Monoclonal antibodies for podocytopathies: Rationale and clinical responses

Nature Reviews Nephrology

Volumn 5, Issue 6, 2009, Pages 337-348

  Marasà, Maddalena ^a   Kopp, Jeffrey B ^b  

^a OSPEDALI RIUNITI   (Italy)

^b NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ABATACEPT; ADALIMUMAB; ALEMTUZUMAB; BASILIXIMAB; BELATACEPT; CERTOLIZUMAB PEGOL; CONNECTIVE TISSUE GROWTH FACTOR ANTIBODY; CYCLOSPORIN; DACLIZUMAB; ECULIZUMAB; ETANERCEPT; INFLIXIMAB; LEVAMISOLE; MONOCLONAL ANTIBODY; NATALIZUMAB; RITUXIMAB; STEROID; TRANSFORMING GROWTH FACTOR BETA ANTIBODY; TUMOR NECROSIS FACTOR INHIBITOR; IMMUNOLOGIC FACTOR;

ANAPHYLAXIS; ANKYLOSING SPONDYLITIS; AUTOIMMUNE DISEASE; B CELL LYMPHOMA; B LYMPHOCYTE; CELLULAR IMMUNITY; CHRONIC LYMPHATIC LEUKEMIA; CLINICAL TRIAL; CROHN DISEASE; CYTOPENIA; DEMYELINATING DISEASE; DRUG HYPERSENSITIVITY; DRUG MECHANISM; DRUG SAFETY; FOCAL GLOMERULOSCLEROSIS; GLOMERULOPATHY; HEART FAILURE; HEMATOPOIETIC STEM CELL; HEPATITIS B; HUMAN; IMMUNOCOMPETENT CELL; INFECTION; INJECTION SITE REACTION; JUVENILE RHEUMATOID ARTHRITIS; KIDNEY DISEASE; KIDNEY GRAFT REJECTION; LIVER TOXICITY; LUPUS LIKE SYNDROME; MACROPHAGE; MALIGNANT NEOPLASTIC DISEASE; MENINGOCOCCOSIS; MINIMAL CHANGE GLOMERULONEPHRITIS; MULTIPLE SCLEROSIS; NATURAL KILLER T CELL; NEPHROTIC SYNDROME; NONHUMAN; PANCYTOPENIA; PAROXYSMAL NOCTURNAL HEMOGLOBINURIA; PATHOGENESIS; PLASMAPHERESIS; PODOCYTE; PRIORITY JOURNAL; PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; PSORIASIS VULGARIS; PSORIATIC ARTHRITIS; REVIEW; RHEUMATOID ARTHRITIS; SCLEROSIS; SIDE EFFECT; SKIN FIBROSIS; SKIN MANIFESTATION; SYSTEMIC VASCULITIS; T LYMPHOCYTE ACTIVATION; TH2 CELL; THYMOMA; TUMOR LYSIS SYNDROME; ULCERATIVE COLITIS; VASCULITIS; VIRUS REACTIVATION; GLOMERULONEPHRITIS; IMMUNOLOGY; PATHOLOGY;

ANTIBODIES, MONOCLONAL; GLOMERULONEPHRITIS; HUMANS; IMMUNOLOGIC FACTORS; PODOCYTES;

EID: 68549117277     PISSN: 17595061     EISSN: 1759507X     Source Type: Journal    
DOI: 10.1038/nrneph.2009.70     Document Type: Review

References (101)

1. Mundel, P. & shankland, S. J. Podocyte biology and response to injury. J. Am. Soc. Nephrol. 13, 3005-3015 (2002).
2. Pavenstädt, H., Kriz, W. & Kretzler, M. Cell biology of the glomerular podocytE. Physiol. rev. 83, 253-307 (2003).
3. Schnaper, H. et al. Nephrotic syndrome: Minimal change disease, focal segmental glomerulosclerosis, and collapsing glomerulopathy, in Disease of the Kidney and urinary tract, 8th edn (Lippincott williams & wilkins, Philadelphia, 2006).
