Focal segmental glomerulosclerosis plays a major role in the progression of IgA nephropathy. II. Light microscopic and clinical studies

Kidney International

Volumn 79, Issue 6, 2011, Pages 643-654

  El Karoui, Khalil ^a,b   Hill, Gary S ^a   Karras, Alexandre ^a   Moulonguet, Luc ^c   Caudwell, Valérie ^d   Loupy, Alexandre ^a   Bruneval, Patrick ^a   Jacquot, Christian ^a   Nochy, Dominique ^a  

^a HÔPITAL EUROPÉEN GEORGES POMPIDOU   (France)

^b HÔPITAL NECKER ENFANTS MALADES   (France)

^c HÔPITAL AMBROISE PARÉ   (France)

^d CENTRE HOSPITALIER SUD FRANCILIEN   (France)

Author keywords

focal segmental glomerulosclerosis; IgA nephropathy; podocytes; podocytopathy

Indexed keywords

ADULT; AGED; ARTICLE; CONTROLLED STUDY; DISEASE CLASSIFICATION; DISEASE COURSE; FEMALE; FOCAL GLOMERULOSCLEROSIS; HISTOPATHOLOGY; HUMAN; HUMAN TISSUE; HYALINE DEGENERATION; IMMUNOGLOBULIN A NEPHROPATHY; MAJOR CLINICAL STUDY; MALE; MICROSCOPY; PRIORITY JOURNAL; RETROSPECTIVE STUDY; SURVIVAL RATE;

EID: 79952163845     PISSN: 00852538     EISSN: 15231755     Source Type: Journal    
DOI: 10.1038/ki.2010.460     Document Type: Article

References (44)

