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Letter by Tsuda Regarding Article, “Association of Chronic Kidney Disease With Cerebral Microbleeds in Patients With Primary Intracerebral Hemorrhage”
To the Editor: We read with great interest the article by Ovbiagele et al1 dealing with the relationship between chronic kidney disease (CKD) and cerebral microbleeds (CMBs) in patients with a recent history of intracerebral hemorrhage. The results of their study demonstrated that baseline CKD with low estimated glomerular filtration rate was associated with a higher presence and number of CMBs, even after adjusting for confounders, including blood pressure level on stroke admission. In addition, when broken down by race, CKD was particularly linked to the presence and number in black patients, but not in non-Hispanic white patients. The authors proposed that low estimated glomerular filtration rate might be a CMB risk marker or potential therapeutic target for mitigating the development of CMBs and intracerebral hemorrhage, particularly in patients with black race. Epidemiological studies have shown that CKD may be associated with increased risk for both cardiovascular and cerebrovascular outcomes. It was demonstrated that, in young patients with acute ischemic stroke, lower estimated glomerular filtration rate values, even in the normal range, might predict the presence of moderate to severe white matter disease in the brain.2 Accumulating evidence suggests that CKD might strongly be related to impaired endothelial function. It was proposed that the overall production of nitric oxide (NO) might be decreased in CKD, which could contribute to cardiovascular events and further damage of kidney function.3 Recently, we have shown that estimated glomerular filtration rate might be correlated with plasma NO-metabolites, and inversely correlated with plasma oxidative stress levels in hypertensive subjects,4 suggesting that reduced kidney function might be associated with endothelial dysfunction and increased oxidative stress. However, it was demonstrated that endothelium-dependent vasodilation was reduced in black individuals compared with white individuals,5 indicating
that racial differences might exist in endothelial function and NO bioavailability. In this context, we speculate that racial differences in NO production might partially explain the discrepancy between black patients and non-Hispanic white patients on the influences of CKD on CMBs in patients with intracerebral hemorrhage. Therefore, we would like to know whether endothelial function or plasma NO metabolite levels might be altered between black and nonHispanic white patients in the study of Ovbiagele et al. Further studies should be necessary to assess more precisely the relationship between CKD and endothelial function, and their contribution to the pathogenesis of CMBs in intracerebral hemorrhage.
Disclosures None.
Kazushi Tsuda, MD, FAHA Cardiovascular Medicine Cardiovascular and Metabolic Research Center Kansai University of Health Sciences Osaka, Japan 1. Ovbiagele B, Wing JJ, Menon RS, Burgess RE, Gibbons MC, Sobotka I, et al. Association of chronic kidney disease with cerebral microbleeds in patients with primary intracerebral hemorrhage. Stroke. 2013;44:2409–2413. 2. Steinicke R, Gaertner B, Grittner U, Schmidt W, Dichgans M, Heuschmann PU, et al. Kidney function and white matter disease in young stroke patients: analysis of the stroke in young fabry patients study population. Stroke. 2012;43:2382–2388. 3. Baylis C. Nitric oxide deficiency in chronic kidney disease. Am J Physiol Renal Physiol. 2008;294:F1–F9. 4. Tsuda K. Chronic kidney disease predicts impaired membrane microviscosity of red blood cells in hypertensive and normotensive subjects: an electron spin resonance study. Int Heart J. 2013;54:154–159. 5. Campia U, Choucair WK, Bryant MB, Waclawiw MA, Cardillo C, Panza JA. Reduced endothelium-dependent and -independent dilation of conductance arteries in African Americans. J Am Coll Cardiol. 2002;40:754–760.
