Note: This copy is for your personal non-commercial use only. To order presentation-ready copies for distribution to your colleagues or clients, contact us at www.rsna.org/rsnarights.
LETTERS TO THE EDITOR
2. Rudnick MR, Berns JS, Cohen RM, Goldfarb S. Contrast media–associated nephrotoxicity. Semin Nephrol 1997;17(1):15–26. 3. Tumlin J, Stacul F, Adam A, et al. Pathophysiology of contrast-induced nephropathy. Am J Cardiol 2006;98(6A):14K–20K. 4. Maioli M, Toso A, Leoncini M, et al. Sodium bicarbonate versus saline for the prevention of contrast-induced nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. J Am Coll Cardiol 2008;52(8):599–604. 5. Stone GW, McCullough PA, Tumlin JA, et al. Fenoldopam mesylate for the prevention of contrast-induced nephropathy: a randomized controlled trial. JAMA 2003;290(17):2284– 2291. 6. Rashid ST, Salman M, Myint F, et al. Prevention of contrast-induced nephropathy in vascular patients undergoing angiography: a randomized controlled trial of intravenous N-acetylcysteine. J Vasc Surg 2004;40(6): 1136–1141. 7. Pahade JK, LeBedis CA, Raptopoulos VD, et al. Incidence of contrast-induced nephropathy in patients with multiple myeloma undergoing contrast-enhanced CT. AJR Am J Roentgenol 2011;196(5):1094–1101. 8. From AM, Bartholmai BJ, Williams AW, Cha SS, Pflueger A, McDonald FS. Sodium bicarbonate is associated with an increased incidence of contrast nephropathy: a retrospective cohort study of 7977 patients at mayo clinic. Clin J Am Soc Nephrol 2008;3(1):10–18.
Response From Jennifer S. McDonald, PhD,* Robert J. McDonald, MD, PhD,* Rickey E. Carter, PhD,† Richard W. Katzberg, MD,‡ David F. Kallmes, MD,*§ and Eric E. Williamson, MD* Departments of Radiology,* Health Sciences Research,† and Neurosurgery,§ College of Medicine, Mayo Clinic, 200 1st St SW, Rochester, MN 55905 e-mail: [email protected] Department of Radiology, Medical University of South Carolina, Charleston, SC‡ We appreciate Dr Mitchell and colleagues’ interest in our work and the opportunity to clarify the strengths, limitations, and validity of the methodologies used in our study (1).
Our studies of CIN used a common definition of AKI of an increase in serum creatinine level of at least 0.5 mg/ dL over baseline in the 24–72 hours after computed tomography (1–3). When patients had multiple postscan serum creatinine levels, we used the maximum rather than the mean postscan serum creatinine value for exactly the reasons outlined in their letter. We chose a 24– 72-hour postscan window for CIN development because this time frame is defined in both the American College of Radiology and European Society of Urogenital Radiology contrast material administration guidelines (4,5). We are unaware of any recent consensus statements or societal guidelines stating that more severe forms of CIN develop later than 72 hours. Furthermore, serum creatinine increases that occur beyond this time frame are more likely to be confounded by contrast material–independent AKI. Regardless of how AKI is defined, our recent study demonstrating similar rates of 30-day emergent dialysis and mortality in contrast material recipients and matched control patients suggests that intravenous contrast material administration is not a risk factor for these more severe and arguably more clinically important outcomes (3). We acknowledge Dr Mitchell and colleagues’ concern over not including acuity of illness or imaging indication in our propensity score model. Although our model included the major AKI risk factors as defined by the American College of Radiology and European Society of Urogenital Radiology (4,5), including renal function and relevant comorbidities, we were unable to manually retrieve and classify illness acuity or indication from our large cohort. Studies specifically examining the risk of contrast material administration in acutely ill patients are under way. As contrast material use is strongly influenced by indication and anatomy, there are limited instances where one can directly compare patients who underwent the same imaging examination for the same indication in the presence and absence of contrast material. However, by including the major AKI risk factors in
Radiology: Volume 275: Number 3—June 2015 n radiology.rsna.org
our model we were able to compare contrast material recipients and control patients with similar clinical characteristics and reasonably approximate a theoretical randomization of these risk factors. Disclosures of Conflicts of Interest: J.S.M. disclosed no relevant relationships. R.J.M. disclosed no relevant relationships. R.E.C. disclosed no relevant relationships. R.W.K. disclosed no relevant relationships. D.F.K. Activities related to the present article: institution receives money from RSNA for deputy editor position. Activities not related to the present article: institution receives patent money from CEEP; receives patent money from UVA. Other relationships: receives research support from Microvention (ev3), Covidien, NFocus Consulting, Sequent Medical, Penumbra, and Benvenue Medical. E.E.W. disclosed no relevant relationships.
