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The simultaneous occurrence of vasculitic glomerulonephritis and membranous nephropathy is unusual. We report two cases that presented to our outpatient department with rapidly progressive renal failure. On evaluation, in one patient, anti-myeloperoxidase (MPO) titers were high, and renal biopsy was suggestive of concurrent necrotizing and diffuse crescentic anti-MPO anti-neutrophil cytoplasmic antigen-associated glomerulonephritis with the circumferential cellular crescent formation and membranous glomerulopathy.

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Thrombotic microangiopathy (TMA) is a severe condition characterized by microangiopathic hemolytic anemia, thrombocytopenia, and end-organ damage, often involving the kidneys. Complement-mediated hemolytic uremic syndrome (cHUS), a rare form of TMA, arises from dysregulated alternative complement pathway activation, frequently due to genetic mutations. We report the case of a 23-year-old male presenting with TMA secondary to a heterozygous mutation in the membrane cofactor protein (MCP/CD46) gene.

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Background: This study examines the role and effectiveness of double filtration plasmapheresis (DFPP) in managing hyperlipidemiclipidemic acute pancreatitis (HLAP).

Methods: Comparative analysis was conducted between two groups: one treated with DFPP and one without. Comparative parameters included blood lipid levels, inflammatory factors, vital signs, disease severity scores, and complication rates.

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Anti-glomerular basement membrane disease is a rare small vessel vasculitis caused by the deposition of immunoglobulin G (IgG) autoantibodies in the basement membrane of glomerular capillaries and lung alveoli, leading to rapidly progressive renal failure and/or alveolar hemorrhage. We report the case of an 83-year-old female patient presenting with uremic symptoms, rapidly progressive kidney failure, and a high titer of anti-glomerular basement membrane antibodies. Given the urgent need for kidney replacement therapy, the substantial fibrosis and glomerular scarring observed in the kidney biopsy suggesting a chronic process, and the absence of pulmonary involvement, neither immunosuppressive treatment nor plasmapheresis was initiated, since a low likelihood of a favorable response to these interventions was expected.

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Introduction: Guillain-Barré syndrome (GBS) is an inflammatory disorder of the peripheral nervous system, causing acute flaccid paralysis. There have been occasional reports linking Hepatitis A virus (HAV) to GBS. Here we aimed to evaluate the current literature on the association between GBS and HAV, exploring potential mechanisms and clinical implications.

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