Solange Moll Abstract Membranous glomerulonephritis and crescents A 45-year-old Swiss female was diagnosed in 1992 for a seropositive rheumatoid arthritis and treated with different regimens including NSAIDs, gold therapy, methotrexate and anti-TNF antibodies. Since 2006, she decided to take only homeopathic therapy. On August 2009, she was admitted to our hospital with complaints of asthenia, legs swelling and increased body weight (6 kg in 3 months). Physical examination revealed edema of the lower extremities and hypertension (160/90mmHg). Initial laboratory data showed high CRP value (62mg/l), anemia (hemoglobin: 93g/l) and rapidly progressive renal failure (serum creatinine: 313μmol/l on admission, 500μmol/l ten days later). Proteinuria (6.3g/l) with glomerular microhematuria and pyuria was detected on urinalysis. Other laboratory data revealed positive antinuclear antibody (1/320) and pANCA (1/640, MPO) tests. A renal biopsy was performed, which consisted of two cores containing 10 glomerules. Three of them showed foci of fibrinoid necrosis with GBM rupture and extracapillary fibrin, and seven showed cellular crescents. A diffuse moderate-to-severe interstitial inflammation composed of a mixed infiltrate of lymphocytes, histiocytes and plasmocytes was observed. Immunofluorescence revealed granular, global glomerular capillary wall positivity for IgG and weaker staining for C3 and C5b-9. Electron microscopy showed subepithelial electron dense deposits, often accompanied by GBM spikes and overlying neomembrane formation. The diagnosis of membranous glomerulonephritis stage I-II and ANCA-associated necrotizing and crescentic glomerulonephritis was done. Methylprednisolone and cyclophosphamide iv therapy was begun, in association with plasmapheresis and transient hemodialysis. Treatment led to rapid improvement in renal function (serum creatinine:120μmol/l at one month) and to a significant decline in the degree of proteinuria. Mycophenolate mofetyl was substituted for cyclophospamide and doses of prednisone were progressively reduced. Renal function was stable during the next following 6 months. Only rare cases of concurrent membranous glomerulonephritis (MGN) and antineutrophil cytoplasmic antibody (ANCA)-associated necrotizing and crescentic glomerulonephritis (NCGN) have been reported in the literature (1). Recently, Snar et al. reported the clinical and pathologic findings in 14 patients with MGN and ANCA-associated NCGN (2). Clinical presentation included heavy proteinuria (mean 24-hr urine protein 6.5 g/d), hematuria, and acute renal failure (mean creatinine 400μmol/l), as observed in our case. Pathologic