References 1. McDonald JS, McDonald RJ, Carter RE, Katzberg RW, Kallmes DF, Williamson EE. Risk of intravenous contrast material–mediated acute kidney injury: a propensity scorematched study stratified by baseline-estimated glomerular filtration rate. Radiology 2014; 271(1):65–73. 2. McDonald RJ, McDonald JS, Bida JP, et al. Intravenous contrast material–induced nephropathy: causal or coincident phenomenon? Radiology 2013;267(1):106–118. 3. McDonald RJ, McDonald JS, Carter RE, et al. Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology 2014;273(3):714–725. 4. American College of Radiology. ACR Manual on Contrast Media. Version 9.2013. http:// www.acr.org/~/media/ACR/Documents/ PDF/QualitySafety/Resources/Contrast Manual/2013_Contrast_Media.pdf. Accessed December 30, 2014. 5. Stacul F, van der Molen AJ, Reimer P, et al. Contrast induced nephropathy: updated European Society of Urogenital Radiology Contrast Media Safety Committee guidelines. Eur Radiol 2011;21(12):2527–2541.
Perplexing Histologic Classification of Thymic Epithelial Tumor From Qijun Shen, MD,* Wenchao Hu, MD,† and Zhan Feng, MD‡ Department of Radiology, Hangzhou First People’s Hospital, Hangzhou, Zhejiang, China* 929
LETTERS TO THE EDITOR
Department of Radiology, Wenzhou Central Hospital, Wenzhou, Zhejiang, China† Department of Radiology, the First Affiliated Hospital of College of Medicine, Zhejiang University, 79 Qingchun Rd, Hangzhou, Zhejiang, China 310003‡ e-mail: [email protected] Editor: We read with interest the article by Dr Abdel Razek and colleagues in the October 2014 issue of Radiology (1). They report that the apparent diffusion coefficient is a reliable imaging parameter that may help characterize thymic epithelial tumors. We have two questions about pathologic classification in the article. First, 30 consecutive patients were included from 2005 to 2013. According to the statement in the original article, it is clear that the authors are still consulting the 1999 World Health Organization (WHO) histopathologic classification system of thymic epithelial tumors. In the new 2004 version, type C has been eliminated and neuroendocrine thymic tumor has been classified into the category of thymic carcinoma (2). Second, the WHO histopathologic classification of thymic epithelial tumors had created some degree of uncertainty and confusion among various investigators (3). Interobserver reproducibility for pathologists was poor, and there was overlap between some subtypes—especially in type AB and types B1 and B2–5 (4–6). Thus, in many cases, pathologic findings suggest two or even three subtypes of the tumor. Currently, many researchers divide the cases into low-risk thymomas and high-risk thymomas to reduce overlap between the subtypes. However, some cases still cannot be classified into the appropriate group, and it is a pity that most radiologic-pathologic correlation studies of thymic epithelial tumors failed to mention the influence of such a problem on the outcome. Conflicts exist between some results about the correlation between computed tomographic (CT) appearance and WHO histopathologic classification of thymic epithelial tumors, and these 930
may be due in part to the limitations of the WHO classification scheme according to Benveniste et al (7). So, we wish radiologists pay enough attention to the histologic classification of thymic epithelial tumors. Disclosures of Conflicts of Interest: Q.S. disclosed no relevant relationships. W.H. disclosed no relevant relationships. Z.F. disclosed no relevant relationships.
