title: Cyclophosphamide pulse therapy in advanced progressive IgA nephropathy.
abstract: For advanced progressive primary IgA nephropathy (IgAN) no established therapy exists. We conducted a prospective, uncontrolled trial to evaluate the effect of intravenous cyclophosphamide pulse (CyP) therapy on the course of advanced progressive IgAN. Twenty-one patients (mean age 52 +/- 10 years; male/female 20/1) with biopsy-proven IgAN without crescentic extracapillary proliferation and a serum creatinine of more than 2.0 mg/dl and/or an increase more than 25% in the previous 3 months were included. Patients were treated with CyP (750 mg/m(2 )body surface area) every 4 weeks for 6 months and low dose oral prednisolone. The loss of renal function per year was significantly reduced from 16% before therapy to 4% after therapy (p < 0.001). A further increase >25% of serum creatinine after therapy was observed in 8 patients after 0.7 years (range 0.3-3.0 years), and 3 of these patients developed end-stage renal disease. Proteinuria decreased significantly during CyP therapy. A low nadir of white blood cell and platelet count was associated with a better renal outcome (p = 0.025). In conclusion, CyP therapy and low dose oral prednisolone is effective in preserving renal function in a subgroup of patients with advanced progressive IgAN.
authors.affiliation: Division of Nephrology, Department of Internal Medicine II, University of Ulm, Ulm, Germany. maximilian.rasche@medizin.uni-ulm.de
authors.forename: Franz Maximilian
authors.initials: FM
authors.lastname: Rasche
authors.forename: Christoph Hubert
authors.initials: CH
authors.lastname: Klotz
authors.forename: David
authors.initials: D
authors.lastname: Czock
authors.forename: Wolfram
authors.initials: W
authors.lastname: Karges
authors.forename: Rainer
authors.initials: R
authors.lastname: Muche
authors.forename: Peter Michael
authors.initials: PM
authors.lastname: Jehle
authors.forename: Andreas
authors.initials: A
authors.lastname: Mertz
authors.forename: Frieder
authors.initials: F
authors.lastname: Keller
mesh_terms: D000328:Adult; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D003404:Creatinine / Q000097:blood; D003520:Cyclophosphamide / Q000008:administration & dosage* / Q000009:adverse effects; D018450:Disease Progression; D004359:Drug Therapy, Combination; D005260:Female; D005922:Glomerulonephritis, IGA / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage* / Q000009:adverse effects; D007668:Kidney / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000209:etiology; D008297:Male; D008875:Middle Aged; D011239:Prednisolone / Q000627:therapeutic use; D011446:Prospective Studies; D011507:Proteinuria / Q000188:drug therapy; D020551:Pulse Therapy, Drug; D044140:Receptor, Angiotensin, Type 1; D012044:Regression Analysis
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D044140:Receptor, Angiotensin, Type 1; D003520:Cyclophosphamide; D011239:Prednisolone; D003404:Creatinine