title: [Cytokines and adhesion molecules in renal vasculitis and lupus nephritis].
abstract: BACKGROUND
  Plasma levels and urinary excretion of proinflammatory cytokines and soluble adhesion molecules may be useful parameters of the activity of ANCA-positive renal vasculitis and lupus nephritis.
  
  
  RESULTS
  Plasma levels and urinary excretion of TNF alpha, IL-6, IL-8, ICAM-1 and VCAM-1 were measured by ELISA in 14 patients (pts) with ANCA-positive renal vasculitis (8 active-ANCA-A, 6 in remission ANCA-R), 6 pts with active lupus nephritis (L.N), 15 pts with IgA nephropathy (IgAN) 10 pts with autosomal dominant polycystic kidney disease and 9 healthy subjects (Co). Fractional excretion (FE) of selected cytokines and adhesion molecules was also calculated. Pts with LN had in comparison with controls increased plasma levels of ICAM-1, VCAM-1, IL-6, IL-8 and TNF alpha, increased urinary excretion of VCAM-1, IL-8 and TNF alpha and increased fractional excretion of VCAM-1 and IL-8. Patients with ANCA-A had in comparison with controls increased plasma concentrations of ICAM-1 and VCAM-1, increased urinary excretion of VCAM-1, IL-6 and TNF alpha and increased fractional excretion of VCAM-1, IL-6, IL-8 and TNF alpha. Patients with ANCA-R had in comparison with controls higher plasma levels of ICAM-1, VCAM-1, IL-6 and TNF alpha, increased urinary excretion of VCAM-1 and TNF alpha and increased fractional excretion of VCAM-1, IL-6 and TNF alpha.
  
  
  CONCLUSIONS
  Patients with ANCA-positive renal vasculitis had in contradistinction to pts with active LN increased fractional excretion of IL-6 and TNF alpha. Both cytokines are probably produced in renal vasculitis locally in the kidney. Increased plasma levels of soluble adhesion molecules and increased plasma levels and fractional excretion of proinflammatory cytokines in patients with ANCA-positive renal vasculitis in clinical remission may explain the strong propensity of these patients to develop relapses of the diseases on withdrawal of immunosuppressive treatment.
authors.affiliation: I. interní klinika I, LF UK a VFN, Praha.
authors.forename: V
authors.initials: V
authors.lastname: Tesar
authors.forename: Z
authors.initials: Z
authors.lastname: Masek
authors.forename: I
authors.initials: I
authors.lastname: Rychlík
authors.forename: M
authors.initials: M
authors.lastname: Merta
authors.forename: J
authors.initials: J
authors.lastname: Bartůnková
authors.forename: A
authors.initials: A
authors.lastname: Stejskalová
authors.forename: J
authors.initials: J
authors.lastname: Zabka
authors.forename: T
authors.initials: T
authors.lastname: Fucíková
authors.forename: C
authors.initials: C
authors.lastname: Dostál
authors.forename: R
authors.initials: R
authors.lastname: Becvár
mesh_terms: D000328:Adult; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000032:analysis; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D005922:Glomerulonephritis, IGA / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000098:blood supply*; D008181:Lupus Nephritis / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D014657:Vasculitis / Q000276:immunology / Q000378:metabolism*
chemical_list: D019268:Antibodies, Antineutrophil Cytoplasmic; D015815:Cell Adhesion Molecules; D016207:Cytokines