4. Barisoni, L., Schnaper, H. W. & Kopp, J. B. A proposed taxonomy for the podocytopathies: A reassessment of the primary nephrotic diseases. Clin. J. Am. Soc. Nephrol. 2, 529-542 (2007).
5. Shalhoub, R. J. Pathogenesis of lipoid nephrosis: A disorder of T-cell function. Lancet 2, 556-560 (1974).
6. Koenecke, C., Ukena, S. N., Ganser, A. & Franzke, A. regulatory T cells as therapeutic target in Hodgkin's lymphoma. Expert Opin. Ther. Targets 12, 769-782 (2008).
7. Mathieson, P. W. Minimal change nephropathy and focal segmental glomerulosclerosis. Semin. Immunopathol. 29, 415-426 (2007).
8. reiser, J. et al. Induction of B7-1 in podocytes is associated with nephrotic syndrome. J. Clin. Invest. 113, 1390-1397 (2004).
9. Yamada, A., Salama, A. D. & Sayegh, M. H. The role of novel T cell costimulatory pathways in autoimmunity and transplantation. J. Am. Soc. Nephrol. 13, 559-575 (2002).
10. Lai, K. W. et al. Overexpression of interleukin-13 induces minimal-change-like nephropathy in rats. J. Am. Soc. Nephrol. 18, 1476-1485 (2007).
11. Karras, A. et al. renal and thymic pathology in thymoma-associated nephropathy: report of 21 cases and review of the literature. Nephrol. Dial. Transplant. 20, 1075-1082 (2005).
12. Ronco, P. & Debiec, H. Pathophysiological lessons from rare associations of immunological disorderS. Pediatr. Nephrol. 24, 3-8 (2008).
13. Lapillonne, H. et al. Stem cell mobilization in idiopathic steroid-sensitive nephrotic syndrome. Pediatr. Nephrol. 23, 1251-1256 (2008).
14. Araya, C. E. et al. A case of unfulfilled expectations. Cytokines in idiopathic minimal lesion nephrotic syndrome. Pediatr. Nephrol. 21, 603-610 (2006).
15. Sharma, M., Sharma, R., Reddy, S. R., McCarthy, E. T. & Savin, V. J. Proteinuria after injection of human focal segmental glomerulosclerosis factor. Transplantation 73, 366-372 (2002).
16. Zimmerman, S. W. Increased urinary protein excretion in the rat produced by serum from a patient with recurrent focal glomerular sclerosis after renal transplantation. Clin. Nephrol. 22, 32-38 (1984).
17. Koyama, A., Fujisaki, M., Kobayashi, M., Igarashi, M. & Narita, M. A glomerular permeability factor produced by human T cell hybridomas. Kidney Int. 40, 453-460 (1991).
18. Dantal, J. et al. Effect of plasma protein adsorption on protein excretion in kidney- transplant recipients with recurrent nephrotic syndrome. N. Engl. J. med. 330, 7-14 (1994).
19. Le Berre, L. et al. Extrarenal effects on the pathogenesis and relapse of idiopathic nephrotic syndrome in Buffalo/Mna rats. J. Clin. Invest. 109, 491-498 (2002).
20. Le Berre, L. et al. renal macrophage activation and TH2 polarization precedes the development of nephrotic syndrome in Buffalo/Mna rats. Kidney Int. 68, 2079-2090 (2005).
21. Ali, A. A. et al. Minimal-change glomerular nephritis. Normal kidneys in an abnormal environment? Transplantation 58, 849-852 (1994).
22. Savin, V. J. et al. Circulating factor associated with increased glomerular permeability to albumin in recurrent focal segmental glomerulosclerosis. N. Engl. J. med. 334, 878-883 (1996).
23. Ghiggeri, G. M., Carraro, M. & vincenti, F. Recurrent focal glomerulosclerosis in the era of genetics of podocyte proteins: Theory and therapy. Nephrol. Dial. transplant. 19, 1036-1040 (2004).
24. Carraro, M. et al. Nephrotic urine prevents increased rat glomerular albumin permeability induced by serum from the same patient with idiopathic nephrotic syndrome. Nephrol. Dial. transplant. 18, 689-693 (2003).
