In patients with preexisting renal impairment, particularly those who are diabetic, the iodinated radiographic contrast media may cause contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI), that is, an acute renal failure (ARF), usually nonoliguric and asymptomatic, occurring 24 to 72 hours after their intravascular injection in the absence of an alternative aetiology. Radiographic contrast media have different osmolalities and viscosities. They have also a different nephrotoxicity. In order to prevent CIN, the least nephrotoxic contrast media should be chosen, at the lowest dosage possible. Other prevention measures should include discontinuation of potentially nephrotoxic drugs, adequate hydration with i.v. infusion of either normal saline or bicarbonate solution, and eventually use of antioxidants, such as N-acetylcysteine, and statins. 1. Introduction Iodinated radiographic contrast media [1] are widely used in clinical practice, for both diagnostic and therapeutic procedures such as radiography, percutaneous cardiac and arterial interventions, and contrast-enhanced computed tomography (CT). The intravascular injection of CM is usually safe in healthy subjects with normal renal function. But in patients with preexisting renal impairment the CM may express their nephrotoxicity. Since the clinical need for diagnostic and therapeutic procedures using CM is increased in particular in patients with cardiovascular diseases whose renal function is frequently impaired [2], the occurrence of renal damage by CM is quite frequent. Contrast-induced nephropathy (CIN) is defined as an acute renal failure (ARF) occurring 24 to 72 hours after the intravascular injection of radiographic contrast media in the absence of an alternative aetiology [3]. The KDIGO Group [4] “proposes that the term contrast-induced acute kidney injury (CI-AKI) be used for patients developing AKI secondary to intravascular radiocontrast media exposure” rather than CIN. But CIN is still widely used in the literature. It is also questioned whether to use the term ARF to indicate renal impairment by CM. The KDIGO Group also underlines that “the term “acute kidney injury/impairment” has been proposed to encompass the entire spectrum of the syndrome from minor changes in markers of renal function to requirement for renal replacement therapy (RRT)” [4]. However, most authors keep defining AKI as an “ARF,” sometimes “renal insufficiency,” even without the need for dialysis. It is usually a nonoliguric, asymptomatic, and transient decline in renal function. The renal
References
[1]
B. J. Barrett, P. S. Parfrey, H. M. Vavasour et al., “Contrast nephropathy in patients with impaired renal function: high versus low osmolar media,” Kidney International, vol. 41, no. 5, pp. 1274–1279, 1992.
[2]
G. Fuiano, D. Mancuso, C. Indolfi et al., “Early detection of progressive renal dysfunction in patients with coronary artery disease,” Kidney International, vol. 68, no. 6, pp. 2773–2780, 2005.
[3]
M. Andreucci, R. Solomon, and A. Tasanarong, “Side effects of radiographic contrast media: pathogenesis, risk factors, and prevention,” BioMed Research International, vol. 2014, Article ID 741018, 20 pages, 2014.
[4]
Group KDIGOKAKIW, “KDIGO clinical practice guideline for acute kidney injury,” Kidney International, vol. 2, supplement, pp. 1–138, 2012.
[5]
A. S. Levey, J. P. Bosch, J. B. Lewis, T. Greene, N. Rogers, and D. Roth, “A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation,” Annals of Internal Medicine, vol. 130, no. 6, pp. 461–470, 1999.
[6]
D. W. Cockcroft and M. H. Gault, “Prediction of creatinine clearance from serum creatinine,” Nephron, vol. 16, no. 1, pp. 31–41, 1976.
[7]
M. Andreucci, T. Faga, M. Sabbatini, A. Pisani, D. Russo, and A. Michael, “How to prevent contrast-induced nephropathy in clinical practice,” Journal of Clinical Nephrology and Research, vol. 1, no. 1, p. 1002, 2014.
[8]
M. Andreucci, R. Solomon, and A. Tasanarong, “Side effects of radiographic contrast media: pathogenesis, risk factors, and prevention,” BioMed Research International, vol. 2014, Article ID 741018, 20 pages, 2014.
[9]
V. E. Andreucci, G. Fuiano, D. Russo, and M. Andreucci, “Vasomotor nephropathy in the elderly,” Nephrology Dialysis Transplantation, vol. 13, supplement 7, pp. 17–24, 1998.
