Citation

Zeng DH, Chen XH, Li Y, Zhu XY, Wang BL, Ma XG, Cao YL. Clin. Toxicol. (Phila) 2023; ePub(ePub): ePub.

Copyright

(Copyright © 2023, Informa - Taylor and Francis Group)

DOI

10.1080/15563650.2023.2262113

PMID

37882621

Abstract

INTRODUCTION: Diquat poisoning leads to kidney injury, hepatotoxicity, rhabdomyolysis, gastrointestinal hemorrhage, and respiratory failure. Diquat has high mortality and no specific antidote. The pathology of acute kidney injury caused by diquat poisoning has been mainly investigated in animal studies and autopsies, and typically shows renal tubular necrosis. To our knowledge, antemortem renal biopsy has not been reported in humans.Case reports: Two males and one female presented following deliberate diquat self-poisoning. Their main clinical manifestations were abdominal pain, nausea, and emesis. All developed acute kidney injury. Kidney biopsy was performed in two cases which showed acute tubular necrosis with renal interstitial edema and multifocal inflammatory cell infiltration. Treatments given included gastric lavage, catharsis, early hemoperfusion combined with continuous kidney replacement therapy or hemodialysis, administration of glucocorticoids, and antioxidant therapy. All patients survived.

DISCUSSION: Despite potentially lethal ingestions three patients survived oral diquat poisoning with intensive supportive care. No clear relationship can be made between any of the therapies given and patient outcome.

CONCLUSIONS: Kidney biopsy in these patients confirmed proximal renal tubular injury was the major pathological finding although interstitial injury was also present. The role of therapies that address renal pathology requires further study.

Language: en

Keywords

acute kidney injury; corticosteroids; Diquat poisoning; hemoperfusion; pathology