UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate®

Pathogenesis, clinical features, and diagnosis of contrast-induced nephropathy

Author
Michael R Rudnick, MD
Section Editor
Paul M Palevsky, MD
Deputy Editor
Alice M Sheridan, MD

INTRODUCTION

Contrast nephropathy is a generally reversible form of acute kidney injury (AKI) that occurs soon after the administration of radiocontrast media [1-11]. Although AKI is reversible in most cases, its development may be associated with adverse outcomes. (See "Renal and patient outcomes after acute tubular necrosis".)

This topic reviews the pathogenesis, clinical characteristics, and diagnosis of iodinated radiocontrast media-induced nephropathy. The epidemiology of contrast nephropathy, preventive strategies for reducing the risk of contrast nephrotoxicity, and a discussion of acute tubular necrosis (ATN), the most common cause of AKI developing in hospitalized patients, are presented separately. (See "Evaluation of acute kidney injury among hospitalized adult patients" and "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting" and "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults".)

PATHOGENESIS

The best data related to the pathogenesis of contrast nephropathy are from animal models. Studies show evidence of acute tubular necrosis (ATN), but the mechanism by which ATN occurs is not well understood [12-14]. The two major theories are that ATN is caused by renal vasoconstriction resulting in medullary hypoxia, possibly mediated by effects of viscosity and by alterations in nitric oxide, endothelin, and/or adenosine, and that ATN is a direct result of the cytotoxic effects of the contrast agents on tubular cells [12-20]. Tubular cell injury may be exacerbated by renal vasoconstriction [12,13,18].

Compared with other types of ATN (such as ischemic), contrast nephropathy is usually characterized by relatively rapid recovery of renal function (see 'Clinical features' below). If ATN contributes to contrast nephropathy, it is not clear why recovery occurs relatively quickly (ie, within a few days) compared with a longer duration (ie, one to three weeks), as with ATN due to other causes. One possibility is that the degree of tubular necrosis is much less severe than seen in other settings. It is also possible that the decline in glomerular filtration rate (GFR) is due to functional changes in tubule epithelial cells rather than necrosis. This phenomenon may be at least in part due to redistribution of membrane transport proteins from the basolateral to the luminal membrane [21].

In addition, it is possible that prerenal factors or intratubular obstruction contribute to the pathogenesis. This possibility is suggested by the observation that the fractional sodium excretion (FENa) may be <1 percent in patients with contrast nephropathy, which is characteristic of prerenal physiology [22]. (See "Fractional excretion of sodium, urea, and other molecules in acute kidney injury (acute renal failure)", section on 'Fractional excretion of sodium in acute kidney injury' and 'Clinical features' below.)

     

Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: Aug 2017. | This topic last updated: Jun 16, 2017.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
References
Top
  1. Parfrey PS, Griffiths SM, Barrett BJ, et al. Contrast material-induced renal failure in patients with diabetes mellitus, renal insufficiency, or both. A prospective controlled study. N Engl J Med 1989; 320:143.
  2. Rudnick MR, Goldfarb S, Wexler L, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: a randomized trial. The Iohexol Cooperative Study. Kidney Int 1995; 47:254.
  3. Davidson CJ, Hlatky M, Morris KG, et al. Cardiovascular and renal toxicity of a nonionic radiographic contrast agent after cardiac catheterization. A prospective trial. Ann Intern Med 1989; 110:119.
  4. Schwab SJ, Hlatky MA, Pieper KS, et al. Contrast nephrotoxicity: a randomized controlled trial of a nonionic and an ionic radiographic contrast agent. N Engl J Med 1989; 320:149.
  5. Cigarroa RG, Lange RA, Williams RH, Hillis LD. Dosing of contrast material to prevent contrast nephropathy in patients with renal disease. Am J Med 1989; 86:649.
  6. Lautin EM, Freeman NJ, Schoenfeld AH, et al. Radiocontrast-associated renal dysfunction: incidence and risk factors. AJR Am J Roentgenol 1991; 157:49.
  7. Lautin EM, Freeman NJ, Schoenfeld AH, et al. Radiocontrast-associated renal dysfunction: a comparison of lower-osmolality and conventional high-osmolality contrast media. AJR Am J Roentgenol 1991; 157:59.
  8. Rudnick MR, Berns JS, Cohen RM, Goldfarb S. Nephrotoxic risks of renal angiography: contrast media-associated nephrotoxicity and atheroembolism--a critical review. Am J Kidney Dis 1994; 24:713.
  9. Barrett BJ. Contrast nephrotoxicity. J Am Soc Nephrol 1994; 5:125.
  10. Solomon R. Contrast-medium-induced acute renal failure. Kidney Int 1998; 53:230.
  11. Weisbord SD, Palevsky PM. Radiocontrast-induced acute renal failure. J Intensive Care Med 2005; 20:63.
  12. Detrenis S, Meschi M, Musini S, Savazzi G. Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art. Nephrol Dial Transplant 2005; 20:1542.
  13. Persson PB, Hansell P, Liss P. Pathophysiology of contrast medium-induced nephropathy. Kidney Int 2005; 68:14.
  14. Heyman SN, Rosenberger C, Rosen S. Regional alterations in renal haemodynamics and oxygenation: a role in contrast medium-induced nephropathy. Nephrol Dial Transplant 2005; 20 Suppl 1:i6.
  15. Agmon Y, Peleg H, Greenfeld Z, et al. Nitric oxide and prostanoids protect the renal outer medulla from radiocontrast toxicity in the rat. J Clin Invest 1994; 94:1069.
  16. Weisberg LS, Kurnik PB, Kurnik BR. Radiocontrast-induced nephropathy in humans: role of renal vasoconstriction. Kidney Int 1992; 41:1408.
  17. Cantley LG, Spokes K, Clark B, et al. Role of endothelin and prostaglandins in radiocontrast-induced renal artery constriction. Kidney Int 1993; 44:1217.
  18. Katholi RE, Taylor GJ, McCann WP, et al. Nephrotoxicity from contrast media: attenuation with theophylline. Radiology 1995; 195:17.
  19. Russo D, Minutolo R, Cianciaruso B, et al. Early effects of contrast media on renal hemodynamics and tubular function in chronic renal failure. J Am Soc Nephrol 1995; 6:1451.
  20. Pflueger A, Larson TS, Nath KA, et al. Role of adenosine in contrast media-induced acute renal failure in diabetes mellitus. Mayo Clin Proc 2000; 75:1275.
  21. Molitoris BA, Dahl R, Geerdes A. Cytoskeleton disruption and apical redistribution of proximal tubule Na(+)-K(+)-ATPase during ischemia. Am J Physiol 1992; 263:F488.
  22. Fang LS, Sirota RA, Ebert TH, Lichtenstein NS. Low fractional excretion of sodium with contrast media-induced acute renal failure. Arch Intern Med 1980; 140:531.
  23. Rich MW, Crecelius CA. Incidence, risk factors, and clinical course of acute renal insufficiency after cardiac catheterization in patients 70 years of age or older. A prospective study. Arch Intern Med 1990; 150:1237.
  24. Morcos SK, el-Nahas AM, Brown P, Haylor J. Effect of iodinated water soluble contrast media on urinary protein assays. BMJ 1992; 305:29.
  25. Solomon RJ, Mehran R, Natarajan MK, et al. Contrast-induced nephropathy and long-term adverse events: cause and effect? Clin J Am Soc Nephrol 2009; 4:1162.
  26. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 2002; 105:2259.
  27. Giacoppo D, Madhavan MV, Baber U, et al. Impact of Contrast-Induced Acute Kidney Injury After Percutaneous Coronary Intervention on Short- and Long-Term Outcomes: Pooled Analysis From the HORIZONS-AMI and ACUITY Trials. Circ Cardiovasc Interv 2015; 8:e002475.
  28. From AM, Bartholmai BJ, Williams AW, et al. Mortality associated with nephropathy after radiographic contrast exposure. Mayo Clin Proc 2008; 83:1095.
  29. Weisbord SD, Chen H, Stone RA, et al. Associations of increases in serum creatinine with mortality and length of hospital stay after coronary angiography. J Am Soc Nephrol 2006; 17:2871.
  30. Chalikias G, Drosos I, Tziakas DN. Contrast-Induced Acute Kidney Injury: An Update. Cardiovasc Drugs Ther 2016; 30:215.
  31. Sato A, Aonuma K, Watanabe M, et al. Association of contrast-induced nephropathy with risk of adverse clinical outcomes in patients with cardiac catheterization: From the CINC-J study. Int J Cardiol 2017; 227:424.