[10]
V. E. Andreucci, G. Fuiano, P. Stanziale, and M. Andreucci, “Role of renal biopsy in the diagnosis and prognosis of acute renal failure,” Kidney International, Supplement, vol. 53, no. 66, pp. S91–S95, 1998.
[11]
M. Andreucci, T. Faga, A. Pisani, M. Sabbatini, and A. Michael, “Pathogenesis of acute renal failure induced by iodinated radiographic contrast media,” Austin Journal of Nephrology and Hypertension, vol. 1, no. 1, pp. 1–6, 2014.
[12]
A. Caiazza, L. Russo, M. Sabbatini, and D. Russo, “Hemodynamic and tubular changes induced by contrast media,” BioMed Research International, vol. 2014, Article ID 578974, 7 pages, 2014.
[13]
S. W. Murphy, B. J. Barrett, and P. S. Parfrey, “Contrast nephropathy,” Journal of the American Society of Nephrology, vol. 11, no. 1, pp. 177–182, 2000.
[14]
S. Detrenis, M. Meschi, S. Musini, and G. Savazzi, “Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art,” Nephrology Dialysis Transplantation, vol. 20, no. 8, pp. 1542–1550, 2005.
[15]
D. Russo, R. Minutolo, B. Cianciaruso, B. Memoli, G. Conte, and L. de Nicola, “Early effects of contrast media on renal hemodynamics and tubular function in chronic renal failure,” Journal of the American Society of Nephrology, vol. 6, no. 5, pp. 1451–1458, 1995.
[16]
M. Andreucci, T. Faga, A. Pisani, M. Sabbatini, and A. Michael, “Acute kidney injury by radiographic contrast media: pathogenesis and prevention,” BioMed Research International, vol. 2014, Article ID 362725, 21 pages, 2014.
[17]
A. J. Giaccia, M. C. Simon, and R. Johnson, “The biology of hypoxia: the role of oxygen sensing in development, normal function, and disease,” Genes and Development, vol. 18, no. 18, pp. 2183–2194, 2004.
[18]
M. Sabbatini, M. Santillo, A. Pisani et al., “Inhibition of Ras/ERK1/2 signaling protects against postischemic renal injury,” American Journal of Physiology—Renal Physiology, vol. 290, no. 6, pp. F1408–F1415, 2006.
[19]
S. N. Heyman, S. Rosen, M. Khamaisi, J.-M. Idée, and C. Rosenberger, “Reactive oxygen species and the pathogenesis of radiocontrast-induced nephropathy,” Investigative Radiology, vol. 45, no. 4, pp. 188–195, 2010.
[20]
P. Dawson, A. Becker, and J. M. Holton, “The effect of contrast media on the growth of bacteria,” The British Journal of Radiology, vol. 56, no. 671, pp. 809–815, 1983.
[21]
M. M. Sendeski, “Pathophysiology of renal tissue damage by iodinated contrast media,” Clinical and Experimental Pharmacology and Physiology, vol. 38, no. 5, pp. 292–299, 2011.
[22]
A. Pisani, E. Riccio, M. Andreucci et al., “Role of reactive oxygen species in pathogenesis of radiocontrast-induced nephropathy,” BioMed Research International, vol. 2013, Article ID 868321, 6 pages, 2013.
[23]
P. Pacher, J. S. Beckman, and L. Liaudet, “Nitric oxide and peroxynitrite in health and disease,” Physiological Reviews, vol. 87, no. 1, pp. 315–424, 2007.
[24]
A. Pisani, M. Sabbatini, E. Riccio et al., “Effect of a recombinant manganese superoxide dismutase on prevention of contrast-induced acute kidney injury,” Clinical and Experimental Nephrology, vol. 18, pp. 424431–8, 2014.
[25]
C. Quintavalle, M. Brenca, F. de Micco, et al., “In vivo and in vitro assessment of pathways involved in contrast media-induced renal cells apoptosis,” Cell Death & Disease, vol. 2, no. 5, article e155, 2011.
