Urinary level of podocyte damage and self-defence markers in patients with chronic glomerulonephritis


Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

Aim. Assessment of severity of podocyte damage in patients with chronic glomerulonephitis (CGN) according to proteinuria level and urinary excretion of interleuki-6 (IL-6) and heat shock protein-27 (HSP-27). Methods. 73 patients with CGN were included into the study; 30 of the — with nephrotic syndrome. Podocyturia was assessed by floucytometry with podocalixin-marked antibodies, urinary levels of IL-6 and HSP-27 were detetmined by Elisa. Results. Pateints with active CGN demonstrate high levels of podocyturia, correlating with proteinuria, seveirity of nephrotic syndrome and urinary excretion of IL-6. Podocituria detects unfavorable renal prognosis. Conclusion. Podocituria can be used as a marker of disease severity and prognosis in patients with chronic glomerulonephritis.

Full Text

Restricted Access

References

  1. Smoyer W., Mundel P. Regulation of podocyte structur during the development of nephritic syndrome. J Mol Med. 1998; 76: 172-183.
  2. Huh W., Kim D.J., Kim M.-K. et al. Expression of nephrin in acquired human glomerular disease. Nephrol Dial Transplant. 2002; 17: 478-484.
  3. Kanwar Y.S., Rosenzweig L.J. Altered glomerular permeability as a result of focal detachment of the visceral epithelium. Kidney Int. 1982; 21: 565-574.
  4. Smoyer W.E., Gupta A., Mundel P. et al. Altered expression of glomerular heat shock protein 27 in experimental nephrotic syndrome. J Clin Invest. 1996; 97: 2697-2704.
  5. Mehlen P., Hickey E., Weber L.A. et al. Large unphosphorylated aggregates as the active form of hsp27 which controls intracellular reactive oxygen species and glutathione levels and generated a protection against TNFa in NIH-3T3-ras cells. Biochem Biophys Res Commun. 1997; 241: 187-192.
  6. Preville X., Schultz H., Knauf U. et al. Analysis of the role of Hsp25 phosphorylation reveals the importance of the oligomerization state of this small heat shock protein in its protective function against TNF-α and hydrogen peroxide-induced cell death. J Cell Biochem. 1998; 69: 436-452.
  7. Lai K.N., Leung J.C., Chan L.Y. et al. Activation of podocytes by mesangial-derived TNF-α: glomerulopodocytic communication in IgA nephropathy. Am J Physiol Renal Physiol. 2008; 294: 945-955.
  8. Gordon C., Richards N., Howie A.J. et al. Urinary IL-6: a markerformesangial proliferative glomerulonephritis? Clin Exp. Immunol.1991; 8: 145-149.
  9. Horii Y., Muraguchi A., Ivano M. et al. Involvement of IL-6 in mesangial proliferative glomerulonephritis. I. Immunol. 143.
  10. Lee S.J., Borsting E., Decleves A.E. et al. Podocytes express IL-6 and Lipocalin2/Neutrophil gelatinase-associated lipocalin in lipopolysaccharide-induced acute glomerular injury. Nephon Exp Nephrol. 2012; 121: 86-96.
  11. Малышев И.Ю. Феномен адаптационной стабилизации структур и роль в нем белков теплового шока - дисс.. д.м.н. - М., 1982.
  12. Мюлленайзен Б. Синдром стресса. Издательство Казанского Университета, 1993.
  13. Kritz W., Greitz N., Lemley K.V. Progresion of glomeular diseases: is the podocyte the culprit? Kidney Int. 1998; 54: 687-697.
  14. Lemley K.V., Lafayette A., Safai G. et al. Podocytopenia and disease severity in IgA nephropathy. Kidney Int. 2002; 61: 1475-1485.

Supplementary files

Supplementary Files
Action
1. JATS XML

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies