Cited by 377Chronic Kidney Disease and DiabetesRenal Diseases and GlomerulopathiesAdvanced Glycation End Products research

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Interaction of metabolic and haemodynamic factors in mediating experimental diabetic nephropathy

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Cooper, M. E.·2001·Diabetologia

DOI 10.1007/s001250100000

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Abstract

Diabetic nephropathy seems to occur as a result of an interaction of metabolic and haemodynamic factors. Glucose dependent pathways are activated within the diabetic kidney. These include increased oxidative stress, renal polyol formation and accumulation of advanced glycated end-products. Haemodynamic factors are also implicated in the pathogenesis of diabetic nephropathy and include increased systemic and intraglomerular pressure and activation of various vasoactive hormone pathways including the renin-angiotensin system and endothelin. These haemodynamic pathways, independently and with metabolic pathways, activate intracellular second messengers such as protein kinase C and MAP kinase, nuclear transcription factors such as NF-kappaB and various growth factors such as the prosclerotic cytokine, TGF-beta and the angiogenic, permeability enhancing growth factor, VEGF. These pathways ultimately lead to increased renal albumin permeability and extracellular matrix accumulation which results in increasing proteinuria, glomerulosclerosis and tubulointerstitial fibrosis. Therapeutic strategies involved in the management and prevention of diabetic nephropathy include currently available treatments such as intensified glycaemic control and antihypertensive agents, particularly those which interrupt the renin-angiotensin system. More novel strategies to influence vasoactive hormone action or to inhibit various metabolic pathways such as inhibitors of advanced glycation, specific protein kinase C isoforms and aldose reductase are at present under experimental and clinical investigation. It is predicted that multiple therapies will be required to reduce the progression of diabetic nephropathy.

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Self-citation

Authors: Cooper, M. E.
Affiliations: The University of Melbourne (AU)
Corresponding author: Cooper, M. E.
ORCID: Cooper, M. E.
Venue: Diabetologia
Publisher: Springer Science and Business Media LLC
Published: 2001-11-01
Volume: 44
Issue: 11
Pages: 1957-1972
ISSN: 0012-186X (ISSN-L)
1432-0428
DOI: 10.1007/s001250100000
OpenAlex: W1991427290
Cited by: 375
References: 14
Citations by year: 2026: 5 · 2025: 4 · 2024: 10 · 2023: 14 · 2022: 5 · 2021: 19 · 2020: 16 · 2019: 9 · 2018: 8 · 2017: 15 · 2016: 13 · 2015: 10 · 2014: 23 · 2013: 20 · 2012: 14
FWCI: 4.27
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
Locations: Diabetologia (publishedVersion)
PubMed (publishedVersion)
Funders: Kidney Health Australia
Topics: Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
Keywords: diabetic nephropathy, metabolic factors, oxidative stress, advanced glycation end products, intraglomerular pressure, renin-angiotensin system, endothelin, protein kinase C, mitogen-activated protein kinase, NF-κB, TGF-beta, vascular endothelial growth factor, albumin permeability, extracellular matrix accumulation, glomerulosclerosis, tubulointerstitial fibrosis, proteinuria, aldose reductase inhibitors, renin-angiotensin system inhibitors, antihypertensive therapy, glycemic control, pathogenesis
MeSH terms: Animals, Diabetic Nephropathies, Diabetic Retinopathy, Disease Models, Animal, Hemodynamics

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Interaction of metabolic and haemodynamic factors in mediating experimental diabetic nephropathy

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