References 1. Abdel Razek AA, Khairy M, Nada N. Diffusion-weighted MR imaging in thymic epithelial tumors: correlation with World Health Organization classification and clinical staging. Radiology 2014;273(1):268–275. 2. Travis WD, Brambilla E, Muller-Hermelink HK, Harris CC, eds. Pathology and genetics of tumors of the lung, pleura, thymus and heart. Lyon, France: IARC Press, 2004. 3. Suster S, Moran CA. Problem areas and inconsistencies in the WHO classification of thymoma. Semin Diagn Pathol 2005;22(3): 188–197. 4. Suster S, Moran CA. Histologic classification of thymoma: the World Health Organization and beyond. Hematol Oncol Clin North Am 2008;22(3):381–392. 5. Suster S, Moran CA. Thymoma classification: current status and future trends. Am J Clinical Pathol 2006;125(4):542–554. 6. Rieker RJ, Hoegel J, Morresi-Hauf A, et al. Histologic classification of thymic epithelial tumors: comparison of established classification schemes. Int J Cancer 2002; 98(6):900–906. 7. Benveniste MF, Rosado-de-Christenson ML, Sabloff BS, Moran CA, Swisher SG, Marom EM. Role of imaging in the diagnosis, staging, and treatment of thymoma. Radiographics 2011;31(7):1847–1861; discussion 1861–1863.
Response From Ahmed Abdel Khalek Abdel Razek, MD Department of Diagnostic Radiology, Mansoura Faculty of Medicine, Mansoura, Egypt 13351 e-mail: [email protected] I thank Dr Shen and colleagues for their comments. In our study, we applied the recent 2004 WHO classification (1) for the assessment of thymic epithelial tu-
mors (2). We classified thymic epithelial tumors into thymoma and thymic carcinoma according to the 2004 WHO classification. Unfortunately, we misclassified thymic carcinoma as equivalent to type C in the old WHO classification of thymic tumors. In our study, only one expert pathologist performed the histopathologic examination. We could not assess the interobserver variability of the pathologic classification. The recent 2004 WHO classification has gained acceptance by pathologists in the recent years (3); however, there is still some overlap in the subtype classification of thymic epithelial tumors among pathologists (4). Future multicenter studies with larger numbers of patients that assess the intra- and interobserver variability of the pathologic classification and its relationship to the apparent diffusion coefficient may lead to better evaluation and characterization of the subtypes of thymic epithelial tumors with diffusionweighted magnetic resonance (MR) imaging in the future. Finally, we suggest that some conflicting results on the correlation between CT appearance and the WHO classification of thymic epithelial tumors may be related to the fact that CT studies depend on qualitative parameters, whereas diffusion-weighted MR imaging is a quantitative parameter of the apparent diffusion coefficient. Hopefully, further studies in a large number of patients that correlate findings from CT and diffusion-weighted MR imaging with pathologic subtypes of thymic epithelial tumors will decrease the conflicting results and improve the results. Disclosures of Conflicts of Interest: disclosed no relevant relationships.
References 1. Travis WD, Brambilla E, Muller-Hermelink HK, Harris CC, eds. Pathology and genetics of tumors of the lung, pleura, thymus and heart. Lyon, France: IARC Press, 2004. 2. Abdel Razek AA, Khairy M, Nada N. Diffusion-weighted MR imaging in thymic epithelial tumors: correlation with World Health Organization classification and clinical staging. Radiology 2014;273(1):286–275.
radiology.rsna.org n Radiology: Volume 275: Number 3—June 2015
LETTERS TO THE EDITOR
3. Marino M, Piantelli M. Immunohistochemistry of thymic epithelial tumors as a tool in translational research. Thorac Surg Clin 2011;21(1):33–46. 4. Honglin Y, Jun D, Zhenfeng L, et al. The correlation of the World Health Organization histologic classification of thymic epithelial tumors and its prognosis: a clinicopathologic study of 108 patients from China. Int J Surg Pathol 2009;17(3):255–261.
