Open Access
Issue
Med Sci (Paris)
Volume 35, Number 8-9, Août–Septembre 2019
Page(s) 659 - 666
Section M/S Revues
DOI https://doi.org/10.1051/medsci/2019128
Published online 18 September 2019
  1. Puelles VG, Hoy WE, Hughson MD, et al. Glomerular number and size variability and risk for kidney disease. Curr Opin Nephrol Hypertens 2011 ; 20 : 7–15. [CrossRef] [PubMed] [Google Scholar]
  2. Cil O, Perwad F. Monogenic causes of proteinuria in children. Front Med 2018 ; 5 : 55. [Google Scholar]
  3. O’Sullivan ED, Hughes J, Ferenbach DA. Renal aging: causes and consequences. J Am Soc Nephrol 2017 ; 28 : 407–420. [Google Scholar]
  4. D’Agati VD, Kaskel FJ, Falk RJ. Focal segmental glomerulosclerosis. N Engl J Med 2011 ; 365 : 2398–2411. [Google Scholar]
  5. Audard V, Lang P, Sahali D. Pathogénie du syndrome néphrotique à lesions glomérulaires minimes. Med Sci (Paris) 2008 ; 24 : 853–858. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  6. Zhang SY, Audard V, Lang P, Sahali D. Mécanismes moléculaires du syndrome néphrotique idiopathique à rechutes: rôle de c-mip dans les dysfonctions podocytaires. Med Sci (Paris) 2010 ; 26 : 592–596. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  7. Banh TH, Hussain-Shamsy N, Patel V, et al. Ethnic differences in incidence and outcomes of childhood nephrotic syndrome. Clin J Am Soc Nephrol 2016 ; 11 : 1760–1768. [CrossRef] [PubMed] [Google Scholar]
  8. Meyrier A, Niaudet P. Acute kidney injury complicating nephrotic syndrome of minimal change disease. Kidney Int 2018 ; 94 : 861–869. [CrossRef] [PubMed] [Google Scholar]
  9. Uezono S, Hara S, Sato Y, et al. Renal biopsy in elderly patients: a clinicopathological analysis. Renal Failure 2006 ; 28 : 549–555. [CrossRef] [PubMed] [Google Scholar]
  10. Mendonca AC, Oliveira EA, Froes BP, et al. A predictive model of progressive chronic kidney disease in idiopathic nephrotic syndrome. Pediatr Nephrol 2015 ; 30 : 2011–2020. [CrossRef] [PubMed] [Google Scholar]
  11. Han MH, Kim YJ. Practical application of Columbia classification for focal segmental glomerulosclerosis. BioMed Res Int 2016 ; 2016 : 9375753. [Google Scholar]
  12. Wharram BL, Goyal M, Wiggins JE, et al. Podocyte depletion causes glomerulosclerosis: diphtheria toxin-induced podocyte depletion in rats expressing human diphtheria toxin receptor transgene. J Am Soc Nephrol 2005 ; 16 : 2941–2952. [Google Scholar]
  13. Smeets B, Kuppe C, Sicking EM, et al. Parietal epithelial cells participate in the formation of sclerotic lesions in focal segmental glomerulosclerosis. J Am Soc Nephrol 2011 ; 22 : 1262–1274. [Google Scholar]
  14. O’Shaughnessy MM, Hogan SL, Poulton CJ, et al. Temporal and demographic trends in glomerular disease epidemiology in the southeastern United States, 1986–2015. Clin J Am Soc Nephrol 2017 ; 12 : 614–623. [CrossRef] [PubMed] [Google Scholar]
  15. Savin VJ, Sharma M, Zhou J, et al. Multiple targets for novel therapy of FSGS associated with circulating permeability factor. BioMed Res Int 2017 ; 2017 : 6232616. [Google Scholar]
  16. Ehrich JH, Geerlings C, Zivicnjak M, et al. Steroid-resistant idiopathic childhood nephrosis: overdiagnosed and undertreated. Nephrol Dial Transplant 2007 ; 22 : 2183–2193. [CrossRef] [PubMed] [Google Scholar]
  17. Sharma M, Zhou J, Gauchat JF, et al. Janus kinase 2/signal transducer and activator of transcription 3 inhibitors attenuate the effect of cardiotrophin-like cytokine factor 1 and human focal segmental glomerulosclerosis serum on glomerular filtration barrier. Transl Res 2015 ; 166 : 384–398. [Google Scholar]
  18. Fogo AB. Causes and pathogenesis of focal segmental glomerulosclerosis. Nat Rev Nephrol 2015 ; 11 : 76–87. [CrossRef] [PubMed] [Google Scholar]
