Document Detail


The role of endothelial cell injury in thrombotic microangiopathy.
MedLine Citation:
PMID:  20843591     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Thrombotic microangiopathy (TMA) refers to a clinical and pathologic syndrome in which endothelial injury results in the manifestations of thrombocytopenia, microangiopathic hemolytic anemia, and kidney injury. A host of causes may induce endothelial injury and TMA, including enteric bacterial toxins, deficiency or dysfunction of complement regulatory proteins, deficiency or inhibition of von Willebrand factor-cleaving proteases, and factors that inhibit endothelial cell proliferation and turnover. This has led specialists to concentrate on these specific inciting factors in terms of designing treatment and management. However, a key and less recognized factor is the underlying level of endothelial health. Many persons with hereditary causes may remain disease free for years or may never develop disease. Others with acute inciting events, such as Escherichia coli O157 enteritis, never manifest TMA. Experimental studies document the importance of specific factors, such as endothelial nitric oxide levels, in helping protect animals from TMA. This suggests that one might approach the management of TMA not simply with specific treatments aimed at the underlying hereditary cause or inciting event, but rather at general measures that may improve overall endothelial health. We propose studies to determine whether interventions that improve endothelial health, such as the administration of angiotensin-converting enzyme inhibitors, statins, vitamin C, allopurinol, or nitric oxide-producing drugs, may be able to prevent TMA, even in persons with underlying hereditary conditions that otherwise would predispose them to these diseases.
Authors:
Ryan J Goldberg; Takahiko Nakagawa; Richard J Johnson; Joshua M Thurman
Publication Detail:
Type:  Case Reports; Journal Article; Research Support, N.I.H., Extramural     Date:  2010-09-16
Journal Detail:
Title:  American journal of kidney diseases : the official journal of the National Kidney Foundation     Volume:  56     ISSN:  1523-6838     ISO Abbreviation:  Am. J. Kidney Dis.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-24     Completed Date:  2010-12-16     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  8110075     Medline TA:  Am J Kidney Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1168-74     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Adult
Endothelium, Vascular / injuries*,  metabolism,  physiopathology*
Female
Hemolytic-Uremic Syndrome / physiopathology,  therapy
Humans
Nitric Oxide
Plasma Exchange
Thrombotic Microangiopathies / etiology,  physiopathology*,  therapy
Treatment Outcome
Grant Support
ID/Acronym/Agency:
DK-076690/DK/NIDDK NIH HHS; DK-52121/DK/NIDDK NIH HHS; R01 DK052121/DK/NIDDK NIH HHS; R01 DK052121-11/DK/NIDDK NIH HHS; R01 DK076690/DK/NIDDK NIH HHS; R01 DK076690-02/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
31C4KY9ESH/Nitric Oxide
Comments/Corrections

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