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Updated: Jul 30, 2025

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro
Published on: January 31, 2022
Renal toxicity caused by diethylene glycol: an overview
Stanley de Almeida Araújo1,2, Bárbara Caroline Dias Faria3, Júlia Cunha Vasconcelos3
1Instituto de Nefropatologia, Belo Horizonte, MG, Brasil.
Diethylene glycol (DEG) poisoning causes kidney damage through its metabolite, diglycolic acid (DGA), leading to acute kidney injury. Early diagnosis and supportive care, including hemodialysis, are crucial for managing this potentially fatal condition.
Area of Science:
- Nephrology
- Toxicology
- Internal Medicine
Background:
- Diethylene glycol (DEG) is a toxic alcohol known for causing severe kidney damage.
- Diglycolic acid (DGA), a metabolite of DEG, is the primary agent responsible for DEG-induced nephrotoxicity.
- DEG poisoning presents a significant public health concern due to its potential for high morbidity and mortality.
Purpose of the Study:
- To provide a comprehensive overview of diethylene glycol (DEG) poisoning.
- To focus on clinical manifestations, pathophysiology, diagnostic methods, and management strategies for DEG-induced kidney injury.
- To synthesize current literature on DEG intoxication for improved clinical understanding and patient outcomes.
Main Methods:
- This study is a narrative overview based on a review of selected literature.
- The review focused on clinical findings, pathophysiology, diagnostic features (including renal biopsy morphology), and treatment of DEG poisoning.
- Literature search encompassed studies detailing DEG intoxication, its effects on the kidneys, and patient management.
Main Results:
- DEG-induced kidney injury results from proximal tubular necrosis caused by DGA.
- Pathological changes include epithelial cell vacuolization and edema, leading to tubular obstruction, anuria, and uremia.
- Clinical presentation is dose-dependent, often involving gastrointestinal symptoms, metabolic acidosis, renal failure, and neurological complications, with potential overlapping phases.
Conclusions:
- The understanding of DEG's metabolic pathways and its toxic by-product DGA is essential for effective management.
- Prompt diagnosis and intervention, including supportive care, gastric decontamination, acid-base correction, and hemodialysis, are critical.
- Improved comprehension of DEG poisoning mechanisms can aid in preventing mortality, severe sequelae, and irreversible kidney damage.
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