Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/11043
Title: The clinical significance of hyperfiltration in diabetes.
Authors: Jerums, George;Premaratne, Erosha;Panagiotopoulos, Sianna;MacIsaac, Richard J
Affiliation: Endocrine Centre, Austin Health, Heidelberg Repatriation Hospital, Heidelberg West, Victoria, Australia
Issue Date: 23-May-2010
Citation: Diabetologia 2010; 53(10): 2093-104
Abstract: Glomerular filtration rate is commonly elevated in early diabetes and patients with this symptom are arbitrarily considered to have hyperfiltration. The prevalence of hyperfiltration in type 1 diabetes varies from less than 25% to more than 75%. The corresponding figures in type 2 diabetes are significantly lower, ranging between 0% and more than 40%. Several factors, methodological and biological, may contribute to the wide variation in estimates of hyperfiltration prevalence. Methodological differences in measurement and evaluation of GFR apply in particular to the handling of plasma disappearance curves of filtration markers. Biological factors that may influence GFR in the hyperfiltration range include glycaemic control, diabetes duration, BMI, sex, pubertal status in type 1 diabetes and age in type 2 diabetes. Hyperglycaemia may influence GFR and albuminuria, and may therefore confound the evaluation of hyperfiltration as an independent risk factor for diabetic nephropathy. Adequate assessment of the relationship between glycaemic control, GFR and AER therefore requires serial measurements of all three variables followed by multivariate analysis. A recent meta-analysis of ten type 1 diabetes studies concluded that the presence of hyperfiltration at baseline more than doubled the risk of developing micro- or macroalbuminuria at follow-up. However, not all studies allowed for confounding factors or regression dilution bias. Future studies will therefore need to address the independent role of hyperfiltration, not only in the evolution of albuminuria, but also in the subsequent decline of GFR.
Internal ID Number: 20496053
URI: http://ahro.austin.org.au/austinjspui/handle/1/11043
DOI: 10.1007/s00125-010-1794-9
ORCID: 0000-0002-0845-0001
URL: http://www.ncbi.nlm.nih.gov/pubmed/20496053
Type: Journal Article
Subjects: Diabetes Mellitus, Type 1.physiopathology
Diabetes Mellitus, Type 2.physiopathology
Diabetic Nephropathies.physiopathology
Glomerular Filtration Rate.physiology
Humans
Kidney Glomerulus.physiopathology
Appears in Collections:Journal articles

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