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Updated: Dec 5, 2025

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
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Lipoxin (LTX A4 5S, 6R, 15R) levels drastically decrease after 5 years of hemodialysis treatment.

M Szczuko1, J Palma2, A Drozd2

  • 1Department of Human Nutrition and Metabolomics, Pomeranian Medical University, Szczecin, Poland. malgorzata.szczuko@pum.edu.pl.

Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society
|October 20, 2020
PubMed
Summary
This summary is machine-generated.

Chronic kidney disease (CKD) patients show elevated levels of inflammatory mediators like HETES and HODES, linked to atherosclerosis. Lipoxin levels significantly decrease in CKD, suggesting potential antioxidant therapy with LXA4 analogues.

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Area of Science:

  • Biochemistry
  • Nephrology
  • Cardiovascular Research

Background:

  • Chronic kidney disease (CKD) is linked to increased atherosclerosis risk, partly due to elevated omega-6 fatty acids.
  • Oxidation products of arachidonic acid, such as prostaglandins, thromboxanes, HETES, and HODES, contribute to cardiovascular disease pathogenesis via oxidative stress.

Purpose of the Study:

  • To investigate the relationship between the duration of CKD treatment and the levels of inflammatory mediators.
  • To determine if the synthesis of inflammatory mediators becomes insufficient in long-term CKD patients.

Main Methods:

  • Analyzed plasma eicosanoid profiles, including specific HETES, HODES, and lipoxins, in 121 CKD patients and 87 healthy controls.
  • Utilized High-Performance Liquid Chromatography (HPLC) for eicosanoid separation and quantification.

Main Results:

  • CKD patients exhibited significantly higher concentrations of 13(S)-HODE, 5(S)-HETE, 12(S)-HETE, 15(S)-HETE, 5(S)-oxoETE, 16(RS)-HETE, and 5(S),6(R),15(R)-lipoxinA4 compared to controls.
  • Lower concentrations of 9(S)-HODE were observed in the CKD group.
  • Lipoxin levels were found to decrease significantly during the course of CKD.

Conclusions:

  • CKD is associated with increased activity in 15LOX, 12LOX, and 5LOX pathways, and suppressed COX activity.
  • Altered levels of HETE, HODE, and particularly lipoxins, are observed in CKD patients, with lipoxin levels decreasing over time.
  • Synthetic lipoxin A4 (LXA4) analogues represent a potential avenue for antioxidant therapy in CKD, warranting further investigation.