Intravenous Contrast Material and Acute Kidney Injury: A Need for Caution From Aibek E. Mirrakhimov, MD,* and Erkin M. Mirrakhimov, MD† Saint Joseph Hospital, Department of Internal Medicine, 2900 N Lake Shore Dr, Chicago, Ill 60657* e-mail: [email protected] Kyrgyz State Medical Academy, Bishkek, Kyrgyzstan† Editor: We read with great interest the article by Dr McDonald and colleagues (1) in the December 2014 issue of Radiology. In this single-center study, authors retrospectively analyzed the effect of computed tomography (CT) performed with and without contrast material on the incidence of acute kidney injury (AKI), the need for dialysis, or death within 30 days after intravenous contrast material administration. To minimize the risk of selection bias, the researchers used propensity score–based 1:1 matching in their study. It is interesting to note that intravenous contrast material administration was not associated with the risk of AKI, the need for dialysis, or death within 30 days in this study with a large sample. Indeed, in a similar retrospective study by Prasad et al (2) published in the same issue of Radiology, the administration of intravenous contrast material was only associated with the low risk of AKI. We praise the authors of this study for raising the possibility that intravenous contrast material administration for CT studies is not associated with the risk of AKI or dialysis. Indeed, if it is true, our practice should change dramatically and we should eliminate
the entity of contrast material–induced nephropathy (CIN). However, we believe that at least one important variable was not addressed in this study. Dr McDonald and colleagues did not specify whether patients at risk for CIN received preventive measures such as intravenous hydration with isotonic fluids and/or oral N-acetylcysteine, which is a common practice worldwide (3,4). Thus, it is unclear whether the lack of association between AKI and intravenous contrast material was due to preventive measures undertaken or the inherent lack of nephrotoxicity of intravenous contrast material. To answer this question, we will need a representative prospective randomized study evaluating the risk of CIN among patients at risk who received preventive measures and those who did not. However, such study is unlikely to be done due to several reasons, with the major reason being ethics. Given the very high cost of care for CIN and the relative inexpensiveness of preventive measures, we advise assessing the need for intravenous contrast material in every patient at risk and using tools to minimize the risk if intravenous contrast material is to be administered. Disclosures of Conflicts of Interest: A.E.M. disclosed no relevant relationships. E.M.M. disclosed no relevant relationships.
References 1. McDonald RJ, McDonald JS, Carter RE, et al. Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology 2014;273(3):714–725. 2. Prasad V, Gandhi D, Stokum C, Miller T, Jindal G. Incidence of contrast material-induced nephropathy after neuroendovascular procedures. Radiology 2014;273(3):853–858. 3. Seeliger E, Sendeski M, Rihal CS, Persson PB. Contrast-induced kidney injury: mechanisms, risk factors, and prevention. Eur Heart J 2012;33(16):2007–2015. 4. Hosseinjani H, Moghaddas A, Khalili H. Nacetylcysteine for the prevention of non-contrast media agent-induced kidney injury: from preclinical data to clinical evidence. Eur J Clin Pharmacol 2013;69(7):1375–1390.
Radiology: Volume 275: Number 3—June 2015 n radiology.rsna.org
Response From Robert J. McDonald, MD, PhD,* Jennifer S. McDonald, PhD,* Rickey E. Carter, PhD,† Robert P. Hartman, MD,* Richard W. Katzberg, MD,‡ David F. Kallmes, MD,*§ and Eric E. Williamson, MD* Departments of Radiology,* Health Sciences Research,† and Neurosurgery,§ College of Medicine, Mayo Clinic, 200 1st St SW, Rochester, MN 55905 e-mail: [email protected] Department of Radiology, Medical University of South Carolina, Charleston, SC‡ We appreciate Drs Mirrakhimovs’ interest and critical assessment of our recent article on CIN. In our recent propensity score–matched controlled cohort study, we were unable to identify iodinated contrast material as an independent risk factor for AKI, emergent dialysis, or mortality within 30 days of exposure (1). The subset of study patients who developed AKI were at significantly higher risk for both dialysis and mortality, but the risks of these adverse outcomes were not significantly different between contrast material–exposed and unexposed patient groups. Intravenous fluids were excluded from our propensity score model of AKI risk for several reasons. First, a central tenant of propensity score model generation is that all covariates must be present before the treatment of interest is administered; inclusion of a variable after treatment invalidates the logistic model by causal confounding (ie, is the intravenous contrast material or fluid responsible for the change in serum creatinine level?). Intravenous fluid administration data extracted by means of automated software is too coarse to reliably ascertain the exact time of fluid administration near the time of CT. More exhaustive manual review of these records is needed to avoid this source of confounding. Second, there are conflicting data with respect to prevention of CIN with intravenous fluid–based renoprotective treatments 931
