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Acute Kidney Injury II: Pathophysiology

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...

Acute Inflammation II: Local and Systemic Effects

Acute Inflammation II: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...

Acute Kidney Injury I: Introduction

Acute Kidney Injury I: Introduction

Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...

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Related Experiment Video

Updated: Apr 29, 2026

Non-Invasive Monitoring of Microvascular Oxygenation and Reactive Hyperemia using Hybrid, Near-Infrared Diffuse Optical Spectroscopy for Critical Care

Non-Invasive Monitoring of Microvascular Oxygenation and Reactive Hyperemia using Hybrid, Near-Infrared Diffuse Optical Spectroscopy for Critical Care

Published on: May 10, 2024

The renal microcirculation in sepsis.

Bulent Ergin¹, Aysegul Kapucu², Cihan Demirci-Tansel³

¹Department of Translational Physiology, Academic Medical Center, Amsterdam, The Netherlands.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association

|May 23, 2014

Summary

This summary is machine-generated.

Sepsis disrupts kidney oxygen balance, leading to acute kidney injury (AKI) through microcirculatory dysfunction. Restoring oxygen homeostasis and managing reactive species are key to treating septic AKI.

Keywords:

AKI microcirculation nitric oxide oxygen radicals oxygenation

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Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

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Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Published on: December 9, 2022

Area of Science:

Nephrology
Critical Care Medicine
Physiology

Background:

Septic acute kidney injury (AKI) pathophysiology remains incompletely understood despite known cellular mechanisms.
The renal microcirculation (MC) integrates multiple cellular failures contributing to AKI.
Kidneys are vulnerable to hypoxemic injury due to their structure, high energy demand, and borderline ischemic state.

Purpose of the Study:

To review the renal microcirculation's response to sepsis.
To discuss factors influencing renal MC (dys)function in sepsis.
To elucidate the role of renal MC dysfunction in the pathogenesis of renal failure during sepsis.

Main Methods:

Review of existing literature on renal microcirculation in sepsis.
Analysis of oxygen supply-demand balance in the kidney.
Examination of the interplay between oxygen handling, nitric oxide metabolism, and radical formation in septic AKI.

Main Results:

Sepsis disturbs the renal oxygen supply-demand balance, causing microcirculatory dysfunction.
Renal tissue oxygenation is heterogeneous, with MC deterioration being a key factor in septic AKI development.
Experimental therapies improving MC oxygenation show promise in restoring renal function.

Conclusions:

Integrative correction of homeostasis for oxygen and reactive species is crucial for kidney resuscitation in sepsis.
Further clinical studies are needed to validate experimental therapeutic approaches.
Development of MC-focused clinical biomarkers for AKI is essential for monitoring treatment efficacy.