- Email: [email protected]
Letter to the editor concerning the article by Kooiman et al
Letters to the Editor
Letter to the editor concerning the article by Kooiman et al
We read with interest the recently published article titled “Contrast-induced acute kidney injury and clinical outcomes after intra-arterial and intravenous contrast administration: risk comparison adjusted for patient characteristics by design” by Kooiman et al 1 in your journal. The risk of contrast-induced acute kidney injury (CI-AKI) and its clinical course were similar after intra-arterial and intravenous contrast media (CM) administration, after adjustment by design for patient-related risk factors. We have some comments about this study. Contrast media dose is a risk factor that has not receive adequate attention. Regardless of CM type, the amount of CM a patient receives is a powerful predictor of CI-AKI. 2 In the current study, Kooiman et al did not denote in the text the CM doses and the injection site (femoral, brachial, radial) that have been used in the study population. Some early study results indicated that intravenous CM were less risky than intra-arterial CM, 3 particularly if the arterial injection was suprarenal. 4 Khoury et al 5 found that intravenous injection posed a significantly lower risk to kidney function than did renal arterial injection, and Gomes et al 6 found that for aortography, the closer to the renal arteries the injection occurred, the higher the risk of CI-AKI. In a recently published meta-analysis, the mean incidence of CI-AKI after intravenous iodinated contrast enhancement computed tomography was low and associated with renal insufficiency, diabetes, presence of malignancy, old age, and nonsteroidal antiinflammatory drug use. 7 Nyman et al 8 reported an CM-dose (in grams)/estimated glomerular filtration rate ratio (eGFR) of less than 1.0 to be a relatively safe cutoff point to avoid CI-AKI. They also reported an estimated 10% risk of unspecified CI-AKI and a 1% risk of severe CI-AKI at a mean CM-dose (in grams)/ estimated glomerular filtration rate ratio of 1, increasing to approximately 50% and 15% risk at a mean ratio of 3, respectively. Because the patients' profile in Kooiman et al was proned to develop CI-AKI, they could use a risk score like this in their study. Serum creatinine (SCr) is determined by the interplay of creatinine production, GFR, and the kinetics of creatinine distribution among the body's fluid compartments. Owing to the exponential relationship between SCr and GFR, SCr is very insensitive in patients with normal preexisting renal function. To allow evaluation of kidney
injury, more accurate markers such as cystatin C will have to be included in the methodology and design of clinical trials. 9,10 Finally, the authors did not cite the definition of CI-AKI in the outcomes heading. Am Heart J 2013;166:e41. 0002-8703/$ - see front matter http://dx.doi.org/10.1016/j.ahj.2013.08.013
Yavuzer Koza, MD Muhammed Hakan Tas, MD Ziya Simsek, MD Ataturk University Faculty of Medicine Department of Cardiology, Erzurum, Turkey E-mail: [email protected]
References 1. Kooiman J, Le Haen PA, Gezgin G, et al. Contrast-induced acute kidney injury and clinical outcomes after intra-arterial and intravenous contrast administration: risk comparison adjusted for patient characteristics by design. Am Heart J 2013;165:793-9. 2. Kane GC, Doyle BJ, Lerman A, et al. Ultra-low contrast volumes reduce rates of contrast-induced nephropathy in patients with chronic kidney disease undergoing coronary angiography. J Am Coll Cardiol 2008;51:89-90. 3. Harkonen S, Kjellstrand C. Contrast nephropathy. Am J Nephrol 1981;1:69-77. 4. Campbell DR, Flemming BK, Mason WF, et al. A comparative study of the nephrotoxicity of iohexol, iopamidol and ioxaglate in peripheral angiography. Can Assoc Radiol J 1990;41:133-7. 5. Khoury GA, Hopper JC, Varghese Z, et al. Nephrotoxicity of ionic and non-ionic contrast material in digital vascular imaging and selective renal arteriography. Br J Radiol 1983;56:631-5. 6. Gomes AS, Baker JD, Martin-Paredero V, et al. Acute renal dysfunction after majör arteriography. Am J Roentgenol 1985;145: 1249-53. 7. Moos SI, van Vemde DN, Stoker J, et al. Contrast induced nephropathy in patients undergoing intravenous (IV) contrast enhanced computed tomography (CECT) and the relationship with risk factors: a meta-analysis. Eur J Radiol 2013. http://dx.doi.org/10.1016/j.ejrad.2013.04.029. 8. Nyman U, Almen T, Aspelin P, et al. Contrast medium-induced nephropathy correlated to the ratio between dose in gram iodine and estimated GFR in ml/min. Acta Radiol 2005;46:830-42. 9. Haase M, Devarajan P, Haase-Fielitz A, et al. The outcome of neutrophil gelatinase–associated lipocalin-positive subclinical acute kidney injury: a multicenter pooled analysis of prospective studies. J Am Coll Cardiol 2011;57:1752-61. 10. Solomon R, Dauerman HL. Contrast-induced acute kidney injury. Circulation 2010;122:2451-5.
Letter to the editor concerning the article by Kooiman et al
We read with interest the recently published article titled “Contrast-induced acute kidney injury and clinical outcomes after intra-arterial and intravenous contrast administration: risk comparison adjusted for patient characteristics by design” by Kooiman et al 1 in your journal. The risk of contrast-induced acute kidney injury (CI-AKI) and its clinical course were similar after intra-arterial and intravenous contrast media (CM) administration, after adjustment by design for patient-related risk factors. We have some comments about this study. Contrast media dose is a risk factor that has not receive adequate attention. Regardless of CM type, the amount of CM a patient receives is a powerful predictor of CI-AKI. 2 In the current study, Kooiman et al did not denote in the text the CM doses and the injection site (femoral, brachial, radial) that have been used in the study population. Some early study results indicated that intravenous CM were less risky than intra-arterial CM, 3 particularly if the arterial injection was suprarenal. 4 Khoury et al 5 found that intravenous injection posed a significantly lower risk to kidney function than did renal arterial injection, and Gomes et al 6 found that for aortography, the closer to the renal arteries the injection occurred, the higher the risk of CI-AKI. In a recently published meta-analysis, the mean incidence of CI-AKI after intravenous iodinated contrast enhancement computed tomography was low and associated with renal insufficiency, diabetes, presence of malignancy, old age, and nonsteroidal antiinflammatory drug use. 7 Nyman et al 8 reported an CM-dose (in grams)/estimated glomerular filtration rate ratio (eGFR) of less than 1.0 to be a relatively safe cutoff point to avoid CI-AKI. They also reported an estimated 10% risk of unspecified CI-AKI and a 1% risk of severe CI-AKI at a mean CM-dose (in grams)/ estimated glomerular filtration rate ratio of 1, increasing to approximately 50% and 15% risk at a mean ratio of 3, respectively. Because the patients' profile in Kooiman et al was proned to develop CI-AKI, they could use a risk score like this in their study. Serum creatinine (SCr) is determined by the interplay of creatinine production, GFR, and the kinetics of creatinine distribution among the body's fluid compartments. Owing to the exponential relationship between SCr and GFR, SCr is very insensitive in patients with normal preexisting renal function. To allow evaluation of kidney
injury, more accurate markers such as cystatin C will have to be included in the methodology and design of clinical trials. 9,10 Finally, the authors did not cite the definition of CI-AKI in the outcomes heading. Am Heart J 2013;166:e41. 0002-8703/$ - see front matter http://dx.doi.org/10.1016/j.ahj.2013.08.013
Yavuzer Koza, MD Muhammed Hakan Tas, MD Ziya Simsek, MD Ataturk University Faculty of Medicine Department of Cardiology, Erzurum, Turkey E-mail: [email protected]
References 1. Kooiman J, Le Haen PA, Gezgin G, et al. Contrast-induced acute kidney injury and clinical outcomes after intra-arterial and intravenous contrast administration: risk comparison adjusted for patient characteristics by design. Am Heart J 2013;165:793-9. 2. Kane GC, Doyle BJ, Lerman A, et al. Ultra-low contrast volumes reduce rates of contrast-induced nephropathy in patients with chronic kidney disease undergoing coronary angiography. J Am Coll Cardiol 2008;51:89-90. 3. Harkonen S, Kjellstrand C. Contrast nephropathy. Am J Nephrol 1981;1:69-77. 4. Campbell DR, Flemming BK, Mason WF, et al. A comparative study of the nephrotoxicity of iohexol, iopamidol and ioxaglate in peripheral angiography. Can Assoc Radiol J 1990;41:133-7. 5. Khoury GA, Hopper JC, Varghese Z, et al. Nephrotoxicity of ionic and non-ionic contrast material in digital vascular imaging and selective renal arteriography. Br J Radiol 1983;56:631-5. 6. Gomes AS, Baker JD, Martin-Paredero V, et al. Acute renal dysfunction after majör arteriography. Am J Roentgenol 1985;145: 1249-53. 7. Moos SI, van Vemde DN, Stoker J, et al. Contrast induced nephropathy in patients undergoing intravenous (IV) contrast enhanced computed tomography (CECT) and the relationship with risk factors: a meta-analysis. Eur J Radiol 2013. http://dx.doi.org/10.1016/j.ejrad.2013.04.029. 8. Nyman U, Almen T, Aspelin P, et al. Contrast medium-induced nephropathy correlated to the ratio between dose in gram iodine and estimated GFR in ml/min. Acta Radiol 2005;46:830-42. 9. Haase M, Devarajan P, Haase-Fielitz A, et al. The outcome of neutrophil gelatinase–associated lipocalin-positive subclinical acute kidney injury: a multicenter pooled analysis of prospective studies. J Am Coll Cardiol 2011;57:1752-61. 10. Solomon R, Dauerman HL. Contrast-induced acute kidney injury. Circulation 2010;122:2451-5.