Abstract
Acute kidney injury (AKI) significantly contributes to morbidity and mortality in critically ill patients. AKI is also an independent risk factor for the development and progression of chronic kidney disease. Effective therapeutic strategies for AKI are limited, but emerging evidence indicates a prominent role of mitochondrial dysfunction and altered tubular metabolism in the pathogenesis of AKI. Therefore, a comprehensive, mechanistic understanding of mitochondrial function and renal metabolism in AKI may lead to the development of novel therapies in AKI. In this review, we provide an overview of current state of research on the role of mitochondria and tubular metabolism in AKI from both pre-clinical and clinical studies. We also highlight current therapeutic strategies which target mitochondrial function and metabolic pathways for the treatment of AKI.
Highlights
Acute kidney injury (AKI) is the abrupt decline in kidney function
We focus on mechanisms of intrinsic AKI with tubular injury, which is caused by three common etiologies including renal ischemia, nephrotoxins, and sepsis
We summarize the current evidence linking mitochondrial dysfunction and metabolic reprogramming with the development and progression of AKI
Summary
Acute kidney injury (AKI) is the abrupt decline in kidney function. Several definitions have been used for AKI in the past. In addition to increasing the risk of death, AKI is an independent risk factor for progression to chronic kidney disease (CKD) and end-stage renal disease [6,7,8]. Despite this unacceptably high morbidity and mortality, effective strategies to prevent or reverse AKI are extremely limited due to its multifactorial pathogenesis. The proximal tubule in the cortex and thick ascending limb in the outer medulla are rich in mitochondria and are the most metabolically active segments in the kidney These segments are more susceptible to injury in AKI. We present our current knowledge regarding mitochondrial function and tubular energy metabolism in AKI. We discuss potential therapeutic approaches targeting mitochondrial dysfunction and tubular metabolism
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