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| http://dx.doi.org/10.18502/cjn.v22i2.13342 | DOI Listing |
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Eculizumab treatment for Chinese patients with hemolytic paroxysmal nocturnal hemoglobinuria (PNH): efficacy and safety - a single-center study.
Hematology
December 2025
Department of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, People's Republic of China.
Objective: To evaluate the short-term efficacy and safety of eculizumab for the treatment of paroxysmal nocturnal hemoglobinuria (PNH) in China.
Method: Data were retrospectively collected from patients with PNH who received at least 3 months of full-dose eculizumab. Changes in clinical and laboratory indicators after 1, 3, and 6 months of eculizumab therapy and at the end of follow-up were documented.
Complement-Mediated Hemolytic Uremic Syndrome Due to MCP/CD46 Mutation: A Case Report.
J Investig Med High Impact Case Rep
January 2025
Marshall University, Huntington, WV, USA.
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.
View Article and Find Full Text PDFSwitch from eculizumab to satralizumab in aquaporin 4 immunoglobulin G-seropositive neuromyelitis optica spectrum disorder: a case series report.
Front Immunol
January 2025
Genentech, Inc., South San Francisco, CA, United States.
Objectives: This case series describes adults with aquaporin 4 immunoglobulin G-seropositive (AQP4-IgG+) neuromyelitis optica spectrum disorder (NMOSD) who switched treatment from eculizumab to satralizumab.
Methods: Case information for patients with AQP4-IgG+ NMOSD who received satralizumab for ≥6 months was obtained from US healthcare providers from April 2022 to January 2024. Patient characteristics, examination findings, diagnostic test results, treatment response, and adverse events were recorded.
Improved therapeutic efficacy of a bifunctional anti-C5 mAb-FH SCR1-5 fusion protein over anti-C5 mAb in an accelerated mouse model of C3 glomerulopathy.
Immunohorizons
January 2025
Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
C3 glomerulopathy (C3G), a rare kidney disease caused by dysregulation of alternative pathway complement activation, is characterized by glomerular C3 deposition, proteinuria, crescentic glomerulonephritis, and renal failure. The anti-C5 monoclonal antibody (mAb) drug eculizumab has shown therapeutic effects in some but not all patients with C3G, and no approved therapy is currently available. Here, we developed and used a triple transgenic mouse model of fast progressing lethal C3G (FHm/mP-/-hFDKI/KI) to compare the therapeutic efficacy of a bifunctional anti-C5 mAb fused to a functional factor H (FH) fragment (short consensus repeat 1-5 [SCR1-5]) and the anti-C5 mAb itself.
View Article and Find Full Text PDFExploring Potential Complement Modulation Strategies for Ischemia-Reperfusion Injury in Kidney Transplantation.
Antioxidants (Basel)
January 2025
Nephrology, Dialysis and Transplantation Unit, Advanced Research Center on Kidney Aging (A.R.K.A.), Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy.
The complement system plays a crucial role in regulating the inflammatory responses in kidney transplantation, potentially contributing to early decline in kidney function. Ischemia-reperfusion injury (IRI) is among the factors affecting graft outcomes and a primary contributor to delayed graft function. Complement activation, particularly the alternative pathway, participates in the pathogenesis of IRI, involving all kidney compartments.
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