LETTERS TO THE EDITOR
2. Rudnick MR, Berns JS, Cohen RM, Goldfarb S. Contrast media–associated nephrotoxicity. Semin Nephrol 1997;17(1):15–26. 3. Tumlin J, Stacul F, Adam A, et al. Pathophysiology of contrast-induced nephropathy. Am J Cardiol 2006;98(6A):14K–20K. 4. Maioli M, Toso A, Leoncini M, et al. Sodium bicarbonate versus saline for the prevention of contrast-induced nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. J Am Coll Cardiol 2008;52(8):599–604. 5. Stone GW, McCullough PA, Tumlin JA, et al. Fenoldopam mesylate for the prevention of contrast-induced nephropathy: a randomized controlled trial. JAMA 2003;290(17):2284– 2291. 6. Rashid ST, Salman M, Myint F, et al. Prevention of contrast-induced nephropathy in vascular patients undergoing angiography: a randomized controlled trial of intravenous N-acetylcysteine. J Vasc Surg 2004;40(6): 1136–1141. 7. Pahade JK, LeBedis CA, Raptopoulos VD, et al. Incidence of contrast-induced nephropathy in patients with multiple myeloma undergoing contrast-enhanced CT. AJR Am J Roentgenol 2011;196(5):1094–1101. 8. From AM, Bartholmai BJ, Williams AW, Cha SS, Pflueger A, McDonald FS. Sodium bicarbonate is associated with an increased incidence of contrast nephropathy: a retrospective cohort study of 7977 patients at mayo clinic. Clin J Am Soc Nephrol 2008;3(1):10–18.
Response From Jennifer S. McDonald, PhD,* Robert J. McDonald, MD, PhD,* Rickey E. Carter, PhD,† Richard W. Katzberg, MD,‡ David F. Kallmes, MD,*§ and Eric E. Williamson, MD* Departments of Radiology,* Health Sciences Research,† and Neurosurgery,§ College of Medicine, Mayo Clinic, 200 1st St SW, Rochester, MN 55905 e-mail: [email protected] Department of Radiology, Medical University of South Carolina, Charleston, SC‡ We appreciate Dr Mitchell and colleagues’ interest in our work and the opportunity to clarify the strengths, limitations, and validity of the methodologies used in our study (1).
Our studies of CIN used a common definition of AKI of an increase in serum creatinine level of at least 0.5 mg/ dL over baseline in the 24–72 hours after computed tomography (1–3). When patients had multiple postscan serum creatinine levels, we used the maximum rather than the mean postscan serum creatinine value for exactly the reasons outlined in their letter. We chose a 24– 72-hour postscan window for CIN development because this time frame is defined in both the American College of Radiology and European Society of Urogenital Radiology contrast material administration guidelines (4,5). We are unaware of any recent consensus statements or societal guidelines stating that more severe forms of CIN develop later than 72 hours. Furthermore, serum creatinine increases that occur beyond this time frame are more likely to be confounded by contrast material–independent AKI. Regardless of how AKI is defined, our recent study demonstrating similar rates of 30-day emergent dialysis and mortality in contrast material recipients and matched control patients suggests that intravenous contrast material administration is not a risk factor for these more severe and arguably more clinically important outcomes (3). We acknowledge Dr Mitchell and colleagues’ concern over not including acuity of illness or imaging indication in our propensity score model. Although our model included the major AKI risk factors as defined by the American College of Radiology and European Society of Urogenital Radiology (4,5), including renal function and relevant comorbidities, we were unable to manually retrieve and classify illness acuity or indication from our large cohort. Studies specifically examining the risk of contrast material administration in acutely ill patients are under way. As contrast material use is strongly influenced by indication and anatomy, there are limited instances where one can directly compare patients who underwent the same imaging examination for the same indication in the presence and absence of contrast material. However, by including the major AKI risk factors in
Radiology: Volume 275: Number 3—June 2015 n radiology.rsna.org
our model we were able to compare contrast material recipients and control patients with similar clinical characteristics and reasonably approximate a theoretical randomization of these risk factors. Disclosures of Conflicts of Interest: J.S.M. disclosed no relevant relationships. R.J.M. disclosed no relevant relationships. R.E.C. disclosed no relevant relationships. R.W.K. disclosed no relevant relationships. D.F.K. Activities related to the present article: institution receives money from RSNA for deputy editor position. Activities not related to the present article: institution receives patent money from CEEP; receives patent money from UVA. Other relationships: receives research support from Microvention (ev3), Covidien, NFocus Consulting, Sequent Medical, Penumbra, and Benvenue Medical. E.E.W. disclosed no relevant relationships.
