HEMOLYSIS-DERIVED FACTORS ARE ASSOCIATED WITH HEPATIC ISCHEMIA-REPERFUSION-INDUCED REMOTE KIDNEY INJURY

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HEMOLYSIS-DERIVED FACTORS ARE ASSOCIATED WITH HEPATIC ISCHEMIA-REPERFUSION-INDUCED REMOTE KIDNEY INJURY

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Co-author 1

Yong Kwon Han yonkwon3583@gmail.com Cardiovascular Research Institute Anatomy Daegu Korea (Republic of) * Kyungpook National University Anatomy Daegu Korea (Republic of)

Co-author 2

Hui Jae Lim ok980304@gmail.com Kyungpook National University Anatomy Daegu Korea (Republic of) -

Co-author 3

Min Ji Kim mzkim826@gmail.com Kyungpook National University Anatomy Daegu Korea (Republic of) -

Co-author 4

You Ri Park youri0212@naver.com Kyungpook National University Anatomy Daegu Korea (Republic of) -

Co-author 5

Kwon Moo Park kmpark@knu.ac.kr Cardiovascular Research Institute Anatomy Daegu Korea (Republic of) - Kyungpook National University Anatomy Daegu Korea (Republic of)

Co-author 6

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Introduction

Hepatic ischemia-reperfusion injury (HIRI) often induces remote organ injury, which leads to poor outcomes. However, the mechanism of HIR-induced remote organ injury remains to be defined. Here, we investigated the molecular mechanisms of HIRI-induced remote kidney injury.

Methods

To induce HIRI, portal triad just above the branch point to the right liver lobe was occluded with a non-traumatic microaneurysm clamp for 60 minutes. Kidney function and morphology were evaluated 24 hours after reperfusion.

Results

HIRI induced functional and histological damage of kidneys. HIRI caused hemolysis, along with increased plasma heme levels and hemoglobinuria. In addition, HIRI led to the accumulation of hemoglobin in proximal tubule cells. Furthermore, HIRI increased heme oxygenase-1 expression and iron content, and lipid peroxidation in kidneys, indicating that HIRI induces ferroptosis in proximal tubule cells.

Conclusion

These findings demonstrated that HIRI-induced remote kidney injury is associated with hemolysis, increased of cell-free hemoglobin and heme, and subsequent ferroptosis in kidney tubule cells. Our study suggests that hemolysis-derived products act as a mediators of HIRI-induced remote kidney injury.

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