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Advanced Glycation End Products (AGEs) and Chronic Kidney Disease: Does the Modern Diet AGE the Kidney?
Fotheringham, Amelia K; Gallo, Linda A; Borg, Danielle J; Forbes, Josephine M.
  • Fotheringham AK; Glycation and Diabetes Complications, Mater Research Institute, Translational Research Institute, The University of Queensland, Brisbane, QLD 4102, Australia.
  • Gallo LA; Faculty of Medicine, University of Queensland, Brisbane, QLD 4072, Australia.
  • Borg DJ; School of Health and Behavioural Science, University of the Sunshine Coast, Sippy Downs, QLD 4556, Australia.
  • Forbes JM; Faculty of Medicine, University of Queensland, Brisbane, QLD 4072, Australia.
Nutrients ; 14(13)2022 Jun 28.
Article in English | MEDLINE | ID: covidwho-1974857
ABSTRACT
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.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Uremia / Renal Insufficiency, Chronic Type of study: Prognostic study Topics: Long Covid Limits: Animals Language: English Year: 2022 Document Type: Article Affiliation country: Nu14132675

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Uremia / Renal Insufficiency, Chronic Type of study: Prognostic study Topics: Long Covid Limits: Animals Language: English Year: 2022 Document Type: Article Affiliation country: Nu14132675