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• W1897968716 abstract "HomeHypertensionVol. 52, No. 4Response to the Malignant Hypertension-Thrombotic Microangiopathy Link Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse to the Malignant Hypertension-Thrombotic Microangiopathy Link Bert-Jan H. van den Born and Gert A. van Montfrans Bert-Jan H. van den BornBert-Jan H. van den Born Departments of Internal and Vascular Medicine, Academic Medical Centre, Amsterdam, The Netherlands Search for more papers by this author and Gert A. van MontfransGert A. van Montfrans Departments of Internal and Vascular Medicine, Academic Medical Centre, Amsterdam, The Netherlands Search for more papers by this author Originally published11 Aug 2008https://doi.org/10.1161/HYPERTENSIONAHA.108.118836Hypertension. 2008;52:e33Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 11, 2008: Previous Version 1 We read with interest the comments by Thachil1 regarding our article on the association between ADAMTS-13 and thrombotic microangiopathy (TMA) in malignant hypertension.2 Thachil1 proposes a role for NO as a link between malignant hypertension and TMA. We believe that the lack of NO may be an important mediator, but believe it is not the “missing link” between malignant hypertension and TMA. Although previous experiments have shown that administration of the endothelial NO synthase inhibitor NG-nitro-l-arginine methyl ester results in more severe tissue injury and end-organ dysfunction in various animal models of TMA,3,4 the effects of NG-nitro-l-arginine methyl ester were only observed on a permissive background for the development of TMA. For example, in the study by Sethi et al,4 administration of NG-nitro-l-arginine methyl ester led to the development of TMA in mice that were transgenic for the human renin and angiotensinogen genes. The same degree of tissue injury was also observed when these mice were placed on a high-salt diet. Administration of NG-nitro-l-arginine methyl ester in control animals did not lead to tissue injury and fibrin thrombi associated with TMA.We agree that free hemoglobin may be important as an NO scavenger in situations where endothelial damage is associated with severe hemolysis (eg, sickle cell disease). In the TMA of malignant hypertension, hemolysis is usually not a prominent feature, because only a few fragmented red blood cells are present.5 In our study, free hemoglobin levels did not differ between patients with and without TMA, nor was there an association between free hemoglobin and the severity of TMA.Although the sequence of events that lead to TMA in malignant hypertension are still incompletely understood, a further increase in blood pressure, by whatever mechanism, appears to be necessary to provoke TMA in experimental models.6 Treatment directed at lowering blood pressure, either via NO-dependent or via NO-independent mechanisms, leads to resolution of the TMA associated with malignant hypertension and helps to restore organ function. Therefore, the damage to the endothelium and vascular wall elicited by the high arterial pressures may be the trigger that leads to coagulation activation and TMA. This includes the expression of large amounts of prothrombogenic von Willebrand factor (VWF) multimers in the circulation. As discussed in our article, even low-normal levels of ADAMTS-13 have been associated with the appearance of ultra large VWF multimers in situations of endothelial stimulation, possibly because of a misbalance between the amount of VWF and its cleaving protease. We were unable to detect ultra large VWF multimers, because our technique, which was developed to demonstrate decreases in VWF size, may not have been sensitive enough to detect more subtle increases in VWF size. Other than a role for VWF and ADAMTS-13, we agree with the author that other (coagulation) factors that are released on endothelial damage and injury to the vascular wall may be important in the development of TMA. In addition to lowering blood pressure, therapy aimed at inhibiting vital procoagulant pathways in the acute phase of this condition may assist in further ameliorating the vascular damage and organ dysfunction observed in this condition.DisclosuresNone.1 Thachil J. The malignant hypertension-thrombotic microangiopathy link. Hypertension. 2008; 52: e32.LinkGoogle Scholar2 van den Born BJ, van der Hoeven NV, Groot E, Lenting PJ, Meijers JC, Levi M, van Montfrans GA. Association between thrombotic microangiopathy and reduced ADAMTS13 activity in malignant hypertension. Hypertension. 2008; 51: 862–866.LinkGoogle Scholar3 Shao J, Miyata T, Yamada K, Hanafusa N, Wada T, Gordon KL, Inagi R, Kurokawa K, Fujita T, Johnson RJ, Nangaku M. Protective role of nitric oxide in a model of thrombotic microangiopathy in rats. J Am Soc Nephrol. 2001; 12: 2088–2097.CrossrefMedlineGoogle Scholar4 Sethi S, Iida S, Sigmund CD, Heistad DD. Renal thrombotic microangiopathy in a genetic model of hypertension in mice. Exp Biol Med (Maywood). 2006; 231: 196–203.CrossrefMedlineGoogle Scholar5 van den Born BJ, Honnebier UP, Koopmans RP, van Montfrans GA. Microangiopathic hemolysis and renal failure in malignant hypertension. Hypertension. 2005; 45: 246–251.LinkGoogle Scholar6 Gavras H, Brunner HR, Laragh JH, Vaughan ED Jr, Koss M, Cote LJ, Gavras I. Malignant hypertension resulting from deoxycorticosterone acetate and salt excess: role of renin and sodium in vascular changes. Circ Res. 1975; 36: 300–309.CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetails October 2008Vol 52, Issue 4 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.108.118836 Originally publishedAugust 11, 2008 PDF download Advertisement SubjectsEndothelium/Vascular Type/Nitric Oxide" @default.
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