Open AccessPD42 ‐ Is rituximab a trigger for persistent hypogammaglobulinemia in idiopathic nephrotic syndrome?
Author(s) -
Trujillo Juan Enrique,
Bosque Montserrat,
Asensio Òscar,
Ranera Adrián,
Rojo Juan Cristobal,
Vilella Mireia,
Guijarro Elisabet,
Domingo Xavier,
Valdesoiro Laura,
Larramona Helena
Publication year - 2014
Publication title -
clinical and translational allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.979
H-Index - 37
ISSN - 2045-7022
DOI - 10.1186/2045-7022-4-s1-p42
Subject(s) - hypogammaglobulinemia , medicine , nephrotic syndrome , rituximab , immunology , proteinuria , cyclophosphamide , immunodeficiency , gastroenterology , pediatrics , antibody , chemotherapy , kidney , immune system
Rituximab (RTX) is a monoclonal antibody; recently it has been use as a new treatment strategy in patients with high-degree steroid-dependent nephrotic syndrome. It provokes a lymphocyte B depletion in some cases that interacts with Immunoglobulins creating decreased plasma IgG levels and hypogammaglobulinemia. We report the case of a 2.5 year old male diagnosed of idiopathic nephrotic syndrome. He presented resistance to systemic steroids as well as second line treatments (cyclophosphamide and mycophenolate). Patient started with intravenous infussion of rituximab at 375mg/m2. Baseline analysis before RTX treatment evidenced low IgG levels, although these values are not conclusive because they were taken during nephrotic state. Twenty days later, the patient presented severe hypogammaglobulinemia with IgG levels of 149 mg/dL, without nephrotic proteinuria. We decided to start intravenous gammaglobulin (IVIG) every 4-6 weeks. Analysis showed low levels of lymphocytes (predominantly B type) four days after initiated the treatment. Follow up demonstrated complete recovery of lymphocyte count two years later. After 3 years of RTX administration the patient continues to have hypogammaglobulimenia, requiring IVIG until now.