Breaking old and new paradigms regarding urinary sodium in acute kidney injury diagnosis and management

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dc.contributor Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.author MACIEL, Alexandre Toledo FMUSP-HC
dc.date.issued 2013
dc.identifier.citation CRITICAL CARE, v.17, n.1, article ID 115, 2p, 2013
dc.identifier.issn 1466-609X
dc.identifier.uri http://observatorio.fm.usp.br/handle/OPI/4443
dc.description.abstract Urinary sodium (NaU) is one of the oldest parameters used in the evaluation of azotemia and oliguria. Over the past years, however, it has progressively been considered as obsolete and useless, especially in sepsis. It is common sense that NaU frequently does not correlate well with global renal blood flow. If intra-renal microcirculatory changes are more important in acute kidney injury (AKI) than changes in global renal blood flow, we speculate that decreases in NaU may be viewed as a possible marker of microcirculatory impairment in the kidneys. Recent findings by our group (some not yet published) in which sodium retentive capacity is preserved until advanced stages of AKI and the observation of decreases in NaU preceding increases in creatinine bring us to conclude that the new paradigm of abolishing NaU consideration from daily approaches to managing patients at risk for AKI must be reevaluated.
dc.language.iso eng
dc.publisher BIOMED CENTRAL LTD
dc.relation.ispartof Critical Care
dc.rights restrictedAccess
dc.subject.other acute-renal-failure; critically-ill patients; biochemistry; microscopy; biomarkers; azotemia; blood
dc.title Breaking old and new paradigms regarding urinary sodium in acute kidney injury diagnosis and management
dc.type article
dc.rights.holder Copyright BIOMED CENTRAL LTD
dc.identifier.doi 10.1186/cc11926
dc.identifier.pmid 23384365
dc.type.category editorial material
dc.type.version publishedVersion
hcfmusp.author MACIEL, Alexandre Toledo:HC:ICHC
hcfmusp.origem.id WOS:000320161900015
hcfmusp.origem.id 2-s2.0-84873525607
hcfmusp.publisher.city LONDON
hcfmusp.publisher.country ENGLAND
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dc.description.index MEDLINE
hcfmusp.citation.scopus 3
hcfmusp.citation.wos 3


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