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
Hepatitis B
The most frequent glomerulopathy in patients infected with hepatitis B virus is MGN followed by membranoproliferative GN. The antigens Core (HBcAg) and e (HBeAg) seem the most important in the pathogenesis of hepatitis B-associated MGN. In these cases the antigens, or their antibodies, are identified in the glomerular immune deposits. It is not clear what is first deposited: the Ag., the Ac. or the Ag-Ac complex previously formed (circulating). Prevalence of MGN in the infection is not known, but in children with MGN the carrier stage is detected in around 20% of cases, with higher rates in endemic countries. In adults the percentage of patients with MGN carrying hepatitis B virus is lower than in children. In GNM cases associated with this infection there are more frequently mesangial hypercellularity, endocapillary proliferation, subendothelial immune deposits, and tubuloreticular endothelial structures (electron microscopy). It is frequent that appears with hypocomplementemia. The prognosis of MGN in hepatitis B patients seem more favorable, with most frequency of remission and less probability of evolution to terminal renal damage.
Hepatitis C
In this infection disease also secondary MGN can appear, although membranoproliferative GN is more frequent. In many studies have not been identified antigens of the virus, or Acs against these, in the glomerular deposits. Clinic expression can be similar to idiopathic MGN or it may appear with asymptomatic proteinuria.
Congenital Syphilis
MGN is a rare complication in congenital syphilis, but it is a well-recognized cause of NS in children with this infection. Other glomerular disease in congenital syphilis include nephritic syndrome and crescentic GN with rapidly progressive disease. We have seen cases with these types of glomerular disease and there is a dramatic improvement with the antibiotic treatment. Several studies have demonstrated the presence of antigens of Treponema pallidum in the immune glomerular deposits.
Systemic Lupus Erythematosis
the histopathologic presentation is very variable and there is combination of morphologic changes: MGN with subendothelial deposits, endocapillary and/or mesangial proliferation, crescents, combination with characteristics of membranoproliferative GN, and other patterns. In the most recent lupus nephritis classification, pure MGN (class V) is only diagnosed if there are no other active lesions; if there is combination with active lesions it is diagnosed as combination of class V and class III or IV only if there are lesions with membranous characteristics in more than 50% of the tuft in more than 50% of glomeruli. Occasional subepithelial deposits and “spikes” formation are very frequent in class III and IV lupus nephritis. In most of these cases we find C1q glomerular deposits.
Malignancy
The neoplasms more frequently associated with MGN are lung, breast, colon, stomach and kidney carcinomas, leukemia and lymphomas (Hodgkin’s and non-Hodgkin’s), but there is information of MGN in many other cancer types. Incidence of cancer in patients with MGN is approximately 1%. The histologic and immunopathologic findings and the clinical presentation are similar to those of idiopathic forms of MGN. The association between MGN and neoplasms is supported by the clinical course, the immune response of the host to the tumor and the glomerular pathology, nevertheless, in very few cases is documented an antigen of the tumor, or its antibody, in glomerular deposits. It is possible that the immune response against the neoplasm, in a propitious genetic context, allow the development of MGN. The prognosis of the glomerulopathy depend on that of the neoplasm. If there are treatment and response of this last one, the MGN tends to disappear.
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.