References 1. McDonald JS, McDonald RJ, Carter RE, Katzberg RW, Kallmes DF, Williamson EE. Risk of intravenous contrast material–mediated acute kidney injury: a propensity scorematched study stratified by baseline-estimated glomerular filtration rate. Radiology 2014; 271(1):65–73. 2. McDonald RJ, McDonald JS, Bida JP, et al. Intravenous contrast material–induced nephropathy: causal or coincident phenomenon? Radiology 2013;267(1):106–118. 3. McDonald RJ, McDonald JS, Carter RE, et al. Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology 2014;273(3):714–725. 4. American College of Radiology. ACR Manual on Contrast Media. Version 9.2013. http:// www.acr.org/~/media/ACR/Documents/ PDF/QualitySafety/Resources/Contrast Manual/2013_Contrast_Media.pdf. Accessed December 30, 2014. 5. Stacul F, van der Molen AJ, Reimer P, et al. Contrast induced nephropathy: updated European Society of Urogenital Radiology Contrast Media Safety Committee guidelines. Eur Radiol 2011;21(12):2527–2541.
Perplexing Histologic Classification of Thymic Epithelial Tumor From Qijun Shen, MD,* Wenchao Hu, MD,† and Zhan Feng, MD‡ Department of Radiology, Hangzhou First People’s Hospital, Hangzhou, Zhejiang, China* 929
LETTERS TO THE EDITOR
Department of Radiology, Wenzhou Central Hospital, Wenzhou, Zhejiang, China† Department of Radiology, the First Affiliated Hospital of College of Medicine, Zhejiang University, 79 Qingchun Rd, Hangzhou, Zhejiang, China 310003‡ e-mail: [email protected] Editor: We read with interest the article by Dr Abdel Razek and colleagues in the October 2014 issue of Radiology (1). They report that the apparent diffusion coefficient is a reliable imaging parameter that may help characterize thymic epithelial tumors. We have two questions about pathologic classification in the article. First, 30 consecutive patients were included from 2005 to 2013. According to the statement in the original article, it is clear that the authors are still consulting the 1999 World Health Organization (WHO) histopathologic classification system of thymic epithelial tumors. In the new 2004 version, type C has been eliminated and neuroendocrine thymic tumor has been classified into the category of thymic carcinoma (2). Second, the WHO histopathologic classification of thymic epithelial tumors had created some degree of uncertainty and confusion among various investigators (3). Interobserver reproducibility for pathologists was poor, and there was overlap between some subtypes—especially in type AB and types B1 and B2–5 (4–6). Thus, in many cases, pathologic findings suggest two or even three subtypes of the tumor. Currently, many researchers divide the cases into low-risk thymomas and high-risk thymomas to reduce overlap between the subtypes. However, some cases still cannot be classified into the appropriate group, and it is a pity that most radiologic-pathologic correlation studies of thymic epithelial tumors failed to mention the influence of such a problem on the outcome. Conflicts exist between some results about the correlation between computed tomographic (CT) appearance and WHO histopathologic classification of thymic epithelial tumors, and these 930
may be due in part to the limitations of the WHO classification scheme according to Benveniste et al (7). So, we wish radiologists pay enough attention to the histologic classification of thymic epithelial tumors. Disclosures of Conflicts of Interest: Q.S. disclosed no relevant relationships. W.H. disclosed no relevant relationships. Z.F. disclosed no relevant relationships.
