Association of advanced glycation end products and chronic kidney disease with macroangiopathy in type 2 diabetes

Progression of skin autofluorescence of AGEs over 4 years in patients with type 1 diabetes

“…16 This age-dependent increase is slow,~+1%/year, so it cannot The first determinant of the progression of sAF in our patients was their initial mildly impaired eGFR, in line with the association between initial creatinine and follow-up sAF in T2D as shown by Gerrits et al 17 Independent of diabetes, the sAF is well known to increase with the duration, the stage, and the progression of CKD. [21][22][23] We have recently shown that sAF is related to the eGFR measured 10 years before in older subjects from the general population, 5 and it is increased in patients with T2D and CKD. 24 In type 1 diabetes, cross-sectional studies have shown associations of AER and estimated GFR with sAF.…”

Fluorophores advanced glycation end products (AGEs)-to-NADH ratio is predictor for diabetic chronic kidney and cardiovascular disease

“…Common pathways are suggested for the role of AGEs in developing both diabetic CKD and CVD. Rigalleau et al (2014) showed that AGEs were independent predictor for diabetic CKD and macroangiopathy. Recent findings indicate that increased AGEs levels in the vascular walls and cardiac tissue that were associated with the presence of CVD (Brodeur et al, 2014;Hanssen et al, 2015;Hofmann et al, 2014).…”

“…Galler et al (2003) described an agedependent increase of fluorescent AGEs in type 1 diabetes compared to controls, but in patients with T2DM confounding factors such as obesity must be taken into consideration. Other authors (Rigalleau et al, 2014) found that AGEs were associated with age, renal function and smoking habits, rather than to diabetes duration and control. Interestingly, when analyzing patients with or without diabetes, Kiuchi et al (2001) found that serum AGE were associated with mean value of HbA1c in the past four years, but not with recent HbA1c measurements, suggesting that long term poor glycemic control is related to AGEs production.…”

The AGE receptor, OST48 drives podocyte foot process effacement and basement membrane expansion in experimental diabetic kidney disease via promotion of endoplasmic reticulum stress

“…The kidneys are a major site of AGE detoxification through the filtration of circulating AGEs and their subsequent active uptake and excretion [15,16]. Therefore, AGE accumulation is seen in diabetic patients with chronic kidney disease [17,18]. Therapies which lower AGE accumulation have shown benefit in Phase II clinical trials for the treatment DKD in individuals with Type 2 diabetes [19].…”