Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2021 Dec 15;10(12):1994.
doi: 10.3390/antiox10121994.

AGEs and sRAGE Variations at Different Timepoints in Patients with Chronic Kidney Disease

Paolo Molinari  1 , Lara Caldiroli  1 , Elena Dozio  2 , Roberta Rigolini  3 , Paola Giubbilini  3 , Massimiliano M Corsi Romanelli  2   3 , Piergiorgio Messa  1   4 , Simone Vettoretti  1
Affiliations

AGEs and sRAGE Variations at Different Timepoints in Patients with Chronic Kidney Disease

Paolo Molinari et al. Antioxidants (Basel). .

Abstract

Patients with chronic kidney disease (CKD) are affected by enhanced oxidative stress and chronic inflammation, and these factors may contribute to increase advanced glycation end-products (AGEs). In this study we quantified AGEs and soluble receptors for AGE (sRAGE) isoforms and evaluated the association between their variations and eGFR at baseline and after 12 months. We evaluated 64 patients. AGEs were quantified by fluorescence intensity using a fluorescence spectrophotometer, and sRAGE by ELISA. Median age was 81 years, male patients accounted for 70%, 63% were diabetic, and eGFR was 27 ± 10 mL/min/1.73 m2. At follow up, sRAGE isoforms underwent a significant decrement (1679 [1393;2038] vs. 1442 [1117;2102], p < 0.0001), while AGEs/sRAGE ratios were increased (1.77 ± 0.92 vs. 2.24 ± 1.34, p = 0.004). Although AGEs and AGEs/sRAGE ratios were inversely related with eGFR, their basal values as well their variations did not show a significant association with eGFR changes. In a cohort of patients with a stable clinical condition at 1 year follow-up, AGEs/sRAGE was associated with renal function. The lack of association with eGFR suggests that other factors can influence its increase. In conclusion, AGEs/sRAGE can be an additional risk factor for CKD progression over a longer time, but its role as a prognostic tool needs further investigation.

Keywords: advanced glycation end-products (AGE); chronic kidney disease (CKD); cleaved RAGE (cRAGE); endogenous secretory RAGE (esRAGE); soluble receptor for AGE (sRAGE).

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Population selection criteria.
Figure 2
Figure 2
Distribution of advanced glycation end products (AGEs), and soluble receptor for AGE (sRAGE) and its isoforms’ distribution at baseline and follow-up. BS: baseline; FU: follow-up; AGEs: advanced glycation end products; sRAGE: soluble receptor for advanced glycation end products receptor; esRAGE: endogenous secretory receptor for AGE; cRAGE: clivated receptor for AGE.
Figure 3
Figure 3
Linear regression analyses between the differences (basal–FU) of advanced glycation end products (ΔAGEs), soluble receptor for AGEs (ΔsRAGE) and its isoforms (ΔesRAGE and ΔcRAGE) and eGFR (ΔeGFR). Δ: difference; BS: baseline; FU: follow-up; AGEs: advanced glycation end products; sRAGE: soluble receptor for advanced glycation end products receptor; esRAGE: spliced soluble receptor for AGE; cRAGE: cleaved receptor for AGE.
Figure 4
Figure 4
Distribution of advanced glycation end products/soluble receptor for advanced glycation end products ratio. AGEs/sRAGE at baseline and follow-up (panel (A)). Linear regression analysis between the differences (basal–FU) of ΔAGEs/ΔsRAGE and eGFR (ΔeGFR) (panel (B)). BS: baseline; FU: follow-up; AGEs: advanced glycation end products; sRAGE: soluble receptor for advanced glycation end products receptor; eGFR: estimated glomerular filtration rate.
See this image and copyright information in PMC

References

    1. Ahmed N. Advanced glycation endproducts--role in pathology of diabetic complications. Diabetes Res. Clin. Pract. 2005;67:3–21. doi: 10.1016/j.diabres.2004.09.004. - DOI - PubMed
    1. Goldin A., Beckman J.A., Schmidt A.M., Creager M.A. Advanced glycation end products: Sparking the development of diabetic vascular injury. Circulation. 2006;114:597–605. doi: 10.1161/CIRCULATIONAHA.106.621854. - DOI - PubMed
    1. Dozio E., Vettoretti S., Lungarella G., Messa P., Romanelli M.M.C. Sarcopenia in Chronic Kidney Disease: Focus on Advanced Glycation End Products as Mediators and Markers of Oxidative Stress. Biomedicines. 2021;9:405. doi: 10.3390/biomedicines9040405. - DOI - PMC - PubMed
    1. Bucala R., Vlassara H. Advanced glycosylation end products in diabetic renal and vascular disease. Am. J. Kidney Dis. 1995;26:875–888. doi: 10.1016/0272-6386(95)90051-9. - DOI - PubMed
    1. Shimoike T., Inoguchi T., Umeda F., Nawata H., Kawano K., Ochi H. The meaning of serum levels of advanced glycosylation end products in diabetic nephropathy. Metabolism. 2000;49:1030–1035. doi: 10.1053/meta.2000.7738. - DOI - PubMed