title: Predominant tubulointerstitial nephritis in a patient with systemic lupus nephritis.
abstract: In most cases of systemic lupus erythematosus (SLE), glomerular lesions are the main renal complication. Although tubulointerstitial lesions are often associated with severe glomerular lesions, predominant or isolated tubulointerstitial injury in the presence of minimal glomerular abnormalities with SLE, so-called predominant tubulointerstitial lupus nephritis, is rare. Only ten cases are reported in the English literature. Herein, we describe the case of a 64-year-old man with SLE who presented with acute renal deterioration attributable to acute tubulointerstitial nephritis. Renal biopsy showed diffuse infiltration of inflammatory mononuclear cells in the interstitium and tubulitis without significant glomerular lesions. Immunofluorescence study revealed positive staining for IgG, C3, and C1q along the renal tubular basement membrane (TBM). Electron microscopy also showed electron-dense deposits in the TBM. Other causes of tubulointerstitial injury, such as drug use and infection, were ruled out. Taking these findings together with the presence of antitubular basement membrane antibody, predominant tubulointerstitial lupus nephritis was diagnosed. Treatment with oral corticosteroids for 6 weeks improved renal function. Even after tapering of the corticosteroid, renal function and serological markers of SLE activity have remained stable in this patient for more than 12 months.
authors.affiliation: Renal Division, Department of Medicine II, Kansai Medical University, Moriguchi, Osaka 571-8506, Japan. moriy@takii.kmu.ac.jp
authors.forename: Yasukiyo
authors.initials: Y
authors.lastname: Mori
authors.forename: Noriko
authors.initials: N
authors.lastname: Kishimoto
authors.forename: Hideki
authors.initials: H
authors.lastname: Yamahara
authors.forename: Yasuaki
authors.initials: Y
authors.lastname: Kijima
authors.forename: Atsuko
authors.initials: A
authors.lastname: Nose
authors.forename: Yoko
authors.initials: Y
authors.lastname: Uchiyama-Tanaka
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Fukui
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Kitamura
authors.forename: Toshiko
authors.initials: T
authors.lastname: Tokoro
authors.forename: Hiroya
authors.initials: H
authors.lastname: Masaki
authors.forename: Toshiko
authors.initials: T
authors.lastname: Nagata
authors.forename: Yukihisa
authors.initials: Y
authors.lastname: Umeda
authors.forename: Mitsushige
authors.initials: M
authors.lastname: Nishikawa
authors.forename: Toshiji
authors.initials: T
authors.lastname: Iwasaka
mesh_terms: D000284:Administration, Oral; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use; D001485:Basement Membrane / Q000378:metabolism / Q000473:pathology; D015922:Complement C1q / Q000378:metabolism; D003176:Complement C3 / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D005938:Glucocorticoids / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D008180:Lupus Erythematosus, Systemic / Q000150:complications*; D008297:Male; D008775:Methylprednisolone / Q000008:administration & dosage / Q000627:therapeutic use; D008854:Microscopy, Electron; D008875:Middle Aged; D009395:Nephritis, Interstitial / Q000209:etiology* / Q000378:metabolism / Q000473:pathology
chemical_list: D000893:Anti-Inflammatory Agents; D003176:Complement C3; D005938:Glucocorticoids; D007074:Immunoglobulin G; D015922:Complement C1q; D008775:Methylprednisolone