S100A12 gene expression is increased in peripheral leukocytes in chronic kidney disease stage 4-5 patients with

Masaki Hara1, Minoru Ando, Taku Morito

  • 1Division of Nephrology, Department of Internal Medicine, Tokyo Metropolitan Komagome General Hospital, Tokyo, Japan.

Insights

Elevated S100A12 in chronic kidney disease (CKD) stems from increased gene expression in leukocytes, particularly in those with cardiovascular disease (CVD). This finding links S100A12 to CKD pathogenesis and CVD complications.

Area of Science:

  • Biochemistry
  • Immunology
  • Nephrology

Background:

  • S100A12 protein promotes vascular inflammation and atherosclerosis development.
  • Elevated serum S100A12 is observed in chronic kidney disease (CKD) patients, but the underlying cause is not fully understood.

Purpose of the Study:

  • To investigate the reason for elevated serum S100A12 concentrations in CKD patients.
  • To explore the relationship between S100A12 gene expression and serum levels in CKD.
  • To assess the association of S100A12 with cardiovascular disease (CVD) in CKD patients.

Main Methods:

  • Quantitative real-time RT-PCR was used to measure S100A12 and RAGE mRNA levels in peripheral leukocytes.
  • Serum concentrations of S100A12 and soluble RAGE were quantified using ELISA.
  • Study included 40 CKD patients (stages 4-5) and 20 healthy controls, with subgroup analysis for CVD presence.

Main Results:

  • CKD patients exhibited significantly higher serum S100A12 concentrations and S100A12 mRNA levels in leukocytes compared to healthy subjects.
  • Serum S100A12 levels strongly correlated with S100A12 mRNA expression in uremic CKD patients.
  • Both serum S100A12 and its gene expression were significantly elevated in CKD patients with concurrent CVD.

Conclusions:

  • Increased S100A12 gene expression in leukocytes of CKD patients contributes to elevated serum S100A12 levels.
  • This elevated expression is particularly pronounced in CKD patients with cardiovascular disease.
  • S100A12 may play a significant role in the pathogenesis of vascular complications in CKD.
Abstract

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