Efficacy of Combined Desensitization Therapy Based on Protein A Immunoadsorption on Anti-human Leukocyte Antigen Antibodies in Sensitized Kidney Transplant Recipients: A Retrospective Study.

Background and objectives Protein A immunoadsorption (PA-IA) therapy is an immunoglobulin selective apheresis for pre-transplantation desensitization therapy and treatment of post-transplantation antibody-mediated rejection. There is no unified protocol for the timing of PA-IA therapy or its combination with other drug therapy. This study aimed to investigate and analyze the clearance effects of desensitization therapy on human leukocyte antigen (HLA) antibodies to provide a reference for the formulation of clinical desensitization therapy regimens.

Treatment of Severe Japanese Encephalitis Complicated With Hashimoto's Thyroiditis and Guillain-Barré Syndrome With Protein A Immunoadsorption: A Case Report.

A severely comatose female patient was diagnosed with Japanese encephalitis (JE). Her condition was complicated by Hashimoto's thyroiditis (HT) and Guillain-Barré syndrome (GBS). After antiviral, glucocorticoid, and immunoglobulin treatment, the patient's consciousness was restored, and she could breathe spontaneously.

Protein A immunoadsorption for the treatment of refractory anti-N-methyl-d-aspartate receptor encephalitis: A single-center prospective study.

Objective: The aim of this study was to evaluate the efficacy and safety of protein A immunoadsorption (IA) for anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis resistant to intravenous methylprednisolone (IVMP) and intravenous immunoglobulin (IVIG).

Methods: We prospectively evaluated patients with refractory anti-NMDAR encephalitis, treated with protein A IA. Demographic data, clinical characteristics, modified Rankin Score (mRS), and anti-NMDAR antibodies were documented before and after IA and at follow-up.

Protein A Immunoadsorption Relieves Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy after Unsuccessful Methylprednisolone Treatment.

Background: Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy (GFAP-A) is a recently defined autoimmune inflammatory disease of the central nervous system in which GFAP IgG is present in the cerebrospinal fluid (CSF). Its primary clinical manifestation is meningoencephalitis, and it usually responds well to corticosteroids. Herein, we report a case of a patient with GFAP-A with initial symptoms of psychological and cognitive impairment, which did not respond to high-dose methylprednisolone therapy but was successfully treated with protein A immunoadsorption (PAIA) therapy.

Rescue immunoadsorption treatment for neuromyelitis optica spectrum disorder attacks unresponsive to intravenous methylprednisolone.

We aimed to evaluate the value of immunoadsorption (IA) treatment after the failure of intravenous methylprednisolone (IVMP) therapy for neuromyelitis optica spectrum disorder (NMOSD). Sixty-one NMOSD attacks unresponsive to IVMP were included: 22 patients received rescue IA (IVMP+IA), 24 underwent rescue plasma exchange (PE) (IVMP+PE), and 21 received no further rescue therapy (IVMP alone). The improvement frequencies were higher in the IVMP+IA and IVMP+PE groups than in the IVMP-alone group (P = 0.

Soluble expression of a strong thrombolytic pro-urokinase mutant in Escherichia coli.

A recombinant pro-urokinase mutant GZ5-sPA was successfully constructed by fusion of a high fibrin-affinity fragment GZ5 to the N-terminus of the serine protease domain of pro-urokinase (sPA). The fragment GZ5 contains a tetrapeptide GPRP and a tripeptide RGD, and was synthesized in bacterial preferred expressing codons. The mutant was then fused to the C-terminus of maltose binding protein (MBP) carried by pMAL-C2x vector, and expressed in Escherichia coli strain Origami (DE3).