[26]
H.-C. Lee, J.-G. Chang, H.-W. Yen, I.-H. Liu, W.-T. Lai, and S.-H. Sheu, “Ionic contrast media induced more apoptosis in diabetic kidney than nonionic contrast media,” Journal of Nephrology, vol. 24, no. 3, pp. 376–380, 2011.
[27]
R. W. Katzberg, “Urography into the 21st century: new contrast media, renal handling, imaging characteristics, and nephrotoxicity,” Radiology, vol. 204, no. 2, pp. 297–312, 1997.
[28]
P. Aspelin, P. Aubry, S.-G. Fransson, R. Strasser, R. Willenbrock, and K. J. Berg, “Nephrotoxic effects in high-risk patients undergoing angiography,” The New England Journal of Medicine, vol. 348, no. 6, pp. 491–499, 2003.
[29]
C. P. Taliercio, R. E. Vlietstra, D. M. Ilstrup et al., “A randomized comparison of the nephrotoxicity of iopamidol and diatrizoate in high risk patients undergoing cardiac angiography,” Journal of the American College of Cardiology, vol. 17, no. 2, pp. 384–390, 1991.
[30]
B. J. Barrett and E. J. Carlisle, “Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media,” Radiology, vol. 188, no. 1, pp. 171–178, 1993.
[31]
B. J. Barrett, “Contrast nephrotoxicity,” Journal of the American Society of Nephrology, vol. 5, no. 2, pp. 125–137, 1994.
[32]
M. Dong, Z. Jiao, T. Liu, F. Guo, and G. Li, “Effect of administration route on the renal safety of contrast agents: a meta-analysis of randomized controlled trials,” Journal of Nephrology, vol. 25, no. 3, pp. 290–301, 2012.
[33]
M. C. Heinrich, L. H?berle, V. Müller, W. Bautz, and M. Uder, “Nephrotoxicity of iso-osmolar iodixanol compared with nonionic low-osmolar contrast media: meta-analysis of randomized controlled trials,” Radiology, vol. 250, no. 1, pp. 68–86, 2009.
[34]
K. J. Hardiek, R. E. Katholi, R. S. Robbs, and C. E. Katholi, “Renal effects of contrast media in diabetic patients undergoing diagnostic or interventional coronary angiography,” Journal of Diabetes and Its Complications, vol. 22, no. 3, pp. 171–177, 2008.
[35]
R. Mehran and E. Nikolsky, “Contrast-induced nephropathy: definition, epidemiology, and patients at risk,” Kidney International. Supplement, no. 100, pp. S11–S15, 2006.
[36]
M. R. Rudnick, S. Goldfarb, and J. Tumlin, “Contrast-induced nephropathy: is the picture any clearer?” Clinical Journal of the American Society of Nephrology, vol. 3, no. 1, pp. 261–262, 2008.
[37]
J. A. Neyra, S. Shah, R. Mooney, G. Jacobsen, J. Yee, and J. E. Novak, “Contrast-induced acute kidney injury following coronary angiography: a cohort study of hospitalized patients with or without chronic kidney disease,” Nephrology Dialysis Transplantation, vol. 28, no. 6, pp. 1463–1471, 2013.
[38]
A. C. Schoolwerth, D. A. Sica, B. J. Ballermann, and C. S. Wilcox, “Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the council on the kidney in cardiovascular disease and the council for high blood pressure research of the american heart association,” Circulation, vol. 104, no. 16, pp. 1985–1991, 2001.
[39]
M. Cirit, O. Toprak, M. Yesil et al., “Angiotensin-converting enzyme inhibitors as a risk factor for contrast-induced nephropathy,” Nephron Clinical Practice, vol. 104, no. 1, pp. c20–c27, 2006.
[40]
D. Kiski, W. Stepper, E. Brand, G. Breithardt, and H. Reinecke, “Impact of renin-angiotensin-aldosterone blockade by angiotensin-converting enzyme inhibitors or AT-1 blockers on frequency of contrast medium-induced nephropathy: a post-hoc analysis from the Dialysis-versus-Diuresis (DVD) trial,” Nephrology Dialysis Transplantation, vol. 25, no. 3, pp. 759–764, 2010.