25. Sharma, R., Sharma, M., McCarthy, E. T., Ge, X. L. & Savin, V. J. Components of normal serum block the focal segmental glomerulosclerosis factor activity in vitro. Kidney Int. 58, 1973-1979 (2000).
26. Kemper, M. J., Wolf, G. & Müller-wiefel, D. E. Transmission of glomerular permeability factor from a mother to her child. N. Engl. J. med. 344, 386-387 (2001).
27. Kemper, M. J., Meyer-Jark, T., Lilova, M. & Müller-Wiefel, D. E. Combined T- and B-cell activation in childhood steroid-sensitive nephrotic syndrome. Clin. Nephrol. 60, 242-247 (2003).
28. Vivier, E., Tomasello, E., Baratin, M., Walzer, T. & Ugolini, S. Functions of natural killer cellS. Nat. Immunol. 9, 503-510 (2008).
29. Daniel, V., trautmann, Y., Konrad, M., Nayir, A. & Schärer, K. T-lymphocyte populations, cytokines and other growth factors in serum and urine of children with idiopathic nephrotic syndrome. Clin. Nephrol. 47, 289-297 (1997).
30. Bagga, A., Vasudev, A. S., Moudgil, A. & Srivastava, R. N. Peripheral blood lymphocyte subsets in idiopathic nephrotic syndrome of childhood. Indian J. med. res. 104, 292-295 (1996).
31. Pawluczyk, I. Z. & Harris, K. P. Macrophages promote prosclerotic responses in cultured rat mesangial cells: A mechanism for the initiation of glomerulosclerosis. J. Am. Soc. Nephrol. 8, 1525-1536 (1997).
32. Lin, C. Y. & Chien, J. W. Increased interleukin-12 release from peripheral blood mononuclear cells in nephrotic phase of minimal change nephrotic syndrome. Acta Paediatr. Taiwan 45, 77-80 (2004).
33. Nishimura, M. et al. Focal segmental glomerular sclerosis, a type of intractable chronic glomerulonephritis, is a stem cell disorder. J. Exp. med. 179, 1053-1058 (1994).
34. Yoshida, F., Matsuo, S., Fujishima, H., Kim, H. K. & Tomita, T. Renal lesions of the FGs strain of mice: A spontaneous animal model of progressive glomerulosclerosis. Nephron 66, 317-325 (1994).
35. Humphreys, B. D., vanguri, V. K., Henderson, J. & Antin, J. H. Minimal-change nephrotic syndrome in a hematopoietic stem-cell transplant recipient. Nat. Clin. Pract. Nephrol. 2, 535-539 (2006).
36. Heras, M. et al. Nephrotic syndrome resulting from focal segmental glomerulosclerosis in a peripheral blood stem cell transplant patient. J. Nephrol. 20, 495-498 (2007).
37. Colombo, A. A. et al. Nephrotic syndrome after allogeneic hematopoietic stem cell transplantation as a late complication of chronic graft-versus-host disease. Transplantation 81, 1087-1092 (2006).
38. Sellier-Leclerc, A. L. et al. A humanized mouse model of idiopathic nephrotic syndrome suggests a pathogenic role for immature cellS. J. Am. Soc. Nephrol. 18, 2732-2739 (2007).
39. FDA Approved Drug Products [online]. http:// wwW.accessdata.fda.gov/ scripts/cder/ drugsatfda/index.cfm
40. world Health Organization international Nonproprietary Names program [online]. http:// wwW.who.int/medicines/services/inn/en/
41. Hudson, P. J. & Souriau, C. Engineered antibodies. Nat. med. 9, 129-134 (2003).
42. Mottershead, M. & Neuberger, J. Daclizumab. Expert Opin. Biol. Ther. 7, 1583-1596 (2007).
43. Church, A. C. Clinical advances in therapies targeting the interleukin-2 receptor. QJM 96, 91-102 (2003).
44. Francois, H., Daugas, E., Bensman, A. & Ronco, P. Unexpected efficacy of rituximab in multirelapsing minimal change nephrotic syndrome in the adult: First case report and pathophysiological considerations. Am. J. Kidney Dis. 49, 158-161 (2007).