(Stroke. 2013;44:e231.) © 2013 American Heart Association, Inc. Stroke is available at http://stroke.ahajournals.org
DOI: 10.1161/STROKEAHA.113.003341
Downloaded from http://stroke.ahajournals.org/ by guest on November 14, 2015 e231
Letter by Tsuda Regarding Article, ''Association of Chronic Kidney Disease With Cerebral Microbleeds in Patients With Primary Intracerebral Hemorrhage'' Kazushi Tsuda Stroke. 2013;44:e231; originally published online November 5, 2013; doi: 10.1161/STROKEAHA.113.003341 Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2013 American Heart Association, Inc. All rights reserved. Print ISSN: 0039-2499. Online ISSN: 1524-4628
The online version of this article, along with updated information and services, is located on the World Wide Web at: http://stroke.ahajournals.org/content/44/12/e231
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Stroke can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Stroke is online at: http://stroke.ahajournals.org//subscriptions/
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Letter by Tsuda Regarding Article, “Association of Chronic Kidney Disease With Cerebral Microbleeds in Patients With Primary Intracerebral Hemorrhage”
To the Editor: We read with great interest the article by Ovbiagele et al1 dealing with the relationship between chronic kidney disease (CKD) and cerebral microbleeds (CMBs) in patients with a recent history of intracerebral hemorrhage. The results of their study demonstrated that baseline CKD with low estimated glomerular filtration rate was associated with a higher presence and number of CMBs, even after adjusting for confounders, including blood pressure level on stroke admission. In addition, when broken down by race, CKD was particularly linked to the presence and number in black patients, but not in non-Hispanic white patients. The authors proposed that low estimated glomerular filtration rate might be a CMB risk marker or potential therapeutic target for mitigating the development of CMBs and intracerebral hemorrhage, particularly in patients with black race. Epidemiological studies have shown that CKD may be associated with increased risk for both cardiovascular and cerebrovascular outcomes. It was demonstrated that, in young patients with acute ischemic stroke, lower estimated glomerular filtration rate values, even in the normal range, might predict the presence of moderate to severe white matter disease in the brain.2 Accumulating evidence suggests that CKD might strongly be related to impaired endothelial function. It was proposed that the overall production of nitric oxide (NO) might be decreased in CKD, which could contribute to cardiovascular events and further damage of kidney function.3 Recently, we have shown that estimated glomerular filtration rate might be correlated with plasma NO-metabolites, and inversely correlated with plasma oxidative stress levels in hypertensive subjects,4 suggesting that reduced kidney function might be associated with endothelial dysfunction and increased oxidative stress. However, it was demonstrated that endothelium-dependent vasodilation was reduced in black individuals compared with white individuals,5 indicating
that racial differences might exist in endothelial function and NO bioavailability. In this context, we speculate that racial differences in NO production might partially explain the discrepancy between black patients and non-Hispanic white patients on the influences of CKD on CMBs in patients with intracerebral hemorrhage. Therefore, we would like to know whether endothelial function or plasma NO metabolite levels might be altered between black and nonHispanic white patients in the study of Ovbiagele et al. Further studies should be necessary to assess more precisely the relationship between CKD and endothelial function, and their contribution to the pathogenesis of CMBs in intracerebral hemorrhage.
Disclosures None.
Kazushi Tsuda, MD, FAHA Cardiovascular Medicine Cardiovascular and Metabolic Research Center Kansai University of Health Sciences Osaka, Japan 1. Ovbiagele B, Wing JJ, Menon RS, Burgess RE, Gibbons MC, Sobotka I, et al. Association of chronic kidney disease with cerebral microbleeds in patients with primary intracerebral hemorrhage. Stroke. 2013;44:2409–2413. 2. Steinicke R, Gaertner B, Grittner U, Schmidt W, Dichgans M, Heuschmann PU, et al. Kidney function and white matter disease in young stroke patients: analysis of the stroke in young fabry patients study population. Stroke. 2012;43:2382–2388. 3. Baylis C. Nitric oxide deficiency in chronic kidney disease. Am J Physiol Renal Physiol. 2008;294:F1–F9. 4. Tsuda K. Chronic kidney disease predicts impaired membrane microviscosity of red blood cells in hypertensive and normotensive subjects: an electron spin resonance study. Int Heart J. 2013;54:154–159. 5. Campia U, Choucair WK, Bryant MB, Waclawiw MA, Cardillo C, Panza JA. Reduced endothelium-dependent and -independent dilation of conductance arteries in African Americans. J Am Coll Cardiol. 2002;40:754–760.
(Stroke. 2013;44:e231.) © 2013 American Heart Association, Inc. Stroke is available at http://stroke.ahajournals.org
DOI: 10.1161/STROKEAHA.113.003341
Downloaded from http://stroke.ahajournals.org/ by guest on November 14, 2015 e231
Letter by Tsuda Regarding Article, ''Association of Chronic Kidney Disease With Cerebral Microbleeds in Patients With Primary Intracerebral Hemorrhage'' Kazushi Tsuda Stroke. 2013;44:e231; originally published online November 5, 2013; doi: 10.1161/STROKEAHA.113.003341 Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2013 American Heart Association, Inc. All rights reserved. Print ISSN: 0039-2499. Online ISSN: 1524-4628
The online version of this article, along with updated information and services, is located on the World Wide Web at: http://stroke.ahajournals.org/content/44/12/e231
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Stroke can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Stroke is online at: http://stroke.ahajournals.org//subscriptions/
Downloaded from http://stroke.ahajournals.org/ by guest on November 14, 2015
