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Uremic Toxicity of Advanced Glycation End Products in CKD
Andréa E M Stinghen1, Ziad A Massy2, Helen Vlassara3
1Institut National de la Santé et de la Recherche Médicale (INSERM) U-1088, Jules Verne University of Picardie, Amiens, France;
Abstract:
Advanced glycation end products (AGEs), a heterogeneous group of compounds formed by nonenzymatic glycation reactions between reducing sugars and amino acids, lipids, or DNA, are formed not only in the presence of hyperglycemia, but also in diseases associated with high levels of oxidative stress, such as CKD. In chronic renal failure, higher circulating AGE levels result from increased formation and decreased renal clearance. Interactions between AGEs and their receptors, including advanced glycation end product-specific receptor (RAGE), trigger various intracellular events, such as oxidative stress and inflammation, leading to cardiovascular complications. Although patients with CKD have a higher burden of cardiovascular disease, the relationship between AGEs and cardiovascular disease in patients with CKD is not fully characterized. In this paper, we review the various deleterious effects of AGEs in CKD that lead to cardiovascular complications and the role of these AGEs in diabetic nephropathy. We also discuss potential pharmacologic approaches to circumvent these deleterious effects by reducing exogenous and endogenous sources of AGEs, increasing the breakdown of existing AGEs, or inhibiting AGE-induced inflammation. Finally, we speculate on preventive and therapeutic strategies that focus on the AGE-RAGE axis to prevent vascular complications in patients with CKD.
Insights
Advanced glycation end products (AGEs) contribute to cardiovascular disease in chronic kidney disease (CKD). Targeting the AGE-RAGE pathway may prevent vascular complications in CKD patients.
Area of Science:
- Biochemistry
- Nephrology
- Cardiology
Background:
- Advanced glycation end products (AGEs) accumulate in chronic kidney disease (CKD) due to increased formation and reduced clearance.
- AGEs trigger oxidative stress and inflammation via receptors like RAGE, contributing to cardiovascular disease (CVD).
- The link between AGEs and CVD in CKD patients requires further characterization.
Purpose of the Study:
- To review the detrimental effects of AGEs in CKD, focusing on cardiovascular complications.
- To examine the role of AGEs in diabetic nephropathy.
- To discuss therapeutic strategies targeting AGEs and the AGE-RAGE axis.
Main Methods:
- Literature review of studies on AGEs, CKD, diabetic nephropathy, and cardiovascular disease.
- Analysis of mechanisms linking AGEs to inflammation and oxidative stress.
- Exploration of pharmacologic interventions targeting AGE formation, breakdown, and signaling.
Main Results:
- AGEs are implicated in CKD progression and diabetic nephropathy.
- AGE accumulation exacerbates oxidative stress and inflammation, driving cardiovascular complications in CKD.
- The AGE-RAGE axis is a key mediator of vascular damage.
Conclusions:
- AGEs play a significant role in the pathogenesis of cardiovascular disease in CKD.
- Pharmacologic strategies aimed at reducing AGE burden or blocking the AGE-RAGE pathway show promise.
- Targeting the AGE-RAGE axis offers a potential therapeutic avenue for preventing vascular complications in CKD.
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