45. Park, S. S., Hahn, W. H., Kim, S. D. & Cho B. S. Remission of refractory minimal change nephrotic syndrome after basiliximab therapy. Pediatric. Nephrol. doi:10.1007/s00467-009- 1145-1146
46. Salama, A. D. & Pusey, C. D. Drug insight: Rituximab in renal disease and transplantation. Nat. Clin. Pract. Nephrol. 2, 221-230 (2006).
47. Ruggenenti, P. et al. Rituximab in idiopathic membranous nephropathy: A one-year prospective study. J. Am. Soc. Nephrol. 14, 1851-1857 (2003).
48. Pescovitz, M. D., Book, B. K. & Sidner, R. A. Resolution of recurrent focal segmental glomerulosclerosis proteinuria after rituximab treatment. N. Engl. J. med. 354, 1961-1963 (2006).
49. Kamar, N. et al. Treatment of focal segmental glomerular sclerosis with rituximab: 2 case reports. Clin. Nephrol. 67, 250-254 (2007).
50. Gossmann, J. et al. Abrogation of nephrotic proteinuria by rituximab treatment in a renal transplant patient with relapsed focal segmental glomerulosclerosis. transpl. Int. 20, 558-562 (2007).
51. Hristea, D. et al. Successful treatment of recurrent focal segmental glomerulosclerosis after kidney transplantation by plasmapheresis and rituximab. transpl. Int. 20, 102-105 (2007).
52. Meyer, T. N., Thaiss, F. & Stahl, R. A. Immunoadsorbtion and rituximab therapy in a second living-related kidney transplant patient with recurrent focal segmental glomerulosclerosis. transpl. Int. 20, 1066-1071 (2007).
53. Apeland, T. & Hartmann, A. Rituximab therapy in early recurrent focal segmental sclerosis after renal transplantation. Nephrol. Dial. transplant. 23, 2091-2094 (2008).
54. Bayrakci, U. S., Baskin, E., Sakalli, H., Karakayali, H. & Haberal, M. Rituximab for posttransplant recurrences of FsGS. Pediatr. Transplant. 13, 240-243 (2008).
55. Yabu, J. M., Ho, B., Scandling, J. D. & Vincenti, F. Rituximab failed to improve nephrotic syndrome in renal transplant patients with recurrent focal segmental glomerulosclerosis. Am. J. transplant. 8, 222-227 (2008).
56. Marks, S. D. & McGraw, M. Does rituximab treat recurrent focal segmental glomerulosclerosis postrenal transplantation? Pediatr. Nephrol. 22, 158-160 (2007).
57. EI-Firjani, A. et al. Post-transplant focal segmental glomerulosclerosis refractory to plasmapheresis and rituximab therapy. Nephrol. Dial. Transplant. 23, 425 (2008).
58. Nozu, K. et al. Rituximab treatment for posttransplant lymphoproliferative disorder (PTLD) induces complete remission of recurrent nephrotic syndrome. Pediatr. Nephrol. 20, 1660-1663 (2005).
59. Guigonis, V. et al. Rituximab treatment for severe steroid- or cyclosporine-dependent nephrotic syndrome: A multicentric series of 22 cases. Pediatr. Nephrol. 23, 1269-1279 (2008).
60. Bagga, A., sinha, A. & Moudgil, A. Rituximab in patients with the steroid-resistant nephrotic syndrome. N. Engl. J. med. 356, 2751-2752 (2007).
61. Nakayama, M. et al. Rituximab for refractory focal segmental glomerulosclerosis. Pediatr. Nephrol. 23, 481-485 (2008).
62. Benz, K. et al. Change of the course of steroid- dependent nephrotic syndrome after rituximab therapy. Pediatr. Nephrol. 19, 794-797 (2004).
63. Gilbert, R. D., Dötsch, J., Rascher, W. & Stachel, D. Rituximab therapy for steroid- dependent minimal change nephrotic syndrome. Pediatr. Nephrol. 21, 1698-1700 (2006).
