Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12057
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dc.contributor.authorMacisaac, Richard Jen
dc.contributor.authorEkinci, Elif Ien
dc.contributor.authorJerums, Georgeen
dc.date.accessioned2015-05-16T01:42:10Z-
dc.date.available2015-05-16T01:42:10Z-
dc.date.issued2014-02-01en
dc.identifier.citationAmerican Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation; 63(2 Suppl 2): S39-62en
dc.identifier.govdoc24461729en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/12057en
dc.description.abstractDiabetic kidney disease (DKD) occurs in 25%-40% of patients with diabetes. Given the dual problems of a significant risk of progression from DKD to end-stage renal disease (ESRD) and increased cardiovascular morbidity and mortality, it is important to identify patients at risk of DKD and ESRD and initiate protective renal and cardiovascular therapies. The importance of preventive therapy is emphasized further by worldwide increases in the incidence of diabetes. This review summarizes the evidence regarding the prognostic value and benefits of targeting established and novel risk markers for DKD development and progression. Family history of DKD, smoking history, and glycemic, blood pressure, and plasma lipid level control are established factors for identifying people at greatest risk of DKD development and progression. Absolute albumin excretion rate (AER) and glomerular filtration rate (GFR) measurements also are important, although AER categorization generally lacks the necessary specificity and sensitivity, and estimates of declining GFR are compromised by methodological limitations for GFRs in the normal-to-high range. Emerging risk markers for progressive loss of kidney function include markers of oxidation and inflammation, profibrotic cytokines, uric acid, advanced glycation end products, functional and structural markers of vascular dysfunction, kidney structural changes, and tubular biomarkers. Among these, the most promising are serum uric acid and soluble tumor necrosis factor receptor (type 1 and type 2) levels, especially in relation to GFR changes. At present, these can only be considered as risk markers because they only identify an individual at increased risk of progressive DKD and not necessarily related to the causal pathway promoting kidney damage. Further work is needed to establish whether modulating these factors improves the prognosis in DKD. Although change in urinary peptidome levels also is a promising marker, there currently is neither a clinical assay nor adequate studies defining its prognostic value. Until these or other novel markers become available for clinical use, predictive accuracy often may be increased with greater attention to established markers.en
dc.language.isoenen
dc.subject.otherDiabetes mellitusen
dc.subject.otherbiomarkeren
dc.subject.otherdisease trajectoryen
dc.subject.otherend-stage renal disease (ESRD)en
dc.subject.otherrisk factoren
dc.subject.otherBiological Markers.metabolismen
dc.subject.otherDiabetic Nephropathies.diagnosis.metabolismen
dc.subject.otherDisease Progressionen
dc.subject.otherHumansen
dc.subject.otherKidney.physiopathologyen
dc.subject.otherKidney Function Testsen
dc.subject.otherPrognosisen
dc.subject.otherRisk Factorsen
dc.titleMarkers of and risk factors for the development and progression of diabetic kidney disease.en
dc.typeJournal Articleen
dc.identifier.journaltitleAmerican journal of kidney diseases : the official journal of the National Kidney Foundationen
dc.identifier.affiliationDepartment of Endocrinology & Diabetes, St Vincent's Hospital Melbourne, Victoria, Australiaen
dc.identifier.affiliationMenzies School of Health Research, Darwin, Australiaen
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationEndocrine Centre, Heidelberg Repatriation Hospital, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1053/j.ajkd.2013.10.048en
dc.description.pagesS39-62en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/24461729en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
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