1. Haas M. IgA nephropathy histologically resembling focal-segmental glomerulosclerosis: a clinicopathologic study of 18 cases. Am J Kidney Dis 1996; 28: 365-371. (Pubitemid 26304415)
2. Packham DK, Yan HD, Hewitson TD et al. The significance of focal and segmental hyalinosis and sclerosis (FSHS) and nephrotic range proteinuria in IgA nephropathy. Clin Nephrol 1996; 46: 225-229. (Pubitemid 26385556)
3. Weber CL, Rose CL, Magil AB. Focal segmental glomerulosclerosis in mild IgA nephropathy: a clinical-pathologic study. Nephrol Dial Transplant 2009; 24: 483-488.
4. Jeong HJ, Kim YS, Kwon KW et al. Segmental glomerulosclerosis in IgA nephropathy after renal transplantation: relationship with proteinuria and therapeutic response to enalapril. Clin Transplant 2003; 17: 108-113. (Pubitemid 36833780)
5. Okubo M, Horata-Takahashi E, Tamura K et al. Mesangial immunoglobulin A deposition and focal glomerulosclerosis in a renal transplant patient with nephrotic syndrome-Berger's disease alone or superimposition of focal glomerulosclerosis? Transplant Proc 1993; 25: 2109-2112.
6. Haas M. Histologic subclassification of IgA nephropathy: a clinicopathologic study of 244 cases. Am J Kidney Dis 1997; 29: 829-842. (Pubitemid 27251835)
7. Roberts IS, Cook HT, Troyanov S et al. The Oxford classification of IgA nephropathy: pathology definitions, correlations, and reproducibility. Kidney Int 2009; 76: 546-556.
8. Cattran DC, Coppo R, Cook HT et al. The Oxford classification of IgA nephropathy: rationale, clinicopathological correlations, and classification. Kidney Int 2009; 76: 534-545.
9. Coppo R, D'Amico G. Factors predicting progression of IgA nephropathies. J Nephrol 2005; 18: 503-512. (Pubitemid 41824469)
10. Wang C, Liu X, Ye Z et al. Mesangial medium with IgA1 from IgA nephropathy inhibits nephrin expression in mouse podocytes. Eur J Clin Invest 2009; 39: 561-567.
11. Wang C, Ye Z, Peng H et al. Effect of aggregated immunoglobulin A1 from immunoglobulin A nephropathy patients on nephrin expression in podocytes. Nephrology (Carlton) 2009; 14: 213-218.
12. Coppo R, Fonsato V, Balegno S et al. Aberrantly glycosylated IgA1 induces mesangial cells to produce platelet-activating factor that mediates nephrin loss in cultured podocytes. Kidney Int 2009; 77: 17-27.
13. Lai KN, Leung JC, Chan LY et al. Podocyte injury induced by mesangialderived cytokines in IgA nephropathy. Nephrol Dial Transplant 2009; 24: 62-72.
14. Ye ZC, Wang C, Tang Y et al. Serum IgA1 from patients with IgA nephropathy up-regulates integrin-linked kinase synthesis and inhibits adhesive capacity in podocytes through indirect pathways. Clin Invest Med 2009; 32: E20-E27.
15. Lai KN, Leung JC, Chan LY et al. Activation of podocytes by mesangial-derived TNF-alpha: glomerulo-podocytic communication in IgA nephropathy. Am J Physiol Renal Physiol 2008; 294: F945-F955.
16. Qiu LQ, Sinniah R, Hong HS. Downregulation of Bcl-2 by podocytes is associated with progressive glomerular injury and clinical indices of poor renal prognosis in human IgA nephropathy. J Am Soc Nephrol 2004; 15: 79-90. (Pubitemid 38020700)
17. Hill GS, El Karoui K, Karras A et al. Focal segmental glomerulosclerosis plays a major role in the progression of IgA nephropathy. I. Immunohistochemical studies. Kidney Int 2010 (in press).
18. Bariety J, Mandet C, Hill GS et al. Parietal podocytes in normal human glomeruli. J Am Soc Nephrol 2006; 17: 2770-2780. (Pubitemid 44484667)
19. Dijkman H, Smeets B, van der J et al. The parietal epithelial cell is crucially involved in human idiopathic focal segmental glomerulosclerosis. Kidney Int 2005; 68: 1562-1572. (Pubitemid 43169901)
20. Barisoni L, Kriz W, Mundel P et al. The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy. J Am Soc Nephrol 1999; 10: 51-61. (Pubitemid 29034942)
21. Bariety J, Nochy D, Mandet C et al. Podocytes undergo phenotypic changes and express macrophagic-associated markers in idiopathic collapsing glomerulopathy. Kidney Int 1998; 53: 918-925. (Pubitemid 28155664)
22. Bariety J, Bruneval P, Hill GS et al. Transdifferentiation of epithelial glomerular cells. J Am Soc Nephrol 2003; 14(Suppl 1): S42-S47. (Pubitemid 36687039)
23. Bariety J, Bruneval P, Hill G et al. Posttransplantation relapse of FSGS is characterized by glomerular epithelial cell transdifferentiation. J Am Soc Nephrol 2001; 12: 261-274. (Pubitemid 32116368)
24. Ohtaka A, Ootaka T, Sato H et al. Significance of early phenotypic change of glomerular podocytes detected by Pax2 in primary focal segmental glomerulosclerosis. Am J Kidney Dis 2002; 39: 475-485. (Pubitemid 34194623)
25. Dijkman HB, Weening JJ, Smeets B et al. Proliferating cells in HIV and pamidronate-associated collapsing focal segmental glomerulosclerosis are parietal epithelial cells. Kidney Int 2006; 70: 338-344. (Pubitemid 44086583)
26. Smeets B, Uhlig S, Fuss A et al. Tracing the origin of glomerular extracapillary lesions from parietal epithelial cells. J Am Soc Nephrol 2009; 20: 2604-2615.
27. Ronconi E, Sagrinati C, Angelotti ML et al. Regeneration of glomerular podocytes by human renal progenitors. J Am Soc Nephrol 2009; 20: 322-332.
28. Smeets B, Angelotti ML, Rizzo P et al. Renal progenitor cells contribute to hyperplastic lesions of podocytopathies and crescentic glomerulonephritis. J Am Soc Nephrol 2009; 20: 2593-2603.
29. D'Agati VD, Fogo AB, Bruijn JA et al. Pathologic classification of focal segmental glomerulosclerosis: a working proposal. Am J Kidney Dis 2004; 43: 368-382. (Pubitemid 38146337)
30. Tian J, Wang HP, Mao YY et al. Reduced glomerular epithelial protein 1 expression and podocyte injury in immunoglobulin A nephropathy. J Int Med Res 2007; 35: 338-345. (Pubitemid 46971354)
31. Gagliardini E, Benigni A, Tomasoni S et al. Targeted downregulation of extracellular nephrin in human IgA nephropathy. Am J Nephrol 2003; 23: 277-286. (Pubitemid 36980723)
32. Koop K, Eikmans M, Baelde HJ et al. Expression of podocyte-associated molecules in acquired human kidney diseases. J Am Soc Nephrol 2003; 14: 2063-2071. (Pubitemid 36909914)
33. Mao J, Zhang Y, DU L et al. Expression profile of nephrin, podocin, and CD2AP in Chinese children with MCNS and IgA nephropathy. Pediatr Nephrol 2006; 21: 1666-1675. (Pubitemid 44390831)
34. Patrakka J, Ruotsalainen V, Ketola I et al. Expression of nephrin in pediatric kidney diseases. J Am Soc Nephrol 2001; 12: 289-296. (Pubitemid 32116370)
35. Huh W, Kim DJ, Kim MK et al. Expression of nephrin in acquired human glomerular disease. Nephrol Dial Transplant 2002; 17: 478-484. (Pubitemid 34211147)
36. Kriz W. The pathogenesis of 'classic' focal segmental glomerulosclerosislessons from rat models. Nephrol Dial Transplant 2003; 18(Suppl 6): vi39-vi44. (Pubitemid 37098593)
37. Schwartz MM. Focal segmental glomerulosclerosis. In: Jennette CE, Olson JL, Schwartz MM, Silva FG (eds). Heptinstall's Pathology of the Kidney, 6th edn, chap. 5, Lippincott Williams & Wilkins: Philadelphia, PA, 2007, pp 155-204.
38. Rennke HG. How does glomerular epithelial cell injury contribute to progressive glomerular damage? Kidney Int Suppl 1994; 45: S58-S63.
39. Schwartz MM. The role of podocyte injury in the pathogenesis of focal segmental glomerulosclerosis. Ren Fail 2000; 22: 663-684.
40. Bariety J, Bruneval P. Activated parietal epithelial cells or dedifferentiated podocytes in FSGS: can we make the difference? Kidney Int 2006; 69: 194.
41. Tanaka R, Iijima K, Murakami R et al. ACE gene polymorphism in childhood IgA nephropathy: association with clinicopathologic findings. Am J Kidney Dis 1998; 31: 774-779. (Pubitemid 28234628)
42. Kondo Y, Akikusa B. Chronic Masugi nephritis in the rat. An electron microscopic study on evolution and consequences of glomerular capsular adhesions. Acta Pathol Jpn 1982; 32: 231-242.
43. 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. (Pubitemid 44743492)
44. Hara M, Yanagihara T, Kihara I. Cumulative excretion of urinary podocytes reflects disease progression in IgA nephropathy and Schonlein-Henoch purpura nephritis. Clin J Am Soc Nephrol 2007; 2: 231-238.