  19. Tejani A, Phadke K, Nicastri A, et al. Efficacy of cyclophosphamide in steroid-sensitive childhood nephrotic syndrome with different morphological lesions. Nephron 1985 ; 41 : 170–173. [CrossRef] [PubMed] [Google Scholar]
  20. Maas RJ, Deegens JK, Smeets B, et al. Minimal change disease and idiopathic FSGS: manifestations of the same disease. Nat Rev Nephrol 2016 ; 12 : 768–776. [CrossRef] [PubMed] [Google Scholar]
  21. Gentili A, Tangheroni W, Gelli G. Proteinuria caused by transfusion of blood from nephrotic to non-nephrotic individuals. Minerva Medica 1954 ; 45 : 603–608. [PubMed] [Google Scholar]
  22. Hoyer JR, Vernier RL, Najarian JS, et al. Recurrence of idiopathic nephrotic syndrome after renal transplantation. Lancet 1972 ; 2 : 343–348. [CrossRef] [PubMed] [Google Scholar]
  23. Rich AR. A hitherto undescribed vulnerability of the juxtamedullary glomeruli in lipoid nephrosis. Bull Johns Hopkins Hosp 1957 ; 100 : 173–186. [PubMed] [Google Scholar]
  24. Hoyer JR, Vernier RL, Najarian JS, et al. Recurrence of idiopathic nephrotic syndrome after renal transplantation. 1972. J Am Soc Nephrol 2001 ; 12 : 1994–2002. [Google Scholar]
  25. Dantal J, Testa A, Bigot E, Soulillou JP. Effects of plasma-protein A immunoadsorption on idiopathic nephrotic syndrome recurring after renal transplantation. Ann Med Interne (Paris) 1992 ; 143 : suppl 1 48–51. [PubMed] [Google Scholar]
  26. Artero ML, Sharma R, Savin VJ, Vincenti F. Plasmapheresis reduces proteinuria and serum capacity to injure glomeruli in patients with recurrent focal glomerulosclerosis. Am J Kidney Dis 1994 ; 23 : 574–581. [CrossRef] [PubMed] [Google Scholar]
  27. Dantal J, Godfrin Y, Koll R, et al. Antihuman immunoglobulin affinity immunoadsorption strongly decreases proteinuria in patients with relapsing nephrotic syndrome. J Am Soc Nephrol 1998 ; 9 : 1709–1715. [Google Scholar]
  28. Zimmerman SW. Increased urinary protein excretion in the rat produced by serum from a patient with recurrent focal glomerular sclerosis after renal transplantation. Clin Nephrol 1984 ; 22 : 32–38. [PubMed] [Google Scholar]
  29. Savin VJ, Sharma R, Sharma M, et al. Circulating factor associated with increased glomerular permeability to albumin in recurrent focal segmental glomerulosclerosis. N Engl J Med 1996 ; 334 : 878–883. [CrossRef] [Google Scholar]
  30. Lagrue G, Branellec A, Niaudet P, et al. Transmission of nephrotic syndrome to two neonates. Spontaneous regression. Presse Med 1991 ; 20 : 255–257. [Google Scholar]
  31. Gallon L, Leventhal J, Skaro A, et al. Resolution of recurrent focal segmental glomerulosclerosis after retransplantation. N Engl J Med 2012 ; 366 : 1648–1649. [CrossRef] [Google Scholar]
  32. Shalhoub RJ. Pathogenesis of lipoid nephrosis: a disorder of T-cell function. Lancet 1974 ; 2 : 556–560. [CrossRef] [PubMed] [Google Scholar]
  33. Janeway CA. The management of nephrosis. Pediatrics 1948 ; 2 : 705. [Google Scholar]
  34. Lagrue G, Xheneumont S, Branellec A, et al. A vascular permeability factor elaborated from lymphocytes. I. Demonstration in patients with nephrotic syndrome. Biomedicine 1975 ; 23 : 37–40. [PubMed] [Google Scholar]
  35. Benz K, Dotsch J, Rascher W, Stachel D. Change of the course of steroid-dependent nephrotic syndrome after rituximab therapy. Pediatr Nephrol 2004 ; 19 : 794–797. [CrossRef] [PubMed] [Google Scholar]
  36. Yoo TH, Pedigo CE, Guzman J, et al. Sphingomyelinase-like phosphodiesterase 3b expression levels determine podocyte injury phenotypes in glomerular disease. J Am Soc Nephrol 2015 ; 26 : 133–147. [CrossRef] [Google Scholar]
  37. Ollero M, Sahali D. Inhibition of the VEGF signalling pathway and glomerular disorders. Nephrol Dial Transplant 2015 ; 30 : 1449–1455. [CrossRef] [PubMed] [Google Scholar]
  38. Delville M, Sigdel TK, Wei C, et al. A circulating antibody panel for pretransplant prediction of FSGS recurrence after kidney transplantation. Sci Transl Med 2014; 6 : 256ra136. [CrossRef] [Google Scholar]
