Literature DB >> 25558821

Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment.

Wei Ling Lai1, Ting Hao Yeh1, Ping Min Chen1, Chieh Kai Chan1, Wen Chih Chiang2, Yung Ming Chen1, Kwan Dun Wu1, Tun Jun Tsai1.   

Abstract

In adults, membranous nephropathy (MN) is a major cause of nephrotic syndrome. However, the etiology of approximately 75% of MN cases is idiopathic. Secondary causes of MN are autoimmune diseases, infection, drugs, and malignancy. The pathogenesis of MN involves formation of immune complex in subepithelial sites, but the definite mechanism is still unknown. There are three hypotheses about the formation of immune complex, including preformed immune complex, in situ immune-complex formation, and autoantibody against podocyte membrane antigen. The formation of immune complex initiates complement activation, which subsequently leads to glomerular damage. Recently, the antiphospholipase A2 receptor antibody was found to be associated with idiopathic MN. This finding may be useful in the diagnosis and prognosis of MN. The current treatment includes best supportive care, which consists of the use of angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers, lipid-lowering agents, and optimal control of blood pressure. Immunosuppressive agents should be used for patients who suffer from refractory proteinuria or complications associated with nephrotic syndrome. Existing evidence supports the use of a combination of steroid and alkylating agents. This article reviews the epidemiology, pathogenesis, diagnosis, and the treatment of MN.
Copyright © 2014. Published by Elsevier B.V.

Entities:  

Keywords:  membranous nephropathy; pathogenesis; phospholipase A(2) receptor antibody; treatment

Mesh:

Substances:

Year:  2015        PMID: 25558821     DOI: 10.1016/j.jfma.2014.11.002

Source DB:  PubMed          Journal:  J Formos Med Assoc        ISSN: 0929-6646            Impact factor:   3.282


  34 in total

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10.  Rapidly Progressing Primary Membranous Nephropathy in a Hispanic Male With Elevated Levels of Anti-phospholipase A2 Receptor Antibodies.

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