Treatment with azathioprine was restarted

Treatment with azathioprine was restarted. amounts of anti-GBM antibodies usually do not remain in the circulation for >6C12 months, even without the use of cytotoxic drugs. After that time, the recurrence of anti-GBM antibodies as well as relapse of glomerulonephritis (GN) is rare [3C5]. Here, we report a case of a clinically and histologically mild form of GN, associated with low levels of anti-GBM antibodies but complicated by a protracted relapsing course. Case report A 71-year-old woman with a medical history that included a peripheral facial paresis and an irritable colon sought medical attention in August 2000 after a 6-month period of general malaise, intermittent subfebrility and myalgia. The weeks preceding the appointment PF 4981517 her condition had worsened. Dipstick tests revealed haematuria and proteinuria. Blood tests indicated a mild renal failure with a serum creatinine of 100 mol/L and an erythrocyte sedimentation rate of 80 mm/h. A week later her creatinine had risen to 130 mol/L and serology was positive for anti-GBM with 61 and myeloperoxidase-antineutrophil cytoplasmic anitbody (MPO-ANCA) >320 ELISA units (above 10 is considered as positive in both the assays). She was transferred to the Lund University Hospital, where she received apheresis with Protein A adsorption columns. A renal biopsy showed focal necrotizing glomerulonephritis with crescents in 6 of 16 glomeruli and a typical linear immunofluorescence pattern for IgG, kappa and lambda. After three Protein A sessions, her anti-GBM antibodies were undetectable. She was discharged with oral cyclophosphamide 75 mg per day and prednisolone. After 5 months, the medication was switched to azathioprine 50 mg daily, which was continued for 12 months. Serum creatinine remained stable at a level of 90 mol/L and anti-GBM antibodies were below the detection limit (Figure 1). Open in a separate window Fig. 1. The solid line represents levels of anti-GBM antibodies measured PF 4981517 by the enzyme-linked immunosorbent assay (ELISA) and expressed in arbitrary ELISA units as indicated by the right vertical axis. The patient exhibited four distinct serological exacerbations separated by intervals with negative tests. The serological relapses coincided with clinical relapses; start (and restart) of immunosuppressive treatment is indicated by Rabbit Polyclonal to FPR1 arrows. Dotted lines represent MPO-ANCA levels measured by three different ELISA methods. Method* was used until June 2007, then method** was used until November the same year when method***, using international units, was introduced. ELISA units for MPO-ANCA are indicated on the left vertical axis, levels differ between the three assays. Two years later in the fall of 2004, she experienced a relapse with re-emergence of anti-GBM antibodies, return of microscopic haematuria and a slight elevation of serum creatinine (maximum 108 mol/L). Treatment with azathioprine was restarted. During 2005, anti-GBM remained positive at low level, but turned negative in April 2006. Haematuria was noted until November 2005. Azatioprine therapy was continued for 25 months. In October 2007, she experienced her second minor relapse with return of anti-GBM antibodies, microscopic haematuria and a slight elevation of creatinine (maximum 131 mol/L). Treatment with pulse cyclophosphamide therapy was initiated, resulting in disappearance of anti-GBM antibodies and haematuria. After six cyclophosphamide pulses, azathioprine was restarted. In November 2010, both haematuria and anti-GBM antibodies returned, like at previous relapses there was no malaise PF 4981517 or other symptoms of general inflammation. This third relapse was curbed with an increase in azathioprine doses to 150.