title: Treatment strategies for Henoch-Schönlein purpura nephritis by histological and clinical severity.
abstract: The management of Henoch-Schönlein purpura nephritis (HSPN) is controversial. It has been revealed that some patients develop end-stage renal disease and aggressive treatment with drugs such as steroids is increasing, and some of them may be overzealous. At our institutes, our treatment decisions are based on the clinical and pathological severity of the case in an attempt to limit the indications for aggressive therapies such as steroids and immunosuppressive agents. Here, we retrospectively examined the efficacy of treatment for HSPN. Renal biopsy was performed in patients with nephrotic syndrome or persistent proteinuria for more than 3 months and patients were classified by treatment. Patients (n=31) with moderately severe HSPN (histological grade I-III and serum albumin [Alb] >2.5 g/dl) were treated with angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers. Patients (n=19) with HSPN exceeding grade III or Alb ≤ 2.5 g/dl received combination therapy comprising prednisolone, immunosuppressants, warfarin, and dipyridamole. All patients showed resolution of proteinuria without renal dysfunction during the observation period (3.76 ± 0.37 years). Our findings support those of some earlier reports that treatment strategies for HSPN should depend on the histological and clinical severity. Furthermore, aggressive therapies, particularly combination therapies, are unnecessary for moderate-severe HSPN.
authors.affiliation: Department of Pediatrics, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 6500017, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Ninchoji
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kaito
authors.forename: Kandai
authors.initials: K
authors.lastname: Nozu
authors.forename: Yuya
authors.initials: Y
authors.lastname: Hashimura
authors.forename: Kyoko
authors.initials: K
authors.lastname: Kanda
authors.forename: Ichiro
authors.initials: I
authors.lastname: Kamioka
authors.forename: Yuko
authors.initials: Y
authors.lastname: Shima
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Hamahira
authors.forename: Koichi
authors.initials: K
authors.lastname: Nakanishi
authors.forename: Ryojiro
authors.initials: R
authors.lastname: Tanaka
authors.forename: Norishige
authors.initials: N
authors.lastname: Yoshikawa
authors.forename: Kazumoto
authors.initials: K
authors.lastname: Iijima
authors.forename: Masafumi
authors.initials: M
authors.lastname: Matsuo
mesh_terms: D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D002648:Child; D004176:Dipyridamole / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D011695:IgA Vasculitis / Q000150:complications* / Q000188:drug therapy; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008297:Male; D009393:Nephritis / Q000188:drug therapy* / Q000209:etiology* / Q000473:pathology*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011239:Prednisolone / Q000627:therapeutic use; D016896:Treatment Outcome; D014859:Warfarin / Q000627:therapeutic use
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000893:Anti-Inflammatory Agents; D000925:Anticoagulants; D007166:Immunosuppressive Agents; D010975:Platelet Aggregation Inhibitors; D014859:Warfarin; D004176:Dipyridamole; D011239:Prednisolone