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Growth factor Midkine is involved in the pathogenesis of renal injury induced by protein overload containing

Kiyonari Kato1, Tomoki Kosugi1, Waichi Sato2

  • 1Division of Nephrology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya, Aichi, 466-8550, Japan.

Clinical and Experimental Nephrology
|March 2, 2011
PubMed
Abstract

Insights

Midkine (MK) exacerbates protein overload-induced glomerulonephritis by promoting inflammation and glomerular damage. MK deficiency protects against kidney injury, highlighting MK's detrimental role in this kidney disease model.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Midkine (MK) is a growth factor involved in inflammation-related kidney diseases.
  • MK mediates biological actions via chemotaxis and chemokine pathways.
  • Post-infectious glomerulonephritis involves immune complex deposition and inflammatory cell infiltration.

Purpose of the Study:

  • To investigate the role of Midkine (MK) in the pathogenesis of acute glomerulonephritis.

Main Methods:

  • Endocapillary proliferative glomerulonephritis was induced in 129/SV mice via intraperitoneal protein injections.
  • Comparison of disease development in Midkine-deficient (Mdk (-/-)) and wild-type (Mdk (+/+)) mice.

Main Results:

  • Wild-type mice showed more severe glomerular and tubulointerstitial injury compared to Midkine-deficient mice.
  • MK appears to contribute to injury through neutrophil infiltration, IgG deposition, and C3 activation.
  • MK expression levels correlated with the severity of glomerular and tubulointerstitial damage.

Conclusions:

  • Midkine (MK) plays a deleterious role in protein overload-induced endocapillary proliferative glomerulonephritis.
  • This study offers new insights into MK's contribution to kidney disease pathogenesis.

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