Skip to main content
Log in

The strong relation between post-hemodialysis blood methylglyoxal levels and post-hemodialysis blood glucose concentration rise

  • Original Article
  • Published:
Clinical and Experimental Nephrology Aims and scope Submit manuscript

Abstract

Background

Hemodialysis is known to decrease blood glucose concentration (BGC), insulin, and methylglyoxal levels. However, the effects of decreases in these factors on the increase in post-hemodialysis BGC remain unknown. This study identifies the effects of hemodialysis-induced changes in concentrations of these elements on post-hemodialysis BGC.

Methods

Study subjects included seventeen insulin-treated diabetes patients receiving hemodialysis. The fluctuations in BGC on hemodialysis-treatment days and non-hemodialysis-treatment days were evaluated using a continuous glucose monitoring system. BGC was evaluated before breakfast, before starting hemodialysis, at the end of hemodialysis, 1 h post-hemodialysis (lunch), and 6 h post-hemodialysis (dinner). BGC, insulin, and methylglyoxal levels were measured at the start and end of hemodialysis. This study also evaluated the changes in the concentrations of glucose and insulin in the arterial line and the venous line during hemodialysis.

Results

Hemodialysis decreases BGC, insulin, and methylglyoxal levels. Concentrations of glucose and insulin in the arterial line gradually decreased during dialysis, while concentrations in the venous line approached their original concentrations in the dialysis solution. BGC rose sharply after eating lunch 1 h post-hemodialysis. The blood glucose, insulin, and methylglyoxal concentrations at the end of hemodialysis were associated with the M values and the mean amplitude of glycemic excursion values between before lunch and dinner. In particular, methylglyoxal concentration at the end of hemodialysis was strongly related to the post-hemodialysis increase in BGC.

Conclusion

Hemodialysis-induced decreases in methylglyoxal concentrations and methylglyoxal concentration at the end of hemodialysis influence post-hemodialysis fluctuations in BGC.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1

Similar content being viewed by others

References

  1. Abe M, Kaizu K, Matsumoto K. Evaluation of the hemodialysis-induced changes in plasma glucose and insulin concentrations in diabetic patients: comparison between the hemodialysis and non-hemodialysis days. Ther Apher Dial. 2007;11:288–95.

    Article  CAS  PubMed  Google Scholar 

  2. Abe M, Kaizu K, Matsumoto K. Plasma insulin is removed by hemodialysis: evaluation of the relation between plasma insulin and glucose by using a dialysate with or without glucose. Ther Apher Dial. 2007;11:280–7.

    Article  CAS  PubMed  Google Scholar 

  3. Abe M, Okada K, Matsumoto K. Plasma insulin and C-peptide concentrations in diabetic patients undergoing hemodialysis: comparison with five types of high-flux dialyzer membranes. Diabetes Res Clin Pract. 2008;82:e17–9.

    Article  CAS  PubMed  Google Scholar 

  4. Abe M, Okada K, Ikeda K, Matsumoto S, Soma M, Matsumoto K. Characterization of insulin adsorption behavior of dialyzer membranes used in hemodialysis. Artif Organs. 2011;35:398–403.

    Article  PubMed  Google Scholar 

  5. Odani H, Shinzato T, Matsumoto Y, Usami J, Maeda K. Increase in three alpha, beta-dicarbonyl compound levels in human uremic plasma: specific in vivo determination of intermediates in advanced Maillard reaction. Biochem Biophys Res Commun. 1999;256:89–93.

    Article  CAS  PubMed  Google Scholar 

  6. O’Byrne D, Devaraj S, Islam KN, Collazo R, McDonald L, Grundy S, Jialal I. Low-density lipoprotein (LDL)-induced monocyte-endothelial cell adhesion, soluble cell adhesion molecules, and autoantibodies to oxidized-LDL in chronic renal failure patients on dialysis therapy. Metabolism. 2001;50:207–15.

    Article  PubMed  Google Scholar 

  7. Guo Q, Mori T, Jiang Y, Hu C, Osaki Y, Yoneki Y, Sun Y, Hosoya T, Kawamata A, Ogawa S, Nakayama M, Miyata T, Ito S. Methylglyoxal contributes to the development of insulin resistance and salt sensitivity in Sprague–Dawley rats. J Hypertens. 2009;27:1664–71.

    Article  CAS  PubMed  Google Scholar 

  8. Randell EW, Vasdev S, Gill V. Measurement of methylglyoxal in rat tissues by electrospray ionization mass spectrometry and liquid chromatography. J Pharmacol Toxicol Methods. 2005;51:153–7.

    Article  CAS  PubMed  Google Scholar 

  9. Ogawa S, Nakayama K, Nakayama M, Mori T, Matsushima M, Okamura M, Senda M, Nako K, Miyata T, Ito S. Methylglyoxal is a predictor in type 2 diabetic patients of intima-media thickening and elevation of blood pressure. Hypertension. 2010;56:471–6.

    Article  CAS  PubMed  Google Scholar 

  10. Beisswenger PJ, Howell SK, O’Dell RM, Wood ME, Touchette AD, Szwergold BS. alpha-Dicarbonyls increase in the postprandial period and reflect the degree of hyperglycemia. Diabetes Care. 2001;24:726–32.

    Article  CAS  PubMed  Google Scholar 

  11. Jia X, Olson DJ, Ross AR, Wu L. Structural and functional changes in human insulin induced by methylglyoxal. FASEB J. 2006;20:1555–7.

    Article  CAS  PubMed  Google Scholar 

  12. Schalkwijk CG, Brouwers O, Stehouwer CD. Modulation of insulin action by advanced glycation endproducts: a new player in the field. Horm Metab Res. 2008;40:614–9.

    Article  CAS  PubMed  Google Scholar 

  13. Dhar A, Desai KM, Wu L. Alagebrium attenuates acute methylglyoxal-induced glucose intolerance in Sprague-Dawley rats. Br J Pharmacol. 2010;159:166–75.

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  14. Jia X, Wu L. Accumulation of endogenous methylglyoxal impaired insulin signaling in adipose tissue of fructose-fed rats. Mol Cell Biochem. 2007;306:133–9.

    Article  CAS  PubMed  Google Scholar 

  15. Dhar A, Dhar I, Jiang B, Desai KM, Wu L. Chronic methylglyoxal infusion by minipump causes pancreatic beta-cell dysfunction and induces type 2 diabetes in Sprague-Dawley rats. Diabetes. 2011;60:899–908.

    Article  CAS  PubMed Central  PubMed  Google Scholar 

Download references

Acknowledgments

The authors acknowledge the editorial assistance and clinical support of Miss Manami Shimizu for her help with preparing the references and for her expert assistance with the management of blood and urinary samples. We would like to express our sincere gratitude to all staff at the facilities involved with the hemodialysis procedures that assisted us with this study. We also acknowledge the clinical support of the doctors who provided expert management of health care support, and for the case registrations. This work was supported by a 21st Century Center of Excellence Program Special Research Grant from the Ministry of Education, Sports, and Culture.

Conflict of interest

No potential conflicts of interest.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Susumu Ogawa.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Supplementary material 1 (DOC 38 kb)

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Senda, M., Ogawa, S., Nako, K. et al. The strong relation between post-hemodialysis blood methylglyoxal levels and post-hemodialysis blood glucose concentration rise. Clin Exp Nephrol 19, 527–533 (2015). https://doi.org/10.1007/s10157-014-1018-6

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10157-014-1018-6

Keywords

Navigation