Acute kidney ischemia-reperfusion (IR) injury is a life-threatening condition that predisposes individuals to chronic kidney disease. Since the kidney is one of the most energy-demanding organs in the human body and mitochondria are the powerhouse of cells, mitochondrial dysfunction plays a central role in the pathogenesis of IR-induced acute kidney injury. Mitochondrial dysfunction causes a reduction in adenosine triphosphate production, loss of mitochondrial dynamics (represented by persistent fragmentation), and impaired mitophagy. Furthermore, the pathological accumulation of succinate resulting from fumarate reduction under oxygen deprivation (ischemia) in the reverse flux of the Krebs cycle can eventually lead to a burst of reactive oxygen species driven by reverse electron transfer during the reperfusion phase. Accumulating evidence indicates that improving mitochondrial function, biogenesis, and dynamics, and normalizing metabolic reprogramming within the mitochondria have the potential to preserve kidney function during IR injury and prevent progression to chronic kidney disease. In this review, we summarize recent advances in understanding the detrimental role of metabolic reprogramming and mitochondrial dysfunction in IR injury and explore potential therapeutic strategies for treating kidney IR injury.
Background Postoperative acute kidney injury (AKI), which increases the risk of postoperative morbidity and mortality, poses a major concern to surgeons. We conducted this study to analyze the risk factors associated with the occurrence of AKI after orthopedic surgery.
Methods This was a retrospective study that included 351 patients who underwent total hip or knee replacement surgery at Inje University Haeundae Paik Hospital between January 2012 and December 2016.
Results AKI occurred in 13 (3.7%) of the 351 patients. The patients’ preoperative estimated glomerular filtration rate (eGFR) was 66.66±34.02 mL/min/1.73 m2 in the AKI group and 78.07±21.23 mL/min/1.73 m2 in the non-AKI group. The hemoglobin levels were 11.21±1.65 g/dL in the AKI group and 12.39±1.52 g/dL in the non-AKI group. Hemoglobin level was related to increased risk of AKI (odds ratio [OR], 0.13; 95% confidence interval [CI], 0.02–0.68; p=0.016). Administration of crystalloid or colloid fluid alone and the perioperative amount of fluid did not show any significant relationship with AKI. Further analysis of the changes in eGFR was performed using a cutoff value of 7.54. The changes in eGFR were significantly related to decreased risk of AKI (OR, 0.74; 95% CI, 0.61–0.89; p=0.002).
Conclusion Renal function should be monitored closely after orthopedic surgery if patients have chronic kidney disease and low hemoglobin level. Predicting the likelihood of AKI occurrence, early treatment of high-risk patients, and monitoring perioperative laboratory test results, including eGFR, will help improve patient prognosis.
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