[41]
M. Y. Rim, H. Ro, W. C. Kang, et al., “The effect of renin-angiotensin-aldosterone system blockade on contrast-induced acute kidney injury: a propensity-matched study,” American Journal of Kidney Diseases, vol. 60, no. 4, pp. 576–582, 2012.
[42]
Z. Umruddin, K. Moe, and K. Superdock, “ACE inhibitor or angiotensin II receptor blocker use is a risk factor for contrast-induced nephropathy,” Journal of Nephrology, vol. 25, no. 5, pp. 776–781, 2012.
[43]
M. A. C. Onuigbo and N. T. C. Onuigbo, “Does renin-angiotensin aldosterone system blockade exacerbate contrast-induced nephropathy in patients with chronic kidney disease? A prospective 50-month mayo clinic study,” Renal Failure, vol. 30, no. 1, pp. 67–72, 2008.
[44]
P. A. McCullough, R. Wolyn, L. L. Rocher, R. N. Levin, and W. W. O’Neill, “Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality,” American Journal of Medicine, vol. 103, no. 5, pp. 368–375, 1997.
[45]
C. P. Taliercio, R. E. Vlietstra, L. D. Fisher, and J. C. Burnett, “Risks for renal dysfunction with cardiac angiography,” Annals of Internal Medicine, vol. 104, no. 4, pp. 501–504, 1986.
[46]
P. McCullough, “Outcomes of contrast-induced nephropathy: Experience in patients undergoing cardiovascular intervention,” Catheterization and Cardiovascular Interventions, vol. 67, no. 3, pp. 335–343, 2006.
[47]
S. T. Cochran, W. S. Wong, and D. J. Roe, “Predicting angiography-induced acute renal function impairment: clinical risk model,” American Journal of Roentgenology, vol. 141, no. 5, pp. 1027–1033, 1983.
[48]
T. G. Gleeson and S. Bulugahapitiya, “Contrast-induced nephropathy,” American Journal of Roentgenology, vol. 183, no. 6, pp. 1673–1689, 2004.
[49]
D. B. Oliveira, “Prophylaxis against contrast-induced nephropathy,” The Lancet, vol. 353, no. 9165, pp. 1638–1639, 1999.
[50]
M. J. Kuhn, N. Chen, D. V. Sahani et al., “The PREDICT study: a randomized double-blind comparison of contrast-induced nephropathy after low- or isoosmolar contrast agent exposure,” The American Journal of Roentgenology, vol. 191, no. 1, pp. 151–157, 2008.
[51]
L. Byrd and R. L. Sherman, “Radiocontrast-induced acute renal failure: a clinical and pathophysiologic review,” Medicine, vol. 58, no. 3, pp. 270–279, 1979.
[52]
S. Harkonen and C. Kjellstrand, “Contrast nephropathy,” American Journal of Nephrology, vol. 1, no. 2, pp. 69–77, 1981.
[53]
G. A. Khoury, J. C. Hopper, Z. Varghese et al., “Nephrotoxicity of ionic and non-ionic contrast material in digital vascular imaging and selective renal arteriography,” The British Journal of Radiology, vol. 56, no. 669, pp. 631–635, 1983.
[54]
R. D. Moore, E. P. Steinberg, N. R. Powe et al., “Nephrotoxicity of high-osmolality versus low-osmolality contrast media: randomized clinical trial,” Radiology, vol. 182, no. 3, pp. 649–655, 1992.
[55]
R. W. Katzberg and B. J. Barrett, “Risk of iodinated contrast material-induced nephropathy with intravenous administration,” Radiology, vol. 243, no. 3, pp. 622–628, 2007.
[56]
D. R. Campbell, B. K. Flemming, W. F. Mason, S. A. Jackson, D. J. Hirsch, and K. J. MacDonald, “A comparative study of the nephrotoxicity of iohexol, iopamidol and ioxaglate in peripheral angiography,” Canadian Association of Radiologists Journal, vol. 41, no. 3, pp. 133–137, 1990.
[57]
A. S. Gomes, J. D. Baker, V. Martin-Paredero et al., “Acute renal dysfunction after major arteriography,” American Journal of Roentgenology, vol. 145, no. 6, pp. 1249–1253, 1985.
