Патогенетические механизмы развития идиопатического нефротического синдрома с минимальными изменениями

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Аннотация

Представлены данные литературы о патогенетических механизмах развития нефротического синдрома с минимальными изменениями, а также описаны клинические и гистологические признаки, особенности течения и принципы лечения.


Об авторе

В. А. Обухова
Научно-исследовательский клинический институт педиатрии
Россия

н.с. отделения наследственных и приобретенных болезней почек



Список литературы

1. Lombel R.M., Gipson D.S, Hodson E.M. Treatment of steroidsensitive nephrotic syndrome: new guidelines from KDIGO. Pediat Nephrol 2013, 28: 415—426.

2. Ponticelli C., Glassock R.J. Treatment of primary glomerulonephritis. Oxford University press 2009: 179—213.

3. Andersen R.F., Thrane N., Noergaard K. et al. Early age at debut is a predictor of steroid-dependent and frequent relapsing nephrotic syndrome. Pediat Nephrol 2010; 25: 1299—1304.

4. Niaudet P., Boyer O. Idiopathic Nephrotic Syndrome in Children: Clinical aspects. Pediat Nephrol 2009: 667—702.

5. McKinney P.A., Feltbower R.G., Brocklebank J.T., Fitzpatrick M.M. Time trends and ethnic patterns of childhood nephrotic syndrome in Yorkshire, UK. Pediat Nephrol 2001; 16: 1040—1044.

6. Primary nephrotic syndrome in children: clinical significance of histopathologic variants of minimal change and of diffuse mesangial hypercellularity. A Report of the International Study of Kidney Disease in Children. Kidney Int 1981; 20: 765—771.

7. Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Groop (2012) KDIGO Clinical Practice Guidelines for Glomerulonephritis. Kidney Int 2012; 2: Suppl: 163—171.

8. Shalhoub R.J. Pathogenesis of lipoid nephrosis: a disorder of T-cell function. Lancet 1974; 7: 556—560.

9. Koyama A., Fujisaki M., Kobayashi M. et al. A glomerular permeability factor produced by human T cell hybridomas. Kidney Int 2001; 40: 453—460.

10. Garin E.H., West L., Zheng W. Interleukin-8 alters glomerular heparan sulfate glycosaminoglycan chain size and charge in rats. Pediat Nephrol 2000; 14: 284—287.

11. Fouqueray B., Suberville S., Isaka Y. et al. Reduction of proteinuria in anti-glomerular basement membrane nephritis by interleukin-10 gene transfer. J Am Soc Nephrol 1996; 7: 9: 2259.

12. Araya C., Diaz L., Wasserfall C. et al. T regulatory cell function in idiopathic minimal lesion nephrotic syndrome. Pediat Nephrol 2009; 24: 1691—1698.

13. Cheung W., Wei C.L., Seah C.C. et al. Atopy, serum IgE, and interleukin-13 in steroidresponsive nephrotic syndrome. Pediat Nephrol 2004; 19: 627—632.

14. Lai K.W., Wei C.L., Tan L.K. et al. Overexpression of interleukin-13 induces minimal-change-like nephropathy in rats. J Am Soc Nephrol 2007; 18: 5: 1476—1485.

15. Jabara H.H., Ahern D.J., Vercelli D., Geha R.S. Hydrocortisone and IL-4 induce IgE isotype switchingin human B cells. J Immunol 1991; 147: 1557—1560.

16. Kimata H., Lindley I., Furusho K. Effect of hydrocortisone on spontaneous IgE and IgG4 production in atopic patients. J Immunol 1995; 154: 3557—3566.

17. Fuke Y., Endo M., Ohsawa I. et al. Implication of elevated serum IgE levels in minimal change nephrotic syndrome. Nephron 2002; 91: 769—770.

18. Lama G., Luongo I., Tirino G. et al. T-lymphocyte populations and cytokines in childhood nephrotic syndrome. Am J Kidney Dis 2002; 39: 958—965.

19. Bustos C., Gonzalez E., Muley R. et al. Increase of tumour necrosis factor alpha synthesis and gene expression in peripheral blood mononuclear cells of children with idiopathic nephrotic syndrome. Eur J Clin Invest 1994; 24: 799—805.

20. Lawrence T. The Nuclear Factor NF-κB Pathway in Inflammation. Cold Spring Harb Perspect Biol 2009; 1: 6: a001651.

21. Sahali D., Pawlak A., Le Gouvello S. et al. Transcriptional and post-transcriptional alterations of IkappaBalpha in active minimal-change nephrotic syndrome. J Am Soc Nephrol 2001; 12: 1648—1658.

22. Stahn C., Löwenberg M., Hommes D. et al. Molecular mechanisms of glucocorticoid action and selective glucocorticoid receptor agonists. Mol Cell Endocrinol 2007; 15: 275 (1—2): 71—78.

23. Zheng Y., Chaudhry A., Kas A. et al. Regulatory T-cell suppressor program co-opts transcription factor IRF4 to control T(H)2 responses. Nature 2009; 458: 351—356.

24. Sellier-Leclerc A., Duval A., Riveron S. et al. A humanized mouse model of idiopathic nephrotic syndrome suggests a pathogenic role for immature cells. J Am Soc Nephrol 2007; 18: 2732—2739.

25. Lapillonne H., Leclerc A, Ulinski T. et al. Stem cell mobilization in idiopathic steroid-sensitive nephrotic syndrome. Pediat Nephrol 2008; 23 :1251—1256.

26. Ransom R.F., Lam N.G., Hallett M.A. et al. Glucocorticoids protect and enhance recovery of cultured murine podocytes via actin filament stabilization. Kidney Int 2005; 68: 2473—2483.

27. Schönenberger E., Ehrich J.H., Haller H. et al. The podocyte as a direct target of immunosuppressive agents. Nephrol Dial Transplant 2011; 26: 18—24.

28. Faul C., Donnelly M., Merscher-Gomez S. et al. The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A. Nat Med 2008; 14: 9: 931—938.

29. Mundel P., Reiser J. Proteinuria: an enzymatic disease of the podocyte? Kidney Int 2010; 77: 571—580.

30. Shimada M., Araya C., Rivard C. et al. Minimal change disease: a “two-hit” podocyte immune disorder? Pediat Nephrol 2011; 26: 645—649.

31. Clement L.C., Avila-Casado C., Macé C. et al. Podocytesecreted angiopoietin-like-4 mediates proteinuria in glucocorticoid-sensitive nephrotic syndrome. Nat Med 2011; 17: 117—122.


Дополнительные файлы

Для цитирования: Обухова В.А. Патогенетические механизмы развития идиопатического нефротического синдрома с минимальными изменениями. Российский вестник перинатологии и педиатрии. 2014;59(4):10-15.

For citation: Obukhova V.A. Pathogenetic mechanisms of idiopathic minimal-change nephrotic syndrome. Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics). 2014;59(4):10-15. (In Russ.)

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