Response to Letter Regarding Article, “Association of Chronic Kidney Disease With Cerebral Microbleeds in Patients With Primary Intracerebral Hemorrhage”
We thank Dr Tsuda for his interest in our recently published article. As he alluded to in his letter, nitrous oxide exerts a powerful influence on the regulation of glomerular filtration rate,1 and mounting evidence suggests that initial renal endothelial damage may lead to superoxide scavenging of nitric oxide, ultimately leading to diffuse severe endothelial dysfunction, including within the cerebrovascular bed.2 However, it must be noted that results from various studies on endogenous nitric oxide conflict, with some studies suggesting a deficiency in nitric oxide with chronic kidney disease,3 and others reporting upregulated nitrous oxide production.4
About the possible interplay of chronic kidney disease, nitric oxide production, and race, reduced nitric oxide bioavailability in the vascular wall may indeed be an important contributor to the observed differences in function and mechanical properties of resistance arteries between blacks and whites,5 but we did not collect data on endothelial function or plasma NO-metabolite levels in the Differences in the Imaging of Primary Hemorrhage based on Ethnicity or Race (DECIPHER) cohort and therefore cannot specifically address this issue directly in the current data set. We share Dr Tsuda’s enthusiasm for future studies aimed at exploring inadequate nitric oxide production as a potential explanation for racial disparities in the influence of chronic kidney disease on vascular brain injury (including cerebral microbleeds).
Bruce Ovbiagele, MD, MSc, MAS
Department of Neurosciences
Medical University of South Carolina
Chelsea S. Kidwell, MD
Department of Neurology
University of Arizona
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- © 2013 American Heart Association, Inc.