[58]
E. Seeliger, B. Flemming, T. Wronski et al., “Viscosity of contrast media perturbs renal hemodynamics,” Journal of the American Society of Nephrology, vol. 18, no. 11, pp. 2912–2920, 2007.
[59]
E. Seeliger, K. Becker, M. Ladwig, T. Wronski, P. B. Persson, and B. Flemming, “Up to 50-fold increase in urine viscosity with iso-osmolar contrast media in the rat,” Radiology, vol. 256, no. 2, pp. 406–414, 2010.
[60]
E. Seeliger, D. C. Lenhard, and P. B. Persson, “Contrast media viscosity versus osmolality in kidney injury: lessons from animal studies,” BioMed Research International, vol. 2014, Article ID 358136, 15 pages, 2014.
[61]
G. Jost, H. Pietsch, J. Sommer et al., “Retention of iodine and expression of biomarkers for renal damage in the kidney after application of iodinated contrast media in rats,” Investigative Radiology, vol. 44, no. 2, pp. 114–123, 2009.
[62]
K. Dyvik, K. Dyrstad, and A. Tronstad, “Relationship between viscosity and determined injection pressure in angiography catheters for common roentgen contrast media,” Acta Radiologica. Supplementum, vol. 399, pp. 43–49, 1995.
[63]
J. Ueda, A. Nygren, P. Hansell, and U. Erikson, “Influence of contrast media on single nephron glomerular filtration rate in rat kidney: a comparison between diatrizoate, iohexol, ioxaglate, and iotrolan,” Acta Radiologica, vol. 33, no. 6, pp. 596–599, 1992.
[64]
J. Ueda, A. Nygren, P. Hansell, and H. R. Ulfendahl, “Effect of intravenous contrast media on proximal and distal tubular hydrostatic pressure in the rat kidney,” Acta Radiologica, vol. 34, no. 1, pp. 83–87, 1993.
[65]
M. C. Heinrich, M. K. Kuhlmann, A. Grgic, M. Heckmann, B. Kramann, and M. Uder, “Cytotoxic effects of ionic high-osmolar, nonionic monomeric, and nonionic iso-osmolar dimeric iodinated contrast media on renal tubular cells in vitro,” Radiology, vol. 235, no. 3, pp. 843–849, 2005.
[66]
A. Michael, T. Faga, A. Pisani et al., “Molecular mechanisms of renal cellular nephrotoxicity due to radiocontrast media,” BioMed Research International, vol. 2014, Article ID 249810, 10 pages, 2014.
[67]
M. Andreucci, “Contrast media and nephrotoxicity: a molecular conundrum,” Giornale Italiano di Nefrologia, vol. 28, no. 4, p. 355, 2011.
[68]
M. Andreucci, G. Fuiano, P. Presta et al., “Radiocontrast media cause dephosphorylation of Akt and downstream signaling targets in human renal proximal tubular cells,” Biochemical Pharmacology, vol. 72, no. 10, pp. 1334–1342, 2006.
[69]
M. Andreucci, G. Lucisano, T. Faga et al., “Differential activation of signaling pathways involved in cell death, survival and inflammation by radiocontrast media in human renal proximal tubular cells,” Toxicological Sciences, vol. 119, no. 2, pp. 408–416, 2011.
[70]
M. Andreucci, T. Faga, D. Russo et al., “Differential activation of signaling pathways by low-osmolar and iso-osmolar radiocontrast agents in human renal tubular cells,” Journal of Cellular Biochemistry, vol. 115, no. 2, pp. 281–289, 2014.
[71]
M. Andreucci, A. Michael, C. Kramers et al., “Renal ischemia/reperfusion and ATP depletion/repletion in LLC-PK1 cells result in phosphorylation of FKHR and FKHRL1,” Kidney International, vol. 64, no. 4, pp. 1189–1198, 2003.
[72]
M. Andreucci, G. Fuiano, P. Presta et al., “Downregulation of cell survival signalling pathways and increased cell damage in hydrogen peroxide-treated human renal proximal tubular cells by alpha-erythropoietin,” Cell Proliferation, vol. 42, no. 4, pp. 554–561, 2009.
