Advanced Glycation End Products (AGEs) and Chronic Kidney Disease: Does the Modern Diet AGE the Kidney?

Since the 1980s, chronic kidney disease (CKD) affecting all ages has increased by almost 25%. This increase may be partially attributable to lifestyle changes and increased global consumption of a “western” diet, which is typically energy dense, low in fruits and vegetables, and high in animal prote...

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Bibliographic Details
Published in:Nutrients 2022-06, Vol.14 (13), p.2675
Main Authors: Fotheringham, Amelia K., Gallo, Linda A., Borg, Danielle J., Forbes, Josephine M.
Format: Article
Language:English
Subjects:
Advanced glycosylation end products
Age
Animal protein
Chemistry
Chronic illnesses
Cooking
Diabetes
Diabetes mellitus
Diet
Food
Food processing
Food sources
Glucose
Glycosylation
Hypertension
Immunology
Inflammation
Kidney diseases
Kidneys
Metabolism
Molecular weight
Mortality
Oxidative stress
Pandemics
Processed foods
Proteins
Renal function
Review
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Summary:Since the 1980s, chronic kidney disease (CKD) affecting all ages has increased by almost 25%. This increase may be partially attributable to lifestyle changes and increased global consumption of a “western” diet, which is typically energy dense, low in fruits and vegetables, and high in animal protein and ultra-processed foods. These modern food trends have led to an increase in the consumption of advanced glycation end products (AGEs) in conjunction with increased metabolic dysfunction, obesity and diabetes, which facilitates production of endogenous AGEs within the body. When in excess, AGEs can be pathological via both receptor-mediated and non-receptor-mediated pathways. The kidney, as a major site for AGE clearance, is particularly vulnerable to AGE-mediated damage and increases in circulating AGEs align with risk of CKD and all-cause mortality. Furthermore, individuals with significant loss of renal function show increased AGE burden, particularly with uraemia, and there is some evidence that AGE lowering via diet or pharmacological inhibition may be beneficial for CKD. This review discusses the pathways that drive AGE formation and regulation within the body. This includes AGE receptor interactions and pathways of AGE-mediated pathology with a focus on the contribution of diet on endogenous AGE production and dietary AGE consumption to these processes. We then analyse the contribution of AGEs to kidney disease, the evidence for dietary AGEs and endogenously produced AGEs in driving pathogenesis in diabetic and non-diabetic kidney disease and the potential for AGE targeted therapies in kidney disease.
ISSN:2072-6643
2072-6643
DOI:10.3390/nu14132675