[Significance of inflammatory cytokines in the pathogenesis of IgA nephropathy]

Vojnosanit Pregl. 1998 Mar-Apr;55(2):141-9.
[Article in Serbian]

Abstract

Prospective study was performed on the concentrations of inflammatory cytokines IL-1, TNF and IL-6 in serum and urine (ELISA tests) were determined in the scope of total clinical-laboratory and histologic treatment in 59 patients with primary IgA nephropathy. Control group consisted of 20 healthy subjects. IL-6 was not detected either in serum of patients with IgAN, or in control examinees. TNF alpha and IL-1 beta were detected in control patients' sera and in patients with IgAN, but detected concentrations were not significantly different. IL-1 beta in urine was detected in 82.8%, TNF alpha in 90.0%, and IL-6 in 40% of our patients with IgAN. The concentrations of IL-1 beta were significantly higher compared to IL-1 beta concentrations in urine of healthy subjects and significantly correlated with the severity of glomerular and tubulointerstitial changes, as well as with the degree of proteinuria. Direct and indirect toxicity of TNF alpha on renal structures was confirmed in significantly higher concentrations of that cytokine in urine of patients with mesangial sclerosis of different percentage compared to the patients with isolated mesangial hypercellularity. Also in the patients with index of chronic lesion over 7 significantly higher TNF alpha concentrations in urine were found compared to the patients with lesion index 0-3 and 4-7. Creatinine clearance was in negative correlation with TNF alpha concentrations in urine of our patients with IgAN. Concentrations of IL-6 in urine were in correlation neither with laboratory parameters of renal function, nor with the degree of histologic changes.

Publication types

  • English Abstract

MeSH terms

  • Adult
  • Female
  • Glomerulonephritis, IGA / metabolism*
  • Humans
  • Inflammation Mediators / analysis
  • Interleukin-1 / analysis*
  • Interleukin-6 / analysis*
  • Male
  • Tumor Necrosis Factor-alpha / analysis*

Substances

  • Inflammation Mediators
  • Interleukin-1
  • Interleukin-6
  • Tumor Necrosis Factor-alpha