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Membranous nephropathy: a review on the pathogenesis, diagnosis, and treatment
Wei Ling Lai1, Ting Hao Yeh1, Ping Min Chen1
1Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
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.
Insights
Membranous nephropathy (MN) causes nephrotic syndrome, often with unknown causes. Research highlights the antiphospholipase A2 receptor antibody in idiopathic MN, aiding diagnosis and prognosis.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Membranous nephropathy (MN) is a leading cause of nephrotic syndrome in adults.
- Idiopathic cases constitute approximately 75% of MN, with secondary causes including autoimmune diseases, infections, drugs, and malignancy.
- The precise mechanism of immune complex formation in MN pathogenesis remains unclear, though hypotheses involve preformed complexes, in situ formation, or autoantibodies against podocyte antigens.
Purpose of the Study:
- To review the epidemiology, pathogenesis, diagnosis, and treatment of membranous nephropathy.
- To highlight recent findings regarding antiphospholipase A2 receptor antibodies in idiopathic MN.
- To discuss current and evidence-based treatment strategies for MN.
Main Methods:
- Review of existing literature on membranous nephropathy.
- Analysis of epidemiological data.
- Synthesis of current understanding of MN pathogenesis and diagnostic markers.
- Evaluation of therapeutic approaches, including supportive care and immunosuppression.
Main Results:
- Immune complex deposition in subepithelial sites initiates complement activation and glomerular damage.
- Antiphospholipase A2 receptor antibody association with idiopathic MN offers potential diagnostic and prognostic value.
- Current management involves supportive care (ACE inhibitors/ARBs, lipid-lowering agents, blood pressure control) and immunosuppression for refractory cases.
Conclusions:
- Membranous nephropathy is a significant cause of nephrotic syndrome with complex pathogenesis.
- The identification of antiphospholipase A2 receptor antibodies represents a breakthrough in understanding and managing idiopathic MN.
- Optimal treatment requires a combination of supportive measures and, in select cases, immunosuppressive therapy, often involving steroids and alkylating agents.
