Related Experiment Video

Updated: Aug 18, 2026

Nephrotoxin Microinjection in Zebrafish to Model Acute Kidney Injury
07:58

Nephrotoxin Microinjection in Zebrafish to Model Acute Kidney Injury

Published on: July 17, 2016

Cell death in toxic nephropathies

Glenda C Gobe1, Zoltan H Endre

  • 1School of Medicine, University of Queensland, Brisbane, Australia. g.gobe@uq.edu.au

Seminars in Nephrology
|September 19, 2003
PubMed

Insights

Toxic nephropathies cause kidney failure by damaging renal tubular cells. Understanding the distinct roles of apoptosis and necrosis in these injuries is crucial for kidney health.

Area of Science:

  • Nephrology
  • Cell Biology
  • Toxicology

Background:

  • Toxic nephropathies are a significant cause of acute and chronic kidney failure.
  • Injury to the renal tubular epithelium is the primary mechanism.
  • The renal nephron exhibits a capacity for both apoptosis and necrosis in toxic insults.

Purpose of the Study:

  • To explore the differing or complementary roles of apoptosis and necrosis in toxic nephropathies.
  • To investigate the blurring features between apoptosis and necrosis in renal diseases.
  • To understand the molecular pathways and role of inflammation in these cell death processes.

Main Methods:

  • Review of existing literature on cell death mechanisms in toxic nephropathies.
  • Analysis of recent evidence regarding apoptosis and necrosis in renal and other diseases.
  • Examination of molecular pathways and inflammatory roles in cell death.

Main Results:

  • Apoptosis and necrosis were once considered mutually exclusive but recent evidence shows overlapping features.
  • The molecular pathways and inflammatory involvement in these cell death modes are complex and interconnected.
  • Defining the heterogeneous pathophysiological response of the nephron is challenging.

Conclusions:

  • Clarifying the types of cell death in toxic nephropathies is significant but presents challenges.
  • Understanding these processes is vital for developing strategies to protect kidney health after injury.
  • Controlling the extent and modalities of cell death through renal-specific molecular features is a key therapeutic goal.

More Related Videos

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Nephrons01:10

Nephrons

The kidneys are intricate organs with millions of working units known as nephrons. Each nephron features two major structures: the renal corpuscle, which facilitates blood plasma filtration, and the renal tubule, which handles the glomerular filtrate. Blood supply is directly linked to the nephrons. The renal corpuscle consists of the glomerulus, a capillary network, and the Bowman's capsule, a double-walled epithelial structure that encases the glomerulus. The filtering of blood plasma happens...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...