64. Hofstra, J. M., Deegens, J. K. & Wetzels, J. F. Rituximab: Effective treatment for severe steroid-dependent minimal change nephrotic syndrome? Nephrol. Dial. Transplant. 22, 2100-2102 (2007).
65. Smith, G. C. Is there a role for rituximab in the treatment of idiopathic childhood nephrotic syndrome? Pediatr. Nephrol. 22, 893-898 (2007).
66. Suri, M., Tran, K., Sharma, A. P., Filler, G. & Grimmer, J. Remission of steroid-resistant nephrotic syndrome due to focal and segmental glomerulosclerosis using rituximab. Int. Urol. Nephrol. 40, 807-810 (2008).
67. Yang, T., Nast, C. C., Vo, A. & Jordan, S. C. Rapid remission of steroid and mycophenolate mofetil (MMF)-resistant minimal change nephrotic syndrome after rituximab therapy. Nephrol. Dial. Transplant. 23, 377-380 (2008).
68. Gray, M., Miles, K., Salter, D., Gray, D. & Savill, J. Apoptotic cells protect mice from autoimmune inflammation by the induction of regulatory B cellS. Proc. Natl Acad. Sci. USA 104, 14080-14085 (2007).
69. Sakaguchi, S., Yamaguchi, T., Nomura, T. & Ono, M. Regulatory T cells and immune tolerance. Cell 133, 775-787 (2008).
70. Taube, D., Brown, Z. & Williams, D. G. Impaired lymphocyte and suppressor cell function in minimal change nephropathy, membranous nephropathy and focal glomerulosclerosis. Clin. Nephrol. 22, 176-182 (1984).
71. Calabrese, L. H. & Molloy, E. S. Progressive multifocal leucoencephalopathy in the rheumatic diseases: assessing the risks of biological immunosuppressive therapies. Ann. Rheum. Dis. 67 (Suppl. 3), iii64-iii65 (2008).
72. Waldmann, H. & Hale, G. CAMPATH: From concept to clinic. Philos. TSrans. R. Soc. Lond. B. Biol. Sci. 360, 1707-1711 (2005).
73. Buttmann, M. & Rieckmann, P. Treating multiple sclerosis with monoclonal antibodies. Expert Rev. Neurother. 8, 433-455 (2008).
74. Pascual, J. et al. Alemtuzumab induction and recurrence of glomerular disease after kidney Transplantation. transplantation 83, 1429-1434 (2007).
75. Ciancio, G. & Burke, G. W. 3rd. Alemtuzumab (Campath-1H) in kidney transplantation. Am. J. Transplant. 8, 15-20 (2008).
76. Noris, M. et al. Regulatory T cells and T cell depletion: Role of immunosuppressive drugS. J. Am. Soc. Nephrol. 18, 1007-1018 (2007).
77. Clatworthy, M. R. et al. Anti-glomerular basement membrane disease after alemtuzumab. N. Engl. J. med. 359, 768-769 (2008).
78. Walsh, M., Wallin, E. F. & Jayne, D. R. Long-term follow-up of relapsing/refractory ANCA associated vasculitis treated with the lymphocyte depleting antibody alemtuzumab (CAMPATH-1H) [abstract]. J. Am. Soc. Nephrol. 18, 48A (2007).
79. Vincenti, F. Costimulation blockade in autoimmunity and transplantation. J. Allergy Clin. Immunol. 121, 299-306 (2008).
80. Kitching, A. R., Huang, X. R., Ruth, A. J., Tipping, P. G. & Holdsworth, S. R. Effects of CTLA4-Fc on glomerular injury in humorally mediated glomerulonephritis in BALB/c mice. Clin. Exp. Immunol. 128, 429-435 (2002).
81. Reynolds, J. et al. CD28-B7 blockade prevents the development of experimental autoimmune glomerulonephritis. J. Clin. Invest. 105, 643-651 (2000).
82. Tracey, D., Klareskog, L., sasso, E. H., salfeld, J. G. & Tak, P. P. Tumor necrosis factor antagonist mechanisms of action: A comprehensive review. Pharmacol. Ther. 117, 244-279 (2008).
