| Low hydrogen sulphide and chronic kidney disease: a dangerous liaison. | |
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MedLine Citation:
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PMID: 22323660 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Hydrogen sulphide, H(2)S, is a gaseous compound involved in a number of biological responses, e.g. blood pressure, vascular function and energy metabolism. In particular, H(2)S is able to lower blood pressure, protect from injury in models of ischaemia-reperfusion and induce a hypometabolic state. In chronic kidney disease (CKD), low plasma hydrogen sulphide levels have been established in humans and in animal models. The enzymes involved in its production are cystathionine β-synthase, cystathionine γ-lyase and 3-mercaptopyruvate sulphurtransferase. The mechanisms for H(2)S decrease in CKD are related to the reduced gene expression (demonstrated in uraemic patient blood cells) and decreased protein levels (in tissues such as liver, kidney, brain in a CKD rat model). In the present Nephrol Dial Transplant issue, in fact, Aminzadeh and Vaziri document that the alterations in this pathway complicate the uraemic state and are linked to CKD progression. They furnish a time frame in CKD and record enzyme tissue distribution. It remains to be established if low H(2)S is causally linked to CKD progression and if interventions aimed to restore the status quo ante are able to modify this picture. |
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Authors:
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Alessandra F Perna; Diego Ingrosso |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association Volume: 27 ISSN: 1460-2385 ISO Abbreviation: Nephrol. Dial. Transplant. Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-02-10 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8706402 Medline TA: Nephrol Dial Transplant Country: England |
Other Details:
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Languages: eng Pagination: 486-93 Citation Subset: IM |
Affiliation:
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Correspondence and offprint requests to: Alessandra F. Perna; E-mail: alessandra.perna@unina2.it. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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