Membranous glomerulonephritis causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Causes
Causes of secondary MN
Drugs
Exposure to a variety of agents that are primarily used to treat rheumatoid arthritis have been implicated in the development of MN, including nonsteroidal antiinflammatory drugs (NSAIDs), penicillamine, parenteral gold salts, bucillamine, and possibly anti-tumor necrosis factor agents (anti-TNF; etanercept, infliximab, or adalimumab) [67-74]. (See "Overview of the systemic and nonarticular manifestations of rheumatoid arthritis", section on 'Kidney disease' and "NSAIDs: Acute kidney injury (acute renal failure)" and "Overview of biologic agents and kinase inhibitors in the rheumatic diseases".)
The association of NSAIDs with MN was illustrated in a study of 125 patients with a biopsy diagnosis of MN [67]. Twenty-nine patients were taking an NSAID, and 13 (10 percent of the study population) fulfilled three criteria suggesting that the NSAID was responsible:
●No other apparent cause for the MN
●Resolution of proteinuria within 1 to 36 weeks of discontinuing NSAIDs
●No recurrence of proteinuria at follow-up (5 months to 13 years)
Many of the patients who developed MN had been treated with diclofenac, but probably any NSAID can be involved [67], including cyclooxygenase (COX)-2 inhibitors [69]. (See "NSAIDs: Acute kidney injury.
The incidence of MN may be as high as 7 percent in patients treated with penicillamine, and 1 to 3 percent in those treated with parenteral gold (the risk with oral gold [auranofin] appears to be lower) [75-77]. Tiopronin (2-mercaptopropionylglycine), an agent structurally similar to penicillamine that is used to treat cystine stones, has also been reported to cause MN, but the incidence is rare [78]. High-dose captopril, which also has a free thiol group, has also been associated with MN. (See "Cystine stones".)
The mechanisms responsible for drug-induced MN are uncertain. Human and experimental data suggest that induction of gold-specific and autoreactive T cells may lead to polyclonal B cell activation and autoantibody production in gold-induced MN [79,80]. Interestingly, it has been suggested that patients carrying the lupus-associated HLA alleles DRB1*0301 (DR3) and DQA1*0501 are particularly susceptible to develop MN, as well as drug-induced lupus, after exposure to gold salts [81].
It should be noted that MN is not the only glomerulopathy seen with these drugs. Gold and NSAIDs can lead to minimal change disease [77], whereas penicillamine can induce an immune complex crescentic glomerulonephritis. Anti-TNF therapy has also been associated with the new onset of lupus nephritis and pauci-immune necrotizing and crescentic glomerulonephritis [72].
Hematopoietic cell transplantation and graft-versus-host disease — Nephrotic syndrome occasionally arises in recipients of allogeneic stem cell or, less commonly, bone marrow transplants and is often temporally correlated with chronic graft-versus-host disease (GVHD).
MN is the most frequently reported underlying histology, although minimal change disease is also seen. The occurrence of MN is often associated with a decrease in immunosuppression. (See "Kidney disease following hematopoietic cell transplantation", section on 'Nephrotic syndrome' and "Clinical manifestations, diagnosis, and grading of chronic graft-versus-host disease".)