Citation

de Almeida Araújo S, Faria BCD, Vasconcelos JC, da Cruz AF, de Souza VS, Wanderley DC, Simões-E-Silva AC. Int. Urol. Nephrol. 2023; ePub(ePub): ePub.

Copyright

(Copyright © 2023, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s11255-023-03604-2

PMID

37186212

Abstract

Diethylene glycol (DEG) is nephrotoxic, potentially resulting in high morbidity and mortality. Its main nephrotoxic by-product is diglycolic acid (DGA). This narrative overview summarizes selected literature with a focus on clinical findings, pathophysiology, diagnosis including morphological features of renal biopsies, and management. The kidney injury in DEG poisoning is secondary to proximal tubular necrosis caused by DGA. Marked vacuolization and edema of epithelial cells obstruct the lumen, reducing urine flow and, consequently, resulting in anuria and uremia. The clinical alterations due to DEG poisoning are dose-dependent. Patients may present with gastrointestinal symptoms and anion gap metabolic acidosis, followed by renal failure, and, later, encephalopathy and neuropathy. Although this three-phase pattern has been described, signs and symptoms may be overlapping. Data about DEG intoxication is scarce. Sometimes the diagnosis is challenging. The management includes supportive care, gastric decontamination, correction of acid-base disorders, and hemodialysis. The understanding of the metabolic processes related to DEG poisoning may contribute to its management, preventing death, serious sequels, or irreversible lesions.

Language: en

Keywords

Intoxication; Acute kidney injury; Diethylene glycol; Metabolic acidosis; Nephrotoxicity