References 1. Abdel Razek AA, Khairy M, Nada N. Diffusion-weighted MR imaging in thymic epithelial tumors: correlation with World Health Organization classification and clinical staging. Radiology 2014;273(1):268–275. 2. Travis WD, Brambilla E, Muller-Hermelink HK, Harris CC, eds. Pathology and genetics of tumors of the lung, pleura, thymus and heart. Lyon, France: IARC Press, 2004. 3. Suster S, Moran CA. Problem areas and inconsistencies in the WHO classification of thymoma. Semin Diagn Pathol 2005;22(3): 188–197. 4. Suster S, Moran CA. Histologic classification of thymoma: the World Health Organization and beyond. Hematol Oncol Clin North Am 2008;22(3):381–392. 5. Suster S, Moran CA. Thymoma classification: current status and future trends. Am J Clinical Pathol 2006;125(4):542–554. 6. Rieker RJ, Hoegel J, Morresi-Hauf A, et al. Histologic classification of thymic epithelial tumors: comparison of established classification schemes. Int J Cancer 2002; 98(6):900–906. 7. Benveniste MF, Rosado-de-Christenson ML, Sabloff BS, Moran CA, Swisher SG, Marom EM. Role of imaging in the diagnosis, staging, and treatment of thymoma. Radiographics 2011;31(7):1847–1861; discussion 1861–1863.
Response From Ahmed Abdel Khalek Abdel Razek, MD Department of Diagnostic Radiology, Mansoura Faculty of Medicine, Mansoura, Egypt 13351 e-mail: [email protected] I thank Dr Shen and colleagues for their comments. In our study, we applied the recent 2004 WHO classification (1) for the assessment of thymic epithelial tu-
mors (2). We classified thymic epithelial tumors into thymoma and thymic carcinoma according to the 2004 WHO classification. Unfortunately, we misclassified thymic carcinoma as equivalent to type C in the old WHO classification of thymic tumors. In our study, only one expert pathologist performed the histopathologic examination. We could not assess the interobserver variability of the pathologic classification. The recent 2004 WHO classification has gained acceptance by pathologists in the recent years (3); however, there is still some overlap in the subtype classification of thymic epithelial tumors among pathologists (4). Future multicenter studies with larger numbers of patients that assess the intra- and interobserver variability of the pathologic classification and its relationship to the apparent diffusion coefficient may lead to better evaluation and characterization of the subtypes of thymic epithelial tumors with diffusionweighted magnetic resonance (MR) imaging in the future. Finally, we suggest that some conflicting results on the correlation between CT appearance and the WHO classification of thymic epithelial tumors may be related to the fact that CT studies depend on qualitative parameters, whereas diffusion-weighted MR imaging is a quantitative parameter of the apparent diffusion coefficient. Hopefully, further studies in a large number of patients that correlate findings from CT and diffusion-weighted MR imaging with pathologic subtypes of thymic epithelial tumors will decrease the conflicting results and improve the results. Disclosures of Conflicts of Interest: disclosed no relevant relationships.
References 1. Travis WD, Brambilla E, Muller-Hermelink HK, Harris CC, eds. Pathology and genetics of tumors of the lung, pleura, thymus and heart. Lyon, France: IARC Press, 2004. 2. Abdel Razek AA, Khairy M, Nada N. Diffusion-weighted MR imaging in thymic epithelial tumors: correlation with World Health Organization classification and clinical staging. Radiology 2014;273(1):286–275.
radiology.rsna.org n Radiology: Volume 275: Number 3—June 2015
LETTERS TO THE EDITOR
3. Marino M, Piantelli M. Immunohistochemistry of thymic epithelial tumors as a tool in translational research. Thorac Surg Clin 2011;21(1):33–46. 4. Honglin Y, Jun D, Zhenfeng L, et al. The correlation of the World Health Organization histologic classification of thymic epithelial tumors and its prognosis: a clinicopathologic study of 108 patients from China. Int J Surg Pathol 2009;17(3):255–261.
