Decrease in reduced-form albumin among chronic kidney disease patients: new insights in cardiovascular complications

Ther Apher Dial. 2011 Apr;15(2):156-60. doi: 10.1111/j.1744-9987.2010.00889.x. Epub 2011 Jan 25.

Abstract

From the perspective of free cysteine residue (Cys-34), human serum albumin (HSA) comprises a mixture of human mercaptoalbumin (HMA), in which the Cys-34 is not oxidized, human non-mercaptoalbumin (HNA)-1, which has a disulfide bond that can be reversibly oxidized, mainly by cysteine, and HNA-2, which is strongly oxidized to form sulfinic (-SO(2) H) or sulfonic (-SO(3) H) species. We have developed a convenient high-performance liquid chromatographic (HPLC) system for the clear separation of HSA into HMA, HNA-1 and HNA-2, and we have studied the dynamic changes of HSA-redox under various states of chronic kidney disease, in both a clinical and an experimental setting. In this article, we discuss the relationship between HSA-redox (especially the decrease of the reduced form), dialyzable uremic toxins and incident cardiovascular disease based on our recent investigations.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Chromatography, High Pressure Liquid / methods*
  • Chronic Disease
  • Cohort Studies
  • Cross-Sectional Studies
  • Female
  • Follow-Up Studies
  • Humans
  • Kidney Diseases / physiopathology*
  • Male
  • Middle Aged
  • Oxidation-Reduction
  • Oxidative Stress*
  • Prospective Studies
  • Serum Albumin / analysis
  • Serum Albumin / metabolism*
  • Serum Albumin, Human

Substances

  • Serum Albumin
  • mercaptoalbumin
  • nonmercaptalbumin
  • Serum Albumin, Human