83. Rigby, W. F. Drug insight: Different mechanisms of action of tumor necrosis factor antagonists- passive-aggressive behavior? Nat. Clin. Pract. Rheumatol. 3, 227-233 (2007).
84. Ehrenstein, M. R. et al. Compromised function of regulatory T cells in rheumatoid arthritis and reversal by anti-TNFá therapy. J. Exp. med. 200, 277-285 (2004).
85. Suranyi, M. G., Guasch, A., Hall, B. M. & Myers, B. D. Elevated levels of tumor necrosis factor-á in the nephrotic syndrome in humans. Am. J. Kidney Dis. 21, 251-259 (1993).
86. Raveh, D., Shemesh, O., Ashkenazi, Y. J., Winkler, R. & Barak, V. Tumor necrosis factor-á blocking agent as a treatment for nephrotic syndrome. Pediatr. Nephrol. 19, 1281-1284 (2004).
87. Leroy, S. et al. Tumor necrosis factor-á blocking agent as a treatment for steroid resistant nephrotic syndrome [abstract]. J. Am. Soc. Nephrol. 18, 565A (2007).
88. Ricklin, D. & Lambris, J. D. Complement- targeted therapeutics. Nat. Biotechnol. 25, 1265-1275 (2007).
89. Cunningham, P. N. & Quigg, R. J. Contrasting roles of complement activation and its regulation in membranous nephropathy. J. Am. Soc. Nephrol. 16, 1214-1222 (2005).
90. Appel, G. et al. Eculizumab (C5 complement inhibitor) in the treatment of idiopathic membranous nephropathy: Preliminary baseline and pharmacokinetic (PK)/ pharmacodynamic (PD) data [abstract]. J. Am. Soc. Nephrol. 13, 668A (2002).
91. Turnberg, D. et al. Complement activation contributes to both glomerular and tubulointerstitial damage in adriamycin nephropathy in mice. J. Immunol. 177, 4094-4102 (2006).
92. rangan, G. K., Pippin, J. W. & Couser, W. G. C5b-9 regulates peritubular myofibroblast accumulation in experimental focal segmental glomerulosclerosis. Kidney Int. 66, 1838-1848 (2004).
93. Abbate, M. et al. Complement-mediated dysfunction of glomerular filtration barrier accelerates progressive renal injury. J. Am. Soc. Nephrol. 19, 1158-1167 (2008).
94. Morita, Y. et al. Complement activation products in the urine from proteinuric patients. J. Am. Soc. Nephrol. 11, 700-707 (2000).
95. Gagliardini, E. & Benigni, A. Therapeutic potential of TGF-â inhibition in chronic renal failure. Expert Opin. Biol. Ther. 7, 293-304 (2007).
96. Wahab, N. A. & Mason, R. M. A critical look at growth factors and epithelial-to-mesenchymal transition in the adult kidney. Interrelationships between growth factors that regulate eMT in the adult kidney. Nephron Exp. Nephrol. 104, e129-e134 (2006).
97. Abbate, M. et al. Transforming growth factor-â1 is up-regulated by podocytes in response to excess intraglomerular passage of proteins: A central pathway in progressive glomerulosclerosis. Am. J. Pathol. 161, 2179-2193 (2002).
98. Ma, L. J. et al. Divergent effects of low versus high dose anti-TGF-â antibody in puromycin aminonucleoside nephropathy in rats. Kidney Int. 65, 106-115 (2004).
99. Kasuga, H. et al. Effects of anti-TGF-â type ii receptor antibody on experimental glomerulonephritis. Kidney Int. 60, 1745-1755 (2001).
100. Dornhöfer, N. et al. Connective tissue growth factor-specific monoclonal antibody therapy inhibits pancreatic tumor growth and metastasis. Cancer Res. 66, 5816-5827 (2006).
101. Ikawa, Y. et al. Neutralizing monoclonal antibody to human connective tissue growth factor ameliorates transforming growth factor-â-induced mouse fibrosis. J. Cell. Physiol. 216, 680-687 (2008).