2010
DOI: 10.1007/s10165-010-0333-3
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Etanercept-induced necrotizing crescentic glomerulonephritis in two patients with rheumatoid arthritis

Abstract: We present two patients with rheumatoid arthritis (RA) who developed necrotizing crescentic glomerulonephritis (NCGN) during etanercept therapy. Both patients developed proteinuria and hematuria, and one progressed to renal failure. Renal biopsy revealed NCGN. In both patients, nephritis improved following discontinuation of etanercept and administration of prednisolone. Physicians should be aware of etanercept-induced GN in patients with RA on anti-tumor necrosis factor therapy.

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Cited by 13 publications
(11 citation statements)
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“…MGN has also been reported to occur with etanercept and adalimumab . Etanercept have also been linked to occurrence of crescentic GN . In addition, use of these agents is associated with increased incidence of infections, which can also affect kidneys.…”
Section: Renal Involvement In Rheumatological Diseases As a Complicatmentioning
confidence: 99%
“…MGN has also been reported to occur with etanercept and adalimumab . Etanercept have also been linked to occurrence of crescentic GN . In addition, use of these agents is associated with increased incidence of infections, which can also affect kidneys.…”
Section: Renal Involvement In Rheumatological Diseases As a Complicatmentioning
confidence: 99%
“…In addition, single reports reveal the presence of FSGS [139] and fibrillary glomerulonephritis [140] in RA patients. Anti-TNF alpha therapy can be causative for the development of necrotizing crescentic glomerulonephritis and proliferative lupus nephritis [141,142]. Besides the renal side effects of gold salts, D-penicillamine and bucillamine, CSA as another DMARD has a serious potential for renal toxicity, which is manifested primarily in a decline in creatinine clearance [143].…”
Section: Reviewmentioning
confidence: 99%
“…In our case, Pronase-aided digestion did not reveal pathologic paraprotein deposits, supporting the idea that such deposits were not present. In addition, though tumor necrosis factor inhibition, including with etanercept, has been linked to PIGN with inconsistent ANCA serologies, the development of RPGN 2 months after stopping etanercept while on immunosuppressive therapy is unlikely [ 9 , 10 ]. With these considerations, we propose that the monoclonal protein in these cases might activate or dysregulate the complement system, or activate neutrophils by mechanisms independent of ANCA.…”
Section: Discussionmentioning
confidence: 99%