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Pathophysiology of AKI

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Acute Kidney Injury and Regenerative Medicine
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Abstract

The causes of acute kidney injury (AKI) are diverse, and the developmental pathological conditions associated with the disease are heterogeneous and complex. The clinical majority of pathological conditions associated with hemodynamics is normotensive ischemic acute kidney injury (AKI) caused by decreased autoregulation of glomerular pressure. It is usually referred to the occurrence of AKI in a patient that already has chronic kidney disease (CKD), what is called acute-on-chronic AKI. In sepsis, changes in renal hemodynamics, particularly in the appearance of shunts in the kidney, are thought to occur during a hyperdynamic state with resultant reduction of renal function. Renal tubule cells are main targets of the pathology of renal parenchymal AKI. Inflammatory cell infiltration into the kidney also exacerbates renal tubule injury. Mechanisms by which the glomerular filtration rate (GFR) decreases due to renal tubule injury include intrarenal vasoconstriction, backleak of primary urine, and renal tubular obstruction. Renal congestion has recently been focused on as a contributing factor in the decrease of renal function. Moreover, innate immunity is associated with the development of AKI in sepsis, and the mitochondrial DNA-TLR9 pathway plays an important role.

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Correspondence to Hideo Yasuda .

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Yasuda, H. (2020). Pathophysiology of AKI. In: Terada, Y., Wada, T., Doi, K. (eds) Acute Kidney Injury and Regenerative Medicine . Springer, Singapore. https://doi.org/10.1007/978-981-15-1108-0_3

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  • DOI: https://doi.org/10.1007/978-981-15-1108-0_3

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