Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/31978
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dc.contributor.authorRabbani, Naila-
dc.contributor.authorAdaikalakoteswari, Antonysunil-
dc.contributor.authorLarkin, James R-
dc.contributor.authorPanagiotopoulos, Sianna-
dc.contributor.authorMacIsaac, Richard J-
dc.contributor.authorYue, Dennis K-
dc.contributor.authorFulcher, Gregory R-
dc.contributor.authorRoberts, Matthew A-
dc.contributor.authorThomas, Merlin-
dc.contributor.authorEkinci, Elif I-
dc.contributor.authorThornalley, Paul J-
dc.date2022-
dc.date.accessioned2023-01-24T03:01:23Z-
dc.date.available2023-01-24T03:01:23Z-
dc.date.issued2022-12-21-
dc.identifier.citationInternational journal of molecular sciences 2022; 24(1): 152en_US
dc.identifier.issn1422-0067-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/31978-
dc.description.abstractAccumulation of advanced glycation endproducts (AGEs) is linked to decline in renal function, particularly in patients with diabetes. Major forms of AGEs in serum are protein-bound AGEs and AGE free adducts. In this study, we assessed levels of AGEs in subjects with and without diabetes, with normal renal function and stages 2 to 4 chronic kidney disease (CKD), to identify which AGE has the greatest progressive change with decline in renal function and change in diabetes. We performed a cross-sectional study of patients with stages 2-4 CKD, with and without diabetes, and healthy controls (n = 135). Nine protein-bound and free adduct AGEs were quantified in serum. Most protein-bound AGEs increased moderately through stages 2-4 CKD whereas AGE free adducts increased markedly. Methylglyoxal-derived hydroimidazolone MG-H1 free adduct was the AGE most responsive to CKD status, increasing 8-fold and 30-fold in stage 4 CKD in patients without and with diabetes, respectively. MG-H1 Glomerular filtration flux was increased 5-fold in diabetes, likely reflecting increased methylglyoxal glycation status. We conclude that serum MG-H1 free adduct concentration was strongly related to stage of CKD and increased in diabetes status. Serum MG-H1 free adduct is a candidate AGE risk marker of non-diabetic and diabetic CKD.en_US
dc.language.isoeng-
dc.subjectchronic kidney diseaseen_US
dc.subjectdiabetesen_US
dc.subjectestimated glomerular filtration rateen_US
dc.subjectglycationen_US
dc.subjectmethylglyoxalen_US
dc.titleAnalysis of Serum Advanced Glycation Endproducts Reveals Methylglyoxal-Derived Advanced Glycation MG-H1 Free Adduct Is a Risk Marker in Non-Diabetic and Diabetic Chronic Kidney Disease.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleInternational journal of molecular sciencesen_US
dc.identifier.affiliationDepartment of Basic Medical Science, College of Medicine, QU Health, Qatar University, Doha P.O. Box 2713, Qatar.en_US
dc.identifier.affiliationClinical Sciences Research Laboratories, Warwick Medical School, University of Warwick, University Hospital, Coventry CV2 2DX, UK.en_US
dc.identifier.affiliationClinical Sciences Research Laboratories, Warwick Medical School, University of Warwick, University Hospital, Coventry CV2 2DX, UK.en_US
dc.identifier.affiliationThe University of Melbourneen_US
dc.identifier.affiliationDepartment of Endocrinology & Diabetes, St Vincent's Hospital Melbourne, Fitzroy, VIC 3065, Australia.en_US
dc.identifier.affiliationDiabetes Centre, Royal Prince Alfred Hospital, Camperdown, NSW 2050, Australia.en_US
dc.identifier.affiliationDepartment of Diabetes, Endocrinology & Metabolism, Royal North Shore Hospital, St Leonards, NSW 2065, Australia.en_US
dc.identifier.affiliationEastern Health Clinical School, Monash University, Box Hill, VIC 3128, Australia.en_US
dc.identifier.affiliationDepartment of Diabetes, Monash University, Melbourne, VIC 3004, Australia.en_US
dc.identifier.affiliationEndocrinologyen_US
dc.identifier.affiliationClinical Sciences Research Laboratories, Warwick Medical School, University of Warwick, University Hospital, Coventry CV2 2DX, UK.en_US
dc.identifier.doi10.3390/ijms24010152en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0002-5819-2506en_US
dc.identifier.orcid0000-0003-2974-3388en_US
dc.identifier.orcid0000-0002-4169-8447en_US
dc.identifier.orcid0000-0001-8058-6977en_US
dc.identifier.orcid0000-0003-1665-3455en_US
dc.identifier.orcid0000-0003-0694-8743en_US
dc.identifier.orcid0000-0001-7659-443Xen_US
dc.identifier.pubmedid36613596-
dc.description.volume24-
dc.description.issue1-
local.name.researcherEkinci, Elif I
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
crisitem.author.deptOffice for Research-
crisitem.author.deptEndocrinology-
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