Opportunistic peritonitis in peritoneal dialysis: The example of .

, a Gram-negative coccobacillus, is an emergent opportunistic pathogen. It originates from soil and water. VITEK and MALDI-TOF are used for identification.

Intravitreal Injection of Anti-VEGF Antibody Induces Glomerular Endothelial Cells Injury.

Introduction: Antiangiogenic agents that inhibit vascular endothelial growth factor have emerged as important tools in cancer therapy and ocular diseases. Their systemic use can induce renal limited microangiopathy. Local use of anti-VEGF agent is supposed to be safe.

Molecular classification of membranous nephropathy.

Purpose Of Review: Continuous expansion of our knowledge in the pathogenesis of membranous nephropathy possible by the identification of antibodies recognized specific podocytes antigens results in unprecedent patient management strategy.

Recent Findings: Circulating anti-phospholipase A2 receptor (PLA2R) and anti-thrombospondin domain 7A (THSD7A) antibodies strongly relate with the modifications of podocytes biology leading to the new molecular diagnosis of membranous nephropathy. Immunization against THSD7A involves extra-renal mechanism.

New insights into immune cells cross-talk during IgG4-related disease.

Immunoglobulin G4-related disease (IgG4-RD) is a newly acknowledged entity, characterized by an immune-mediated fibro-inflammatory process affecting virtually all organs, with infiltration of IgG4 bearing plasma cells. Until today the pathogenesis of IgG4-RD remains unknown. Treatment with anti-CD20 monoclonal antibodies efficiently induced remission and attenuated the secretory phenotype of myofibroblasts responsible of uncontrolled collagen deposition.

Membranous Nephropathy and Anti-Podocytes Antibodies: Implications for the Diagnostic Workup and Disease Management.

The discovery of circulating antibodies specific for native podocyte antigens has transformed the diagnostic workup and greatly improved management of idiopathic membranous nephropathy (iMN). In addition, their identification has clearly characterized iMN as a largely autoimmune disorder. Anti-PLA2R1 antibodies are detected in approximately 70% to 80% and anti-THSD7A antibodies in only 2% of adult patients with iMN.