[73]
M. Andreucci, T. Faga, G. Lucisano, et al., “Mycophenolic acid inhibits the phosphorylation of NF-κB and JNKs and causes a decrease in IL-8 release in H2O2-treated human renal proximal tubular cells,” Chemico-Biological Interactions, vol. 185, no. 3, pp. 253–262, 2010.
[74]
V. E. Andreucci, D. Russo, B. Cianciaruso, and M. Andreucci, “Some sodium, potassium and water changes in the elderly and their treatment,” Nephrology Dialysis Transplantation, vol. 11, supplement 9, pp. 9–17, 1996.
[75]
M. Andreucci, S. Federico, and V. E. Andreucci, “Edema and acute renal failure,” Seminars in Nephrology, vol. 21, no. 3, pp. 251–256, 2001.
[76]
P. A. McCullough, M. E. Bertrand, J. A. Brinker, and F. Stacul, “A meta-analysis of the renal safety of isosmolar iodixanol compared with low-osmolar contrast media,” Journal of the American College of Cardiology, vol. 48, no. 4, pp. 692–699, 2006.
[77]
R. J. Solomon, M. K. Natarajan, S. Doucet et al., “Cardiac angiography in renally impaired patients (CARE) study: a randomized double-blind trial of contrast-induced nephropathy in patients with chronic kidney disease,” Circulation, vol. 115, no. 25, pp. 3189–3196, 2007.
[78]
M. Reed, P. Meier, U. U. Tamhane, K. B. Welch, M. Moscucci, and H. S. Gurm, “The relative renal safety of iodixanol compared with low-osmolar contrast media: a meta-analysis of randomized controlled trials,” JACC: Cardiovascular Interventions, vol. 2, no. 7, pp. 645–654, 2009.
[79]
L. Bolognese, G. Falsini, C. Schwenke et al., “Impact of iso-osmolar versus low-osmolar contrast agents on contrast-induced nephropathy and tissue reperfusion in unselected patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention (from the Contrast Media and Nephrotoxicity Following primary Angioplasty for Acute Myocardial Infarction [CONTRAST-AMI] trial),” The American Journal of Cardiology, vol. 109, no. 1, pp. 67–74, 2012.
[80]
B. J. Barrett, R. W. Katzberg, H. S. Thomsen et al., “Contrast-induced nephropathy in patients with chronic kidney disease undergoing computed tomography: a double-blind comparison of iodixanol and iopamidol,” Investigative Radiology, vol. 41, no. 11, pp. 815–821, 2006.
[81]
M. Andreucci, T. Faga, G. B. De Sarro, and A. Michael, “The toxicity of radiographic contrast agents in the clinical practice,” Journal of Nephrology Advances. In press.
[82]
M. Andreucci, T. Faga, F. Perticone, and A. Michael, “Radiographic contrast agents, drugs useful for diagnostics, but with contrast-induced nephropathy as side effect,” Journal of Nephrology and Urology. In press.
[83]
R. G. Cigarroa, R. A. Lange, R. H. Williams, and D. Hillis, “Dosing of contrast material to prevent contrast nephropathy in patients with renal disease,” The American Journal of Medicine, vol. 86, no. 6, pp. 649–652, 1989.
[84]
W. K. Laskey, C. Jenkins, F. Selzer et al., “Volume-to-creatinine clearance ratio: a pharmacokinetically based risk factor for prediction of early creatinine increase after percutaneous coronary intervention,” Journal of the American College of Cardiology, vol. 50, no. 7, pp. 584–590, 2007.
[85]
H. S. Gurm, S. R. Dixon, D. E. Smith et al., “Renal function-based contrast dosing to define safe limits of radiographic contrast media in patients undergoing percutaneous coronary interventions,” Journal of the American College of Cardiology, vol. 58, no. 9, pp. 907–914, 2011.
[86]
J. J. Keaney, C. M. Hannon, and P. T. Murray, “Contrast-induced acute kidney injury: how much contrast is safe?” Nephrology Dialysis Transplantation, vol. 28, no. 6, pp. 1376–1383, 2013.
