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Klotho deficiency aggravates sepsis-related multiple organ dysfunction.

Lectícia B Jorge1, Fernanda O Coelho1, Talita R Sanches1

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American Journal of Physiology. Renal Physiology
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Klotho deficiency worsens sepsis outcomes, leading to increased organ damage and mortality. Restoring Klotho may protect against sepsis-induced acute kidney injury, particularly in the elderly.

Keywords:
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Area of Science:

  • Nephrology
  • Immunology
  • Gerontology

Background:

  • Sepsis causes organ failure via inflammation and oxidative stress.
  • Acute kidney injury (AKI) affects half of septic shock patients, with high mortality.
  • Klotho protein offers kidney protection and has antioxidant properties.

Purpose of the Study:

  • To investigate Klotho's role in sepsis-induced organ dysfunction and AKI.
  • To analyze sepsis effects on Klotho levels and function.
  • To assess Klotho's protective potential in sepsis.

Main Methods:

  • Utilized a cecal ligation and puncture (CLP) sepsis model in Klotho-haploinsufficient (Kl/+) and wild-type (WT) mice.
  • Compared survival, renal and hepatic function, oxidative stress, and inflammatory markers between CLP-Kl/+ and CLP-WT groups.
  • Evaluated autonomic function, including heart rate variability and baroreflex sensitivity.

Main Results:

  • Klotho-haploinsufficient mice exhibited lower survival rates post-CLP compared to WT mice.
  • CLP-Kl/+ mice showed significantly impaired renal and hepatic function, increased oxidative stress, and heightened inflammatory responses.
  • Sepsis induction led to a state of acute Klotho deficiency, exacerbating organ dysfunction and impacting cardiovascular autonomic regulation.

Conclusions:

  • Klotho deficiency exacerbates sepsis-induced multiple organ dysfunction, including AKI.
  • Klotho plays a protective role in sepsis, mitigating inflammation and oxidative stress.
  • Reduced Klotho levels in sepsis, especially in the elderly, may contribute to severe outcomes.