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Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development
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 shar...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9953191/ https://www.ncbi.nlm.nih.gov/pubmed/36829602 http://dx.doi.org/10.3390/biology12020327 |
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author | Kwiatkowska, Ewa Kwiatkowski, Sebastian Dziedziejko, Violetta Tomasiewicz, Izabela Domański, Leszek |
author_facet | Kwiatkowska, Ewa Kwiatkowski, Sebastian Dziedziejko, Violetta Tomasiewicz, Izabela Domański, Leszek |
author_sort | Kwiatkowska, Ewa |
collection | PubMed |
description | 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. ABSTRACT: 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. |
format | Online Article Text |
id | pubmed-9953191 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99531912023-02-25 Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development Kwiatkowska, Ewa Kwiatkowski, Sebastian Dziedziejko, Violetta Tomasiewicz, Izabela Domański, Leszek Biology (Basel) Review 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. ABSTRACT: 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. MDPI 2023-02-17 /pmc/articles/PMC9953191/ /pubmed/36829602 http://dx.doi.org/10.3390/biology12020327 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Kwiatkowska, Ewa Kwiatkowski, Sebastian Dziedziejko, Violetta Tomasiewicz, Izabela Domański, Leszek Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development |
title | Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development |
title_full | Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development |
title_fullStr | Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development |
title_full_unstemmed | Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development |
title_short | Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development |
title_sort | renal microcirculation injury as the main cause of ischemic acute kidney injury development |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9953191/ https://www.ncbi.nlm.nih.gov/pubmed/36829602 http://dx.doi.org/10.3390/biology12020327 |
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