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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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Senescence marker activin A is increased in human diabetic kidney disease: association with kidney function and

Xiaohui Bian1,2, Tomás P Griffin3,4, Xiangyang Zhu1

  • 1Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA.

BMJ Open Diabetes Research & Care
|January 8, 2020
PubMed
Abstract

Insights

Elevated activin A in blood and urine indicates diabetic kidney disease (DKD) progression and correlates with reduced kidney function. This finding supports activin A as a potential diagnostic marker and therapeutic target for DKD.

Area of Science:

  • Nephrology
  • Endocrinology
  • Inflammation Research

Background:

  • Diabetic kidney disease (DKD) involves kidney injury, adipose tissue dysfunction, and fibrosis, with activin A identified as a key inflammatory mediator.
  • Cellular senescence and inflammation are implicated in DKD pathogenesis, suggesting potential therapeutic targets.
  • Activin A's role in profibrotic kidney injury highlights its potential significance in DKD.

Purpose of the Study:

  • To investigate whether human DKD is associated with increased activin A levels in blood and urine.
  • To examine the correlation between circulating activin A and kidney injury markers in DKD patients.
  • To assess activin A expression in human kidney cells under DKD-mimicking conditions.

Main Methods:

  • Analysis of plasma and urine activin A levels in adult diabetes cohorts and controls from the USA and Ireland.
  • Correlation and logistic regression analyses to assess relationships between activin A, estimated glomerular filtration rate (eGFR), and DKD biomarkers.
  • In vitro studies using human kidney (HK-2) cells exposed to high glucose and transforming growth factor-β1 or albumin to measure activin A, inflammatory, EMT, and senescence markers.

Main Results:

  • Plasma activin A was significantly elevated in individuals with diabetes compared to controls and inversely correlated with eGFR.
  • After eGFR adjustment, high plasma activin A levels were associated with albuminuria and elevated tumor necrosis factor receptor-1.
  • Urinary activin A levels correlated positively with albuminuria, and in vitro studies showed increased activin A, inflammatory, and EMT markers in injured kidney cells.

Conclusions:

  • Circulating activin A is elevated in human DKD and is linked to impaired kidney function and injury markers.
  • DKD-induced human renal tubule cells exhibit a profibrotic and inflammatory phenotype with upregulated activin A.
  • Activin A warrants further investigation as a potential diagnostic biomarker and therapeutic target for diabetic kidney disease.
Keywords:
adipocytokineclinical aspects of diabetesclinical nephrologyrenal fibrosis

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