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Background: Neuroleptic malignant syndrome (NMS) is a psychiatric-neurologic emergency that may require intensive care management. There is a paucity of information about NMS as a critical illness. We reviewed the Mayo Clinic experience.

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Snakebite is a neglected public health problem in tropical countries. Snakebite envenomation-associated acute kidney injury (SBE-AKI) is a major complication accounting for significant morbidity and mortality. The pathogenesis of SBE-AKI may be multifactorial, including prerenal AKI secondary to hemodynamic alterations, intrinsic renal injury, immune-related mechanisms, venom-induced consumptive coagulopathy and capillary leak syndrome.

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Snakebite-associated acute kidney injury (AKI) poses a significant health burden in the South Asia region, resulting in considerable morbidity and mortality. Multiple factors contribute to the pathogenesis of AKI following snakebites, including hypotension, intravascular haemolysis, disseminated intravascular coagulation, rhabdomyolysis, thrombotic microangiopathy (TMA) and direct nephrotoxicity. Clinical features manifest as anuria, oliguria, haematuria, abdominal pain and hypertension.

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Residual hyperglycemia after successful treatment of a patient with severe copper sulfate poisoning.

J Zhejiang Univ Sci B

December 2024

Department of Emergency Medicine, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.

Article Synopsis
  • Copper sulfate is commonly used in labs, with rare cases of poisoning; only 140 exposures were reported in a year, and five were intentional (Gummin et al., 2023).
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Purpose: This study aimed to examine the impact of APS on acute kidney injury induced by rhabdomyolysis (RIAKI), exploring its association with macrophage M1 polarization and elucidating the underlying mechanisms.

Methods: C57BL/6J mice were randomly assigned to one of three groups: a normal control group, a RIAKI model group, and an APS treatment group. Techniques such as flow cytometry and immunofluorescence were employed to demonstrate that APS can inhibit the transition of renal macrophages to the M1 phenotype in RIAKI.

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