[87]
M. Andreucci, T. Faga, A. Pisani, M. Sabbatini, D. Russo, and A. Michael, “Prevention of contrast-induced nephropathy through a knowledge of its pathogenesis and risk factors,” The Scientific World Journal. In press.
[88]
H. S. Thomsen, “Guidelines for contrast media from the European society of urogenital radiology,” American Journal of Roentgenology, vol. 181, no. 6, pp. 1463–1471, 2003.
[89]
H. S. Trivedi, H. Moore, S. Nasr et al., “A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity,” Nephron Clinical Practice, vol. 93, no. 1, pp. C29–C34, 2003.
[90]
C. Mueller, “Prevention of contrast-induced nephropathy with volume supplementation,” Kidney International Supplement, no. 100, pp. S16–S19, 2006.
[91]
G. J. Merten, W. P. Burgess, L. V. Gray, et al., “Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial,” The Journal of the American Medical Association, vol. 291, no. 19, pp. 2328–2334, 2004.
[92]
M. Masuda, T. Yamada, T. Mine et al., “Comparison of usefulness of sodium bicarbonate versus sodium chloride to prevent contrast-induced nephropathy in patients undergoing an emergent coronary procedure,” The American Journal of Cardiology, vol. 100, no. 5, pp. 781–786, 2007.
[93]
E. E. Ozcan, S. Guneri, B. Akdeniz et al., “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, vol. 154, no. 3, pp. 539–544, 2007.
[94]
A. Tamura, Y. Goto, K. Miyamoto et al., “Efficacy of single-bolus administration of sodium bicarbonate to prevent contrast-induced nephropathy in patients with mild renal insufficiency undergoing an elective coronary procedure,” The American Journal of Cardiology, vol. 104, no. 7, pp. 921–925, 2009.
[95]
S. D. Navaneethan, S. Singh, S. Appasamy, R. E. Wing, and A. R. Sehgal, “Sodium bicarbonate therapy for prevention of contrast-induced nephropathy: a systematic review and meta-analysis,” American Journal of Kidney Diseases, vol. 53, no. 4, pp. 617–627, 2009.
[96]
E. A. J. Hoste, J. J. de Waele, S. A. Gevaert, S. Uchino, and J. A. Kellum, “Sodium bicarbonate for prevention of contrast-induced acute kidney injury: a systematic review and meta-analysis,” Nephrology Dialysis Transplantation, vol. 25, no. 3, pp. 747–758, 2010.
[97]
M. Joannidis, M. Schmid, and C. J. Wiedermann, “Prevention of contrast media-induced nephropathy by isotonic sodium bicarbonate: a meta-analysis,” Wiener Klinische Wochenschrift, vol. 120, no. 23-24, pp. 742–748, 2008.
[98]
F. Assadi, “Acetazolamide for prevention of contrast-induced nephropathy: a new use for an old drug,” Pediatric Cardiology, vol. 27, no. 2, pp. 238–242, 2006.
[99]
M. Pakfetrat, M. H. Nikoo, L. Malekmakan et al., “A comparison of sodium bicarbonate infusion versus normal saline infusion and its combination with oral acetazolamide for prevention of contrast-induced nephropathy: a randomized, double-blind trial,” International Urology and Nephrology, vol. 41, no. 3, pp. 629–634, 2009.
[100]
J.-S. Jang, H.-Y. Jin, J.-S. Seo et al., “Sodium bicarbonate therapy for the prevention of contrast-induced acute kidney injury—a systematic review and meta-analysis,” Circulation Journal, vol. 76, no. 9, pp. 2255–2265, 2012.
[101]
C. Briguori, F. Airoldi, D. D'Andrea et al., “Renal insufficiency following contrast media administration trial (REMEDIAL): a randomized comparison of 3 preventive strategies,” Circulation, vol. 115, no. 10, pp. 1211–1217, 2007.
[102]
D. Reddan, M. Laville, and V. D. Garovic, “Contrast-induced nephropathy and its prevention: what do we really know from evidence-based findings?” Journal of Nephrology, vol. 22, no. 3, pp. 333–351, 2009.
[103]
C. S. R. Baker, A. Wragg, S. Kumar, R. De Palma, L. R. I. Baker, and C. J. Knight, “A rapid protocol for the prevention of contrast-induced renal dysfunction: the RAPPID study,” Journal of the American College of Cardiology, vol. 41, no. 12, pp. 2114–2118, 2003.
[104]
M. Andreucci, “Statins inCIN: a problemat least partly solved?” Giornale Italiano di Nefrologia, vol. 30, no. 3, 2013.
[105]
M. Sabbatini, A. Pisani, F. Uccello, et al., “Atorvastatin improves the course of ischemic acute renal failure in aging rats,” Journal of the American Society of Nephrology, vol. 15, no. 4, pp. 901–909, 2004.
[106]
S. Khanal, N. Attallah, D. E. Smith et al., “Statin therapy reduces contrast-induced nephropathy: an analysis of contemporary percutaneous interventions,” The American Journal of Medicine, vol. 118, no. 8, pp. 843–849, 2005.
[107]
G. Patti, A. Nusca, M. Chello et al., “Usefulness of statin pretreatment to prevent contrast-induced nephropathy and to improve long-term outcome in patients undergoing percutaneous coronary intervention,” The American Journal of Cardiology, vol. 101, no. 3, pp. 279–285, 2008.
[108]
B.-C. Zhang, W.-M. Li, and Y.-W. Xu, “High-dose statin pretreatment for the prevention of contrast-induced nephropathy: a meta-analysis,” Canadian Journal of Cardiology, vol. 27, no. 6, pp. 851–858, 2011.
[109]
M. Leoncini, A. Toso, M. Maioli, F. Tropeano, and F. Bellandi, “Statin treatment before percutaneous cononary intervention,” Journal of Thoracic Disease, vol. 5, no. 3, pp. 335–342, 2013.
[110]
G. Patti, E. Ricottini, A. Nusca et al., “Short-term, high-dose atorvastatin pretreatment to prevent contrast-induced nephropathy in patients with acute coronary syndromes undergoing percutaneous coronary intervention (from the ARMYDA-CIN [atorvastatin for reduction of myocardial damage during angioplasty-contrast-induced nephropathy] trial,” The American Journal of Cardiology, vol. 108, no. 1, pp. 1–7, 2011.
[111]
C. Quintavalle, D. Fiore, F. de Micco et al., “Impact of a high loading dose of atorvastatin on contrast-induced acute kidney injury,” Circulation, vol. 126, no. 25, pp. 3008–3016, 2012.
[112]
R. Solomon, C. Werner, D. Mann, J. D'Elia, and P. Silva, “Effects of saline, mannitol, and furosemide on acute decreases in renal function induced by radiocontrast agents,” The New England Journal of Medicine, vol. 331, no. 21, pp. 1416–1420, 1994.
[113]
J.-M. Weinstein, S. Heyman, and M. Brezis, “Potential deleterious effect of furosemide in radiocontrast nephropathy,” Nephron, vol. 62, no. 4, pp. 413–415, 1992.
[114]
L. S. Weisberg, P. B. Kurnik, and B. R. Kurnik, “Risk of radiocontrast nephropathy in patients with and without diabetes mellitus,” Kidney International, vol. 45, no. 1, pp. 259–265, 1994.
[115]
C. Briguori, G. Visconti, B. Ricciardelli, and G. Condorelli, “Renal insufficiency following contrast media administration trial II (REMEDIAL II): renalGuard system in high-risk patients for contrast-induced acute kidney injury: rationale and design,” EuroIntervention, vol. 6, no. 9, pp. 1117–1122, 2011.
[116]
B. Vogt, P. Ferrari, C. Sch?nholzer et al., “Prophylactic hemodialysis after radiocontrast media in patients with renal insufficiency is potentially harmful,” The American Journal of Medicine, vol. 111, no. 9, pp. 692–698, 2001.
[117]
M. Andreucci, “Radiographic contrast nephropathy,” Giornale Italiano di Nefrologia, vol. 31, no. 5, 2014.
[118]
J. J. Pasternak and E. E. Williamson, “Clinical pharmacology, uses, and adverse reactions of iodinated contrast agents: a primer for the non-radiologist,” Mayo Clinic Proceedings, vol. 87, no. 4, pp. 390–402, 2012.