Role of nephrotoxic drugs in contrast-induced nephropathy
Keywords:Contrast-induced nephropathy, Nephrotoxic drugs, Prevention
Background: Elevation of serum creatinine (SCr) more than 0.5 mg/dl or 25% or more of the baseline value in 3 days after contrast administration is considered as contrast-induced nephropathy (CIN). Contrast material (CM) used in the radiological studies like contrast-enhanced computed tomography (CECT) and intravenous urogram (IVU) are nephrotoxic and their ability to cause renal damage is increased when other potential nephrotoxic drugs are given simultaneously. The present study aimed to demonstrate the effects of CM on patients who are on nephrotoxic drugs by studying the incidence of CIN in patients who are on nephrotoxic drugs and need a CECT or IVU (cases presenting with an emergency). The study compares the incidence of CIN in patients on nephrotoxic drugs with that in those not on nephrotoxic drugs and evaluates the importance of withdrawal of nephrotoxic drugs (3 days) in non-emergency contrast studies.
Methods: The study population is divided into three groups. Group A consists of 40 cases undergoing emergency CECT or IVU, who are on nephrotoxic drugs. 40 cases undergoing CECT or IVU after 3 days of holding of nephrotoxic drugs are included in Group B. Group C consists of 40 cases undergoing CECT or IVU who are not on any nephrotoxic drugs. Patients with parenchymal renal disease, renal injury, and renal mass are excluded from the study. All cases having SCr <1.4 mg/dl are included in the study. SCr investigation is repeated 3 days after the contrast study.
Results: The incidence of CIN is more in the patients who are on nephrotoxic drugs (15%) than in those who are not on nephrotoxic drugs (5%). There is no significant difference in the incidence of CIN between Groups B and C. p=0.045 between Groups A and B was noted showing the significance of waiting period in reducing the incidence of CIN.
Conclusions: The incidence of CIN is more in patients who underwent contrast studies without stopping nephrotoxic drugs and stoppage of nephrotoxic drugs for 3 days prior to the procedure is beneficial by reducing the incidence of CIN among them.
McCullough PA. Contrast induced acute kidney injury. J Am Coll Cardiol. 2008;51(15):1419-28.
Rao QA, Newhouse JH. Risk of nephropathy after intravenous administration of contrast material: A critical literature analysis. Radiology. 2006;239(2):392-7.
Gleeson TG, Bulugahapitiya S. Contrast-induced nephropathy. AJR Am J Roentgenol. 2004;183(6):1673-89.
Stevens MA, McCullough PA, Tobin KJ, Speck JP, Westveer DC, Guido-Allen DA, et al. 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. 1999;33(2):403-11.
Guitterez NV, Diaz A, Timmis GC, O’Neill WW, Stevens MA, Sandberg KR, et al. Determinants of serum creatinine trajectory in acute contrast nephropathy. J Interv Cardiol. 2002;15(5):349-54.
Miller JC. Contrast-media induced nephropathy and diagnostic CT. Radiol Rounds. 2007;5(2):1-4.
Bakris GL, Lass N, Gaber AO, Jones JD, Burnett JC Jr. Radiocontrast medium-induced declines in renal function: A role for oxygen free radicals. Am J Physiol. 1990;258:F115-20.
Brunton LL, Chabner BA, Knollaman BC, editors. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th Edition. New York: McGraw-Hill; 2011: 959-1005.
Katzung BG, Masters SB, Trevor AJ. Basic and Clinical Pharmacology. 12th Edition. New York: The McGraw-Hill; 2012: 809-21.
Nunag M, Brogan M, Garrick R. Mitigating contrast-induced acute kidney injury associated with cardiac catheterization. Cardiol Rev. 2009;17(6):263-9.
Rennke HG, Denker BM. Renal Pathophysiology. Baltimore, MD: Lippincott Williams & Wilkins; 2010.
Dirkes S. Acute kidney injury: not just acute renal failure anymore? Crit Care Nurse. 2011;31(1):37-49.
Choudhury D. Acute kidney injury: current perspectives. Postgrad Med. 2010;122(6):29-40.
Martin RK. Acute kidney injury: Advances in definition, pathophysiology, and diagnosis. AACN Adv Crit Care. 2010;21(4):350-6.
Nikolsky E, Mehran R. Hydration protocols to reduce the incidence of contrast-induced nephropathy. J Invasive Cardiol. 2008;20(10):527-38.
Best PJ, Lennon R, Ting HH, Bell MR, Rihal CS, Holmes DR, et al. The impact of renal insufficiency on clinical outcomes in patients undergoing percutaneous coronary interventions. J Am Coll Cardiol. 2002;39(7):1113-9.
Deray G, Bagnis C, Jacquiaud C, Dubois M, Adabra Y, Jaudon C. Renal effects of low and isoosmolar contrast media on renal hemodynamic in a normal and ischemic dog kidney. Invest Radiol. 1999;34(1):1-4.
Trivedi HS, Moore H, Nasr S, Aggarwal K, Agrawal A, Goel P, et al. A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity. Nephron Clin Pract. 2003;93(1):C29-34.
Mueller C, Buerkle G, Buettner HJ, Petersen J, Perruchoud AP, Eriksson U, et al. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med. 2002;162(3):329-36.