A 60-year-old man diagnosed in another hospital in 2000 with extracapillary glomerulonephritis type III associated with C-ANCA. He was treated with 5 intravenous boluses of 6-methylprednisolone followed by oral corticosteroids in a descending pattern associated with oral cyclophosphamide (we were unable to obtain the exact dosage). Cyclophosphamide was discontinued at the time due to myelotoxicity.
In 2002 he was included in a periodic haemodialysis programme.
In September 2006, in another transplant centre, he received a cadaveric kidney graft. The patient was receiving tacrolinus monotherapy, although we cannot be sure whether he had previously received any other combination of immunosuppressants. His serum creatinine levels ranged between 1.5 and 1.7 mg/dl.
In December 2013, on the occasion of the implantation of a percutaneous aortic valve in our hospital, a pre- and post-intervention assessment was performed in our department. At that time, his clinical condition was good, with serum creatinine of 1.5 mg/dl and proteinuria of 0.3 g/day, with normal urinary sediment.
In October 2014, due to the appearance of respiratory symptoms with fever and deterioration of renal function, the patient decided to transfer to our hospital for clinical monitoring. The fever and respiratory symptoms, without microbiological or radiological evidence, improved with empirical treatment with levofloxacin. However, renal function worsened in a few days, reaching serum creatinine levels of 4 mg/dl, with proteinuria of 6.8 g/day and haematuria. C-ANCA determination was 74.2 IU/ml (normal values: 0-5 IU/ml) and P-ANCA 8.4 IU/ml (normal values: 0-6 IU/ml). All other autoimmunity parameters (ANA, anti-GBM antibodies, complement, cryoglobulins, etc.) were negative. HIV, HCV, HBV serology and CMV and BK viraemia were also negative.
A biopsy of the renal graft was performed in which the most relevant findings were: of the 19 assessable glomeruli, 3 showed global glomerular sclerosis, 12 glomeruli showed cellular crescents. Some of them showed disruption of Bowman's capsule causing pseudogranulomatous inflammatory reaction of mononuclear cells. In 2 glomeruli there were lesions compatible with fibrinoid necrosis. We found tubular necrosis in 15%, tubular atrophy in 20% and some haematic casts, as well as interstitial infiltrate in 25% with some eosinophils and foci of recent interstitial haemorrhage and arteriolar hyalinosis, with some images of mucoid degeneration of the wall without transmural infiltrate. The immunofluorescence study was negative. The immunohistochemical study for C4d was negative.

Given the evidence of a recurrence of the underlying disease, the patient received 3 intravenous boluses of 500 mg of 6-methylprednisolone (the patient was diabetic) on consecutive days, followed by oral prednisone at a dose of 0.5 mg/kg/day in a descending pattern. He also underwent 8 sessions of plasmapheresis and was started on treatment with mycophenolate mofetil (1 g/12 h, oral) associated with tacrolimus.
Twelve days after admission, the patient was discharged with a serum creatinine of 2.9 mg/dl. At an outpatient follow-up one month later, creatinine was 2.3 mg/dl and proteinuria was 3.6 g/day.
