Introduction: Rhabdomyolysis, as an acute stage of myopathy, causes kidney damage. It is known that this pathology is caused by the accumulation of muscle breakdown products and is associated with oxidative stress. Therefore, the present study evaluated the effect of intraperitoneal administration (dose 1 mg/kg) of water-soluble C fullerenes, as powerful antioxidants, on the development of rat kidney damage due to rhabdomyolysis caused by mechanical trauma of the of different severity (crush syndrome lasting 1 min under a pressure of 2.5, 3.5, and 4.5 kg/cm, respectively).
Methods: Using tensometry, biochemical and histopathological analyses, the biomechanical parameters of contraction (contraction force and integrated muscle power), biochemical indicators of rat blood (concentrations of creatinine, creatine phosphokinase, urea and hydrogen peroxide, catalase and superoxide dismutase activity), glomerular filtration rate and fractional sodium excretion value, as well as pathohistological and morphometric features of muscle and kidney damages in rats on days 1, 3, 6 and 9 after the initiation of the injury were studied.
Results: Positive changes in biomechanical and biochemical parameters were found during the experiment by about 27-30 ± 2%, as well as a decrease in pathohistological and morphometric features of muscle and kidney damages in rats treated with water-soluble C fullerenes.
Conclusion: These findings indicate the potential application of water-soluble C fullerenes in the treatment of pathological conditions of the muscular system caused by rhabdomyolysis and the associated oxidative stress.
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http://dx.doi.org/10.2147/IJN.S468013 | DOI Listing |
Neurocrit Care
January 2025
Department of Neurology, Mayo Clinic Rochester, Rochester, MN, USA.
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.
View Article and Find Full Text PDFTrans R Soc Trop Med Hyg
January 2025
Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry 605006, India.
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.
View Article and Find Full Text PDFTrans R Soc Trop Med Hyg
January 2025
Department of Clinical Medicine, Faculty of Medicine, University of Colombo, P.O. 00800, Sri Lanka.
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.
View Article and Find Full Text PDFJ Zhejiang Univ Sci B
December 2024
Department of Emergency Medicine, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
J Inflamm Res
December 2024
Department of Traditional Chinese Medicine, The First Affiliated Hospital of Jinan University, Guangzhou, People's Republic of China.
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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