Mouse IgG1 kappa Isotype Control [Biotin]

Immunofluorescence staining plays a vital role in nephropathology, but the panel of antibodies used has not changed for decades. Further classification of immunoglobulin (Ig) G-containing immune-type deposits with IgG subclass staining (IgG1, IgG2, IgG3, and IgG4) has been shown to be of diagnostic utility in glomerular diseases, but their value in the evaluation of renal biopsies has not been addressed systematically in large renal biopsy material. Between January 2007 and June 2014, using direct immunofluorescence, we stained every renal biopsy for the IgG subclasses if there was moderate to prominent glomerular IgG staining and/or IgG-predominant or IgG-codominant glomerular staining. The total number of biopsies stained was 1084, which included 367 cases of membranous glomerulonephritis, 307 cases of lupus nephritis, 74 cases of fibrillary glomerulonephritis, 53 cases of proliferative glomerulonephritis with monoclonal IgG deposits, and 25 cases of antiglomerular basement membrane disease, among others. We found that monoclonality of IgG deposits cannot always be reliably determined on the basis of kappa and lambda light chain staining alone, particularly if concomitant (frequently nonspecific) IgM staining is present. In IgG heavy and heavy and light chain deposition disease (3 cases), subclass staining is very helpful, and in proliferative glomerulonephritis with monoclonal IgG deposits subclass staining is necessary. IgG subclass staining is useful in differentiating primary from secondary membranous glomerulonephritis. In proliferative glomerulonephritis with polyclonal IgG deposition, IgG1 dominance/codominance with concomitant IgG3 and IgG2 but weak or absent IgG4 staining favors an underlying autoimmune disease. IgG subclass staining is a very useful diagnostic method in a selected cohort of renal biopsies, particularly in biopsies with glomerulonephritis with monoclonal IgG deposits.

Cytomegalovirus (CMV) infections are asymptomatic in immunocompetent patients but in immunocompromised patients, CMV infections have varying manifestations depending on their location. Patient who are organ transplant recipients, taking immunosuppressive therapy for a long time are at increased risk of CMV infections. CMV-induced gastric ulcer is very rare but many cases have been reported in the literature. No case describing association between CMV-related gastric ulcer and glomerulonephritis has been reported in the literature so far. In this article, we describe a case of pauci immune crescentic glomerulonephritis in a patient who was on rituximab and long-term steroid therapy and found to have CMV-related gastric ulcer. The association of small vessel vasculitis and CMV-related gastrointestinal infection has not been studied in the literature. Pauci immune crescentic glomerulonephritis is a subtype of rapidly progressive glomerulonephritis manifested by continuous loss of renal functions with features of dysmorphic red blood cells and glomerular proteinuria. Treatment of such condition is a genetically engineered chimeric murine/human monoclonal IgG1 kappa antibody directed against the CD20 antigen known as Rituximab. We also discussed the pathogenesis of CMV- induced gastric ulcer after rituximab therapy. This case emphasizes the importance of opportunistic infections in glomerulonephritis patients and raises the awareness that glomerunephritis patients are at increased risk of opportunistic infections as well. Rituximab was considered to be a safer drug but over the years, the incidence if opportunistic infections in patients on rituximab has been increasing.