title: [Steroid-responsive nephrotic syndrome in IgA nephropathy].
abstract: A 46-year-old male, smoker of half a packet a day and an alcohol intake of 80 grams a day, with an unremarkable medical history, was referred to our service in the year 1988 for a study of nephrotic syndrome. He presented normal renal function, without either microhematuria nor hypertension. In blood analysis an albuminemia of 10 g/l and proteinuria of 22 g/d was observed. A first renal biopsy was carried out which indicated minimal change disease. Steroid treatment was started, as a result the nephrotic syndrome disappeared and the blood analysis normalized. Later he had 4 new outbreaks, all of them steroid-responsive. In 1992 a second renal biopsy was performed after the fourth outbreak and the presence of mild renal failure, that this time indicated a IgA nephropathy. Steroid treatment was tried again, and this time cyclophosphamide was added to try to reduce steroid doses. This result in normalization of renal function and decrease of proteinuria to 2 g/d. The patient remained stable until 1996 when the fifth outbreak occurred, again with mild renal failure and proteinuria in nephrotic range. Therefore a third renal biopsy was performed, that confirmed the presence of IgA nephropathy, but now with signs of histological progression of the disease. Following this, he presented five outbreaks in 3 years, all of them steroid-responsive, with decrease of proteinuria although without renal function normalization. In the year 2000, at his tenth outbreak of nephrotic syndrome it was decided to add cyclosporine to the steroid treatment, achieving the stability of the patient, without further outbreaks until now, with proteinuria of 1.6 g/d and C. creat. 59 ml/min.
authors.affiliation: Servicio de Nefrología, Fundación Puigvert, Barcelona, España. RMGarcía@fundacio-puigvert.es
authors.forename: R M
authors.initials: RM
authors.lastname: García Camín
authors.forename: A
authors.initials: A
authors.lastname: Cabezas
authors.forename: F
authors.initials: F
authors.lastname: Calero
authors.forename: J A
authors.initials: JA
authors.lastname: Ballarín
mesh_terms: D001706:Biopsy; D003520:Cyclophosphamide / Q000008:administration & dosage / Q000627:therapeutic use; D016572:Cyclosporine / Q000008:administration & dosage / Q000627:therapeutic use; D003920:Diabetes Mellitus / Q000139:chemically induced; D004359:Drug Therapy, Combination; D005922:Glomerulonephritis, IGA / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy / Q000473:pathology; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000188:drug therapy / Q000209:etiology* / Q000473:pathology; D010024:Osteoporosis / Q000139:chemically induced; D011241:Prednisone / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use; D011507:Proteinuria / Q000188:drug therapy / Q000209:etiology; D012008:Recurrence
chemical_list: D007166:Immunosuppressive Agents; D016572:Cyclosporine; D003520:Cyclophosphamide; D011241:Prednisone