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Technical Refinement of a Bilateral Renal Ischemia-Reperfusion Mouse Model for Acute Kidney Injury Research
Published on: November 3, 2023
Pharmacological targets in the renal peritubular microenvironment: implications for therapy for sepsis-induced acute
Philip R Mayeux1, Lee Ann MacMillan-Crow
1Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. prmayeux@uams.edu
Abstract:
One of the most frequent and serious complications to develop in septic patients is acute kidney injury (AKI), a disorder characterized by a rapid failure of the kidneys to adequately filter the blood, regulate ion and water balance, and generate urine. AKI greatly worsens the already poor prognosis of sepsis and increases cost of care. To date, therapies have been mostly supportive; consequently there has been little change in the mortality rates over the last decade. This is due, at least in part, to the delay in establishing clinical evidence of an infection and the associated presence of the systemic inflammatory response syndrome and thus, a delay in initiating therapy. A second reason is a lack of understanding regarding the mechanisms leading to renal injury, which has hindered the development of more targeted therapies. In this review, we summarize recent studies, which have examined the development of renal injury during sepsis and propose how changes in the peritubular capillary microenvironment lead to and then perpetuate microcirculatory failure and tubular epithelial cell injury. We also discuss a number of potential therapeutic targets in the renal peritubular microenvironment, which may prevent or lessen injury and/or promote recovery.
Insights
Acute kidney injury (AKI) is a severe complication of sepsis, worsening patient outcomes. This review explores how microenvironment changes cause kidney injury in sepsis and identifies potential therapeutic targets.
Area of Science:
- Nephrology
- Critical Care Medicine
- Pathophysiology
Background:
- Sepsis frequently leads to acute kidney injury (AKI), a serious complication that worsens prognosis and increases healthcare costs.
- Current AKI therapies are primarily supportive, with limited improvement in mortality rates due to delayed diagnosis and a poor understanding of injury mechanisms.
- Understanding the pathophysiology of sepsis-induced AKI is crucial for developing effective treatments.
Purpose of the Study:
- To review recent studies on the development of renal injury during sepsis.
- To elucidate the role of the peritubular capillary microenvironment in sepsis-induced AKI.
- To identify potential therapeutic targets for preventing or mitigating AKI in septic patients.
Main Methods:
- Review of recent scientific literature on sepsis and AKI.
- Analysis of studies investigating microcirculatory changes in the renal peritubular environment.
- Synthesis of findings to propose mechanisms of injury and therapeutic strategies.
Main Results:
- Sepsis induces changes in the peritubular capillary microenvironment, leading to microcirculatory failure.
- These microcirculatory alterations perpetuate tubular epithelial cell injury.
- The peritubular microenvironment is a key factor in the development and persistence of AKI during sepsis.
Conclusions:
- Alterations in the renal peritubular microenvironment are central to sepsis-induced AKI.
- Targeting the peritubular microenvironment offers promising therapeutic avenues for AKI.
- Further research into these targets may lead to novel treatments to prevent or manage AKI in sepsis.
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