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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 Kidney Injury I: Introduction

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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...

Renal Corpuscle

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Related Experiment Video

Updated: Jun 17, 2026

Mouse Model of Acute to Chronic Kidney Disease Transition Induced by Renal Ischemia/Reperfusion Injury

Mouse Model of Acute to Chronic Kidney Disease Transition Induced by Renal Ischemia/Reperfusion Injury

Published on: February 10, 2026

Renal fibrosis.

G Efstratiadis¹, M Divani, E Katsioulis

¹Nephrology Department, Aristotle University, Hippokration Hospital, Thessaloniki, Greece. efstrati@med.auth.gr

|December 17, 2009

Summary

Tubulointerstitial renal fibrosis, a key driver of kidney function decline, is primarily caused by Epithelial to Mesenchymal Transition (EMT). Therapies targeting EMT, like Hepatocyte Growth Factor (HGF) and Bone Morphogenetic Factor-7 (BMF-7), show promise in preventing kidney fibrosis.

Keywords:

TGF-β angiotensin II cytokines epithelial mesenchymal transition fibrosis growth factors hypoxia proteinuria

Related Experiment Videos

Last Updated: Jun 17, 2026

Mouse Model of Acute to Chronic Kidney Disease Transition Induced by Renal Ischemia/Reperfusion Injury

Mouse Model of Acute to Chronic Kidney Disease Transition Induced by Renal Ischemia/Reperfusion Injury

Published on: February 10, 2026

Area of Science:

Nephrology
Cell Biology
Pathology

Background:

Tubulointerstitial renal fibrosis is a detrimental process leading to kidney function loss.
Epithelial to Mesenchymal Transition (EMT) is the primary mechanism driving renal fibrosis.
Proteinuria and hypoxia are key stimuli for EMT.

Purpose of the Study:

To explore the molecular mechanisms of renal fibrosis.
To identify potential therapeutic targets for preventing kidney fibrosis.

Main Methods:

Review of molecular pathways involved in EMT.
Analysis of the roles of TGFbeta-1, HGF, and BMF-7 in renal fibrosis.

Main Results:

TGFbeta-1, via the SMAD pathway, modulates EMT.
HGF and BMF-7 act as inhibitors of EMT.
HGF and BMF-7 administration prevented peritoneal fibrosis in experimental models.

Conclusions:

EMT is a critical target for anti-fibrotic therapies.
HGF and BMF-7 hold therapeutic potential for treating and preventing kidney fibrosis.