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Complement Modulation of Anti-Aging Factor Klotho in Ischemia/Reperfusion Injury and Delayed Graft Function.

G Castellano1, A Intini1, A Stasi1

  • 1Nephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari, Bari, Italy.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|August 18, 2015
PubMed
Summary

Kidney transplant injury reduces the anti-aging factor Klotho, potentially via complement activation. This Klotho deficiency may contribute to long-term kidney transplant dysfunction.

Keywords:
basic (laboratory) research/sciencecomplement biologyimmunobiologyischemia reperfusion injury (IRI)kidney transplantation/nephrology

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Area of Science:

  • Nephrology
  • Immunology
  • Aging Research

Background:

  • Klotho is a key anti-aging protein primarily produced by kidney tubular epithelial cells (TEC).
  • Klotho levels decrease in acute kidney injury, but its role in kidney transplantation is unknown.
  • Reduced Klotho is linked to senescence and fibrosis, processes relevant to chronic allograft dysfunction.

Purpose of the Study:

  • Investigate Klotho modulation in kidney transplantation following ischemia/reperfusion injury (IRI).
  • Determine the role of complement activation in Klotho down-regulation post-transplant.
  • Assess the association between Klotho levels and delayed graft function (DGF) and long-term outcomes.

Main Methods:

  • Utilized a swine model of kidney IRI to assess Klotho expression.
  • Investigated complement inhibition (C1-inhibitor) effects on Klotho and NF-kB signaling.
  • Examined Klotho expression in human kidney biopsies and serum levels in transplant recipients.

Main Results:

  • IRI significantly reduced renal Klotho expression within 24 hours.
  • Complement inhibition preserved Klotho by inhibiting NF-kB signaling.
  • TEC exposed to C5a showed NF-kB-mediated Klotho down-regulation in vitro.
  • Kidney transplant recipients with DGF exhibited lower Klotho expression in biopsies and serum compared to those with early graft function.

Conclusions:

  • Complement activation plays a critical role in the down-regulation of Klotho during kidney IRI.
  • Acquired Klotho deficiency post-transplantation may persist long-term.
  • This Klotho deficiency is hypothesized to contribute to DGF-associated chronic allograft dysfunction.