Intravenous Contrast Material and Acute Kidney Injury: A Need for Caution From Aibek E. Mirrakhimov, MD,* and Erkin M. Mirrakhimov, MD† Saint Joseph Hospital, Department of Internal Medicine, 2900 N Lake Shore Dr, Chicago, Ill 60657* e-mail: [email protected] Kyrgyz State Medical Academy, Bishkek, Kyrgyzstan† Editor: We read with great interest the article by Dr McDonald and colleagues (1) in the December 2014 issue of Radiology. In this single-center study, authors retrospectively analyzed the effect of computed tomography (CT) performed with and without contrast material on the incidence of acute kidney injury (AKI), the need for dialysis, or death within 30 days after intravenous contrast material administration. To minimize the risk of selection bias, the researchers used propensity score–based 1:1 matching in their study. It is interesting to note that intravenous contrast material administration was not associated with the risk of AKI, the need for dialysis, or death within 30 days in this study with a large sample. Indeed, in a similar retrospective study by Prasad et al (2) published in the same issue of Radiology, the administration of intravenous contrast material was only associated with the low risk of AKI. We praise the authors of this study for raising the possibility that intravenous contrast material administration for CT studies is not associated with the risk of AKI or dialysis. Indeed, if it is true, our practice should change dramatically and we should eliminate
the entity of contrast material–induced nephropathy (CIN). However, we believe that at least one important variable was not addressed in this study. Dr McDonald and colleagues did not specify whether patients at risk for CIN received preventive measures such as intravenous hydration with isotonic fluids and/or oral N-acetylcysteine, which is a common practice worldwide (3,4). Thus, it is unclear whether the lack of association between AKI and intravenous contrast material was due to preventive measures undertaken or the inherent lack of nephrotoxicity of intravenous contrast material. To answer this question, we will need a representative prospective randomized study evaluating the risk of CIN among patients at risk who received preventive measures and those who did not. However, such study is unlikely to be done due to several reasons, with the major reason being ethics. Given the very high cost of care for CIN and the relative inexpensiveness of preventive measures, we advise assessing the need for intravenous contrast material in every patient at risk and using tools to minimize the risk if intravenous contrast material is to be administered. Disclosures of Conflicts of Interest: A.E.M. disclosed no relevant relationships. E.M.M. disclosed no relevant relationships.
References 1. McDonald RJ, McDonald JS, Carter RE, et al. Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology 2014;273(3):714–725. 2. Prasad V, Gandhi D, Stokum C, Miller T, Jindal G. Incidence of contrast material-induced nephropathy after neuroendovascular procedures. Radiology 2014;273(3):853–858. 3. Seeliger E, Sendeski M, Rihal CS, Persson PB. Contrast-induced kidney injury: mechanisms, risk factors, and prevention. Eur Heart J 2012;33(16):2007–2015. 4. Hosseinjani H, Moghaddas A, Khalili H. Nacetylcysteine for the prevention of non-contrast media agent-induced kidney injury: from preclinical data to clinical evidence. Eur J Clin Pharmacol 2013;69(7):1375–1390.
Radiology: Volume 275: Number 3—June 2015 n radiology.rsna.org
Response From Robert J. McDonald, MD, PhD,* Jennifer S. McDonald, PhD,* Rickey E. Carter, PhD,† Robert P. Hartman, MD,* Richard W. Katzberg, MD,‡ David F. Kallmes, MD,*§ and Eric E. Williamson, MD* Departments of Radiology,* Health Sciences Research,† and Neurosurgery,§ College of Medicine, Mayo Clinic, 200 1st St SW, Rochester, MN 55905 e-mail: [email protected] Department of Radiology, Medical University of South Carolina, Charleston, SC‡ We appreciate Drs Mirrakhimovs’ interest and critical assessment of our recent article on CIN. In our recent propensity score–matched controlled cohort study, we were unable to identify iodinated contrast material as an independent risk factor for AKI, emergent dialysis, or mortality within 30 days of exposure (1). The subset of study patients who developed AKI were at significantly higher risk for both dialysis and mortality, but the risks of these adverse outcomes were not significantly different between contrast material–exposed and unexposed patient groups. Intravenous fluids were excluded from our propensity score model of AKI risk for several reasons. First, a central tenant of propensity score model generation is that all covariates must be present before the treatment of interest is administered; inclusion of a variable after treatment invalidates the logistic model by causal confounding (ie, is the intravenous contrast material or fluid responsible for the change in serum creatinine level?). Intravenous fluid administration data extracted by means of automated software is too coarse to reliably ascertain the exact time of fluid administration near the time of CT. More exhaustive manual review of these records is needed to avoid this source of confounding. Second, there are conflicting data with respect to prevention of CIN with intravenous fluid–based renoprotective treatments 931
