ACUTE KIDNEY INJURY CAUSES HEPATIC LIPID ACCUMULATION AND MULTIPLE ORGAN DYSFUNCTION

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ACUTE KIDNEY INJURY CAUSES HEPATIC LIPID ACCUMULATION AND MULTIPLE ORGAN DYSFUNCTION

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Co-author 1

Karmin O karmino@sbrc.ca University of Manitoba Animal Science Winnipeg Canada * St. Boniface Hospital Research Centre CCARM Winnipeg Canada University of Manitoba Physiology and Pathophysiology Winnipeg Canada

Co-author 2

Shunshun Jin shunshuj@myumanitoba.ca University of Manitoba Animal Science Winnipeg Canada - St. Boniface Hospital Research Centre CCARM Winnipeg Canada

Co-author 3

Soulmaz Naserli naserli1@myumanitoba.ca University of Manitoba Animal Science Winnipeg Canada -

Co-author 4

Kathy Au-Yeung kau-yeung@sbrc.ca St. Boniface Hospital Research Centre CCARM Winnipeg Canada -

Co-author 5

Susara Madduma Hewage SUSARA.MADDUMAHEWAGE@umanitoba.ca University of Manitoba Animal Science Winnipeg Canada -

Co-author 6

Charith Wijerathne wijekhmc@myumanitoba.ca St. Boniface Hospital Research Centre CCARM Winnipeg Canada -

Co-author 7

Yaw L. Siow csiow@sbrc.ca St. Boniface Hospital Research Centre CCARM Winnipeg Canada - University of Manitoba Physiology and Pathophysiology Winnipeg Canada Agriculture and Agri-Food Canada St. Boniface Winnipeg Canada

Co-author 8

Co-author 9

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Introduction

Kidney dysfunction during acute kidney injury (AKI) can trigger widespread effects to multiple organs, known as distant organ injury. One of the major pathological consequences of AKI is oxidative stress, driven primarily by ischemia-reperfusion events. Oxidative stress results from the overproduction of reactive oxygen species (ROS) and/or a reduction of antioxidant defense, leading to cellular damage, especially in metabolically active organs such as liver, which can lead to hepatic lipid accumulation causing liver injury and hyperlipidemia. The risk of cardiovascular disease is also significantly elevated in patients with kidney disease. AKI complicated by multiple organ injury increases morbidity and mortality. However, the underlying mechanism of AKI-induced distant organ injury is not well understood. This study investigated the mechanisms of AKI-induced oxidative stress (heart, liver) and hepatic lipid accumulation (steatosis).

Methods

AKI was induced in male and female Sprague-Dawley rats through renal ischemia (45 minutes) and reperfusion (24 hours). Kidney and liver function were evaluated.

Results

Kidney and liver function were evaluated. There was a significant increase in plasma creatinine and transaminase levels, indicating kidney and liver injury. AKI caused a significant increase in lipid peroxidation and a decrease in antioxidant glutathione (GSH) and hydrogen sulfide (H2S) levels in plasma, kidney, heart and liver, indicating systemic, local and distant organ oxidative stress. Mechanistic investigation revealed that increased oxidative stress was caused by a decreased Nrf2/GSH synthesis and a reduced transsulfuration/H2S production. The AMP-activated protein kinase (AMPK) pathway is a vital cellular energy metabolic switch involved in the regulation of lipid metabolism in the liver and is regarded as a therapeutic target of fatty liver disease (NAFLD) and hyperlipidemia. Increased oxidative stress impaired AMPK signaling pathway, which decreased fatty acid metabolism and increased lipogenesis, leading to hepatic lipid accumulation (steatosis) and hyperlipidemia during AKI. There was a significant elevation of oxidative stress biomarkers in the heart of rats with AKI.

Conclusion

The results suggest that AKI weakens antioxidant defense and induces oxidative injury to kidney and distant organs (heart, liver). Oxidative stress contributes, in part, to the downregulation of the AMPK signaling pathway leading to hepatic lipid accumulation and dyslipidemia through decreased fatty acid metabolism and increased lipogenesis. Restoration of antioxidant defense and hepatic AMPK signaling may serve as therapeutic targets to improve kidney and its associated distant organ injury.

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