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Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development

Journal

BIOLOGY-BASEL
Volume 12, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/biology12020327

Keywords

kidney microcirculation; acute kidney injury; renin-angiotensin-aldosterone system

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Acute kidney injury (AKI) can occur due to reduced renal perfusion, with the kidneys being susceptible to ischemia because of the anatomical microcirculation around the renal tubules. Impaired blood flow causes damage to the endothelium and thrombosis, leading to the destruction of small vessels. This peritubular rarefaction is believed to be the main cause of irreversible changes in the damaged kidney and the development of chronic kidney disease. This article discusses the structure of renal microcirculation, its regulation, and the mechanisms of acute ischemic damage, with a focus on preventing it through the inhibition of the renin-angiotensin-aldosterone system.
Simple Summary Acute kidney injury can result from multiple factors. The main cause is reduced renal perfusion. Kidneys are susceptible to ischemia due to the anatomy of microcirculation that wraps around the renal tubules. In the kidney, cortical and medullary superficial tubules have a large share in transport and require the supply of oxygen for energy production, while it is the cortex that receives almost 100% of the blood flowing through the kidneys and the medulla only accounts for 5-10% of it. This difference makes the tubules present in the superficial layer of the medulla very susceptible to ischemia. Impaired blood flow causes damage to the inner layer of vessels and thrombosis. The next stage is the disintegration of these vessels. The phenomenon of destruction of small vessels is called peritubular rarefaction, attributed as the main cause of further irreversible changes in the damaged kidney leading to the development of chronic kidney disease. In this article, we will present the characteristic structure of renal microcirculation, its regulation, and the mechanism of damage in acute ischemia, and we will try to find methods of prevention with particular emphasis on the inhibition of the renin-angiotensin-aldosterone system. Acute kidney injury (AKI) can result from multiple factors. The main cause is reduced renal perfusion. Kidneys are susceptible to ischemia due to the anatomy of microcirculation that wraps around the renal tubules-peritubular capillary (PTC) network. Cortical and medullary superficial tubules have a large share in transport and require the supply of oxygen for ATP production, while it is the cortex that receives almost 100% of the blood flowing through the kidneys and the medulla only accounts for 5-10% of it. This difference makes the tubules present in the superficial layer of the medulla very susceptible to ischemia. Impaired blood flow causes damage to the endothelium, with an increase in its prothrombotic and pro-adhesive properties. This causes congestion in the microcirculation of the renal medulla. The next stage is the migration of pericytes with the disintegration of these vessels. The phenomenon of destruction of small vessels is called peritubular rarefaction, attributed as the main cause of further irreversible changes in the damaged kidney leading to the development of chronic kidney disease. In this article, we will present the characteristic structure of renal microcirculation, its regulation, and the mechanism of damage in acute ischemia, and we will try to find methods of prevention with particular emphasis on the inhibition of the renin-angiotensin-aldosterone system.

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