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Genetics of nephrotic syndrome: new insights into molecules acting at the glomerular filtration barrier

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Abstract

Nephrotic syndrome is caused by increased permeability of the glomerular filtration barrier for macromolecules. The identification of mutations of various podocyte-expressed proteins as causes of familial nephrotic syndrome has significantly contributed to shedding light into the molecular pathogenesis of nephrotic proteinuria and into the physiology of the glomerular sieve. More recent findings have changed our conception of the glomerular filtration barrier from a relatively static structure to a highly dynamic one. Both the multiprotein slit diaphragm complex around nephrin and the integrin receptor complex that mediates binding of the podocyte to the glomerular basement membrane, may translate outside–inside signaling and lead to podocyte actin cytoskeleton rearrangement. This may enable the podocyte network to adapt to environmental changes and respond to injury. Disturbance in these processes may not only be involved in the pathogenesis of hereditary nephrotic syndrome but also in that of more common acquired proteinuric diseases. Elucidation of the molecular mechanisms involved will possibly open the way to new therapeutic approaches.

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Abbreviations

GBM:

glomerular basement membrane

SD:

slit diaphragm

NS:

nephrotic syndrome

SRNS:

steroid-resistant nephrotic syndrome

FSGS:

focal and segmental glomerulosclerosis

PI3K:

phosphoinositide-3 kinase

IP3:

inositol 1,4,5-trisphosphate

aPKC:

atypical protein kinase C

DAG:

diacylglycerol

NFAT:

nuclear factor of activated T cells

ILK:

integrin-linked kinase

CsA:

cyclosporin A

References

  1. Jarad G, Miner JH (2009) Update on the glomerular filtration barrier. Curr Opin Nephrol Hypertens 18:226–232

    Article  PubMed  Google Scholar 

  2. Faul C, Asanuma K, Yanagida-Asanuma E, Kim K, Mundel P (2007) Actin up: regulation of podocyte structure and function by components of the actin cytoskeleton. Trends Cell Biol 17:428–437

    Article  PubMed  CAS  Google Scholar 

  3. Holthofer H (2007) Molecular architecture of the glomerular slit diaphragm lessons learnt for a better understanding of disease pathogenesis. Nephrol Dial Transplant. 22:2124–2128

    Article  PubMed  Google Scholar 

  4. Eddy AA, Symons JM (2003) Nephrotic syndrome in childhood. Lancet 362:629–639

    Article  PubMed  Google Scholar 

  5. Antignac C (2002) Genetic models: clues for understanding the pathogenesis of idiopathic nephrotic syndrome. J Clin Invest 109:447