Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16907
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dc.contributor.authorLibianto, Renata-
dc.contributor.authorMoran, John-
dc.contributor.authorO'Callaghan, Christopher J-
dc.contributor.authorBaqar, Sara-
dc.contributor.authorChen, Angela X-
dc.contributor.authorBaker, Scott T-
dc.contributor.authorClarke, Michelle V-
dc.contributor.authorMacisaac, Richard J-
dc.contributor.authorJerums, George-
dc.contributor.authorEkinci, Elif I-
dc.date2017-09-16-
dc.date.accessioned2017-10-15T22:53:51Z-
dc.date.available2017-10-15T22:53:51Z-
dc.date.issued2018-01-
dc.identifier.citationClinical and Experimental Pharmacology and Physiology 2018; 45(1): 94-97en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/16907-
dc.description.abstractPrevious studies investigating the relationship between sodium intake and blood pressure have mostly relied on dietary recall and clinic blood pressure measurement. In this cross-sectional study, we aimed to investigate the relationship between 24h urinary sodium and potassium excretion, and their ratio, with 24h ambulatory blood pressure parameters including nocturnal blood pressure dipping in patients with type 1 and 2 diabetes. We report that in 116 patients with diabetes, systolic blood pressure was significantly predicted by the time of day, age, the interaction between dipping status with time, and 24h urinary sodium-to-potassium ratio (R2 =0.83) with a relative contribution of 53%, 21%, 20% and 6%, respectively. However, there was no interaction between urinary sodium-to-potassium ratio and dipping status.en_US
dc.subjectambulatory blood pressureen_US
dc.subjectdiabetesen_US
dc.subjectpotassiumen_US
dc.subjectsodiumen_US
dc.subjecturinary electrolytesen_US
dc.titleRelationship between Urinary Sodium-to-Potassium Ratio and Ambulatory Blood Pressure in Patients with Diabetes Mellitusen_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleClinical and Experimental Pharmacology and Physiologyen_US
dc.identifier.affiliationMedicine (University of Melbourne)en_US
dc.identifier.affiliationIntensive Care Unit, Queen Elizabeth Hospital, Adelaide, SA, Australiaen_US
dc.identifier.affiliationClinical Pharmacology and Therapeuticsen_US
dc.identifier.affiliationEndocrinologyen_US
dc.identifier.affiliationDepartment of Endocrinology, Flinders Medical Centre, Adelaide, SA, Australiaen_US
dc.identifier.affiliationDepartment of Endocrinology and Diabetes, St Vincent's Hospital Melbourne, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationMenzies School of Health Research, Darwin, NT, Australiaen_US
dc.identifier.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/28921626en_US
dc.identifier.doi10.1111/1440-1681.12852en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0003-2372-395Xen_US
dc.type.austinJournal Articleen_US
local.name.researcherBaker, Scott T
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptClinical Pharmacology and Therapeutics-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
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