  39. Garin EH, Mu W, Arthur JM, et al. Urinary CD80 is elevated in minimal change disease but not in focal segmental glomerulosclerosis. Kidney Int 2010 ; 78 : 296–302. [CrossRef] [PubMed] [Google Scholar]
  40. Yu CC, Fornoni A, Weins A, et al. Abatacept in B7-1-positive proteinuric kidney disease. N Engl J Med 2013 ; 369 : 2416–2423. [CrossRef] [Google Scholar]
  41. Lai KW, Wei CL, Tan LK, et al. Overexpression of interleukin-13 induces minimal-change-like nephropathy in rats. J Am Soc Nephrol 2007 ; 18 : 1476–1485. [CrossRef] [Google Scholar]
  42. McCarthy ET, Sharma M, Savin VJ. Circulating permeability factors in idiopathic nephrotic syndrome and focal segmental glomerulosclerosis. Clin J Am Soc Nephrol 2010 ; 5 : 2115–2121. [CrossRef] [PubMed] [Google Scholar]
  43. Raveh D, Shemesh O, Ashkenazi YJ, et al. Tumor necrosis factor-alpha blocking agent as a treatment for nephrotic syndrome. Pediatr Nephrol 2004 ; 19 : 1281–1284. [CrossRef] [PubMed] [Google Scholar]
  44. Bakker WW, Baller JF, van Luijk WH. A kallikrein-like molecule and plasma vasoactivity in minimal change disease. Increased turnover in relapse versus remission. Contrib Nephrol 1988; 67 : 31–6. [CrossRef] [Google Scholar]
  45. Wei C, Moller CC, Altintas MM, et al. Modification of kidney barrier function by the urokinase receptor. Nat Med 2008 ; 14 : 55–63. [CrossRef] [PubMed] [Google Scholar]
  46. Kemeny E, Mihatsch MJ, Durmuller U, Gudat F. Podocytes loose their adhesive phenotype in focal segmental glomerulosclerosis. Clin Nephrol 1995 ; 43 : 71–83. [PubMed] [Google Scholar]
  47. Clement LC, Avila-Casado C, Mace C, et al. Podocyte-secreted angiopoietin-like-4 mediates proteinuria in glucocorticoid-sensitive nephrotic syndrome. Nat Med 2011 ; 17 : 117–122. [CrossRef] [PubMed] [Google Scholar]
  48. Sever S, Trachtman H, Wei C, Reiser J. Is there clinical value in measuring suPAR levels in FSGS?. Clin J Am Soc Nephrol 2013 ; 8 : 1273–1275. [CrossRef] [PubMed] [Google Scholar]
  49. Schwartz MM, Evans J, Bain R, Korbet SM. Focal segmental glomerulosclerosis: prognostic implications of the cellular lesion. J Am Soc Nephrol 1999 ; 10 : 1900–1907. [Google Scholar]
  50. Campbell KN, Tumlin JA. Protecting podocytes: a key target for therapy of focal segmental glomerulosclerosis. Am J Nephrol 2018 ; 47 : suppl 1 14–29. [CrossRef] [PubMed] [Google Scholar]
  51. Sharma R, Sharma M, McCarthy ET, et al. Components of normal serum block the focal segmental glomerulosclerosis factor activity in vitro. Kidney Int 2000 ; 58 : 1973–1979. [CrossRef] [PubMed] [Google Scholar]
  52. Harita Y, Ishizuka K, Tanego A, et al. Decreased glomerular filtration as the primary factor of elevated circulating suPAR levels in focal segmental glomerulosclerosis. Pediatr Nephrol 2014 ; 29 : 1553–1560. [CrossRef] [PubMed] [Google Scholar]
  53. 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 : 931–938. [CrossRef] [PubMed] [Google Scholar]
  54. Beaudreuil S, Zhang X, Florence H, et al. Circulating CASK is associated with recurrent focal segmental glomerulosclerosis after transplantation. PLoS One 2019 (sous presse). [Google Scholar]
  55. Müller-Deile J, Schenk H, Schroder P, et al. Circulating factors cause proteinuria in parabiotic zebrafish. Kidney Int 2019 Mar 8. pii: S0085–2538(19)30232–7. doi: 10.1016/j.kint.2019.02.013. [Google Scholar]

Current usage metrics show cumulative count of Article Views (full-text article views including HTML views, PDF and ePub downloads, according to the available data) and Abstracts Views on Vision4Press platform.

Data correspond to usage on the plateform after 2015. The current usage metrics is available 48-96 hours after online publication and is updated daily on week days.

Initial download of the metrics may take a while.