPAF I-III clinical trials. The Stroke Prevention in Atrial Fibrillation (SPAF) Investigators". Stroke. 30 (6): 1223–9. PMID 10356104.
  34. ↑ Abizaid AS, Clark CE, Mintz GS, Dosa S, Popma JJ, Pichard AD, Satler LF, Harvey M, Kent KM, Leon MB (1999). "Effects of dopamine and aminophylline on contrast-induced acute renal failure after coronary angioplasty in patients with preexisting renal insufficiency". Am J Cardiol. 83 (2): 260–3, A5. PMID 10073832.
  35. ↑ Briguori C, Visconti G, Focaccio A, Airoldi F, Valgimigli M, Sangiorgi GM; et al. (2011). "Renal Insufficiency After Contrast Media Administration Trial II (REMEDIAL II): RenalGuard System in High-Risk Patients for Contrast-Induced Acute Kidney Injury". Circulation. doi:10.1161/CIRCULATIONAHA.111.030759. PMID 21844075.
  36. ↑ Moscucci M, Rogers EK, Montoye C, Smith DE, Share D, O'Donnell M, Maxwell-Eward A, Meengs WL, De Franco AC, Patel K, McNamara R, McGinnity JG, Jani SM, Khanal S, Eagle KA (2006). "Association of a continuous quality improvement initiative with practice and outcome variations of contemporary percutaneous coronary interventions". Circulation. 113 (6): 814–22. doi:10.1161/CIRCULATIONAHA.105.541995. PMID 16461821. Retrieved 2011-12-06. Unknown parameter |month= ignored (help)
  37. ↑ Bader BD, Berger ED, Heede MB, Silberbaur I, Duda S, Risler T, Erley CM (2004). "What is the best hydration regimen to prevent contrast media-induced nephrotoxicity?". Clinical Nephrology. 62 (1): 1–7. PMID 15267006. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  38. ↑ Trivedi HS, Moore H, Nasr S, Aggarwal K, Agrawal A, Goel P, Hewett J (2003). "A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity". Nephron. Clinical Practice. 93 (1): C29–34. PMID 12411756. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  39. ↑ Marenzi G, Assanelli E, Campodonico J, Lauri G, Marana I, De Metrio M, Moltrasio M, Grazi M, Rubino M, Veglia F, Fabbiocchi F, Bartorelli AL (2009). "Contrast volume during primary percutaneous coronary intervention and subsequent contrast-induced nephropathy and mortality". Annals of Internal Medicine. 150 (3): 170–7. PMID 19189906. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  40. ↑ Russo D, Minutolo R, Cianciaruso B, Memoli B, Conte G, De Nicola L (1995). "Early effects of contrast media on renal hemodynamics and tubular function in chronic renal failure". Journal of the American Society of Nephrology : JASN. 6 (5): 1451–8. PMID 8589322. Retrieved 2011-12-06. Unknown parameter |month= ignored (help)
  41. ↑ Gonzales DA, Norsworthy KJ, Kern SJ, Banks S, Sieving PC, Star RA, Natanson C, Danner RL (2007). "A meta-analysis of N-acetylcysteine in contrast-induced nephrotoxicity: unsupervised clustering to resolve heterogeneity". BMC Medicine. 5: 32. doi:10.1186/1741-7015-5-32. PMC 2200657. PMID 18001477. Retrieved 2011-12-06.
  42. ↑ Ozcan EE, Guneri S, Akdeniz B, Akyildiz IZ, Senaslan O, Baris N, Aslan O, Badak O (2007). "Sodium bicarbonate, N-acetylcysteine, and saline for prevention of radiocontrast-induced nephropathy. A comparison of 3 regimens for protecting contrast-induced nephropathy in patients undergoing coronary procedures. A single-center prospective controlled trial". American Heart Journal. 154 (3): 539–44. doi:10.1016/j.ahj.2007.05.012. PMID 17719303. Retrieved 2011-12-06. Unknown parameter |month= ignored (help)
  43. ↑ Thiele H, Hildebrand L, Schirdewahn C, Eitel I, Adams V, Fuernau G, Erbs S, Linke A, Diederich KW, Nowak M, Desch S, Gutberlet M, Schuler G (2010). "Impact of high-dose N-acetylcysteine versus placebo on contrast-induced nephropathy and myocardial reperfusion injury in unselected patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. The LIPSIA-N-ACC (Prospective, Single-Blind, Placebo-Controlled, Randomized Leipzig Immediate PercutaneouS Coronary Intervention Acute Myocardial Infarction N-ACC) Trial". Journal of the American College of Cardiology. 55 (20): 2201–9. doi:10.1016/j.jacc.2009.08.091. PMID 20466200. Retrieved 2011-12-06. Unknown parameter |month= ignored (help)
  44. ↑ Webb JG, Pate GE, Humphries KH, Buller CE, Shalansky S, Al Shamari A, Sutander A, Williams T, Fox RS, Levin A (2004). "A randomized controlled trial of intravenous N-acetylcysteine for the prevention of contrast-induced nephropathy after cardiac catheterization: lack of effect". American Heart Journal. 148 (3): 422–9. doi:10.1016/j.ahj.2004.03.041. PMID 15389228. Retrieved 2011-12-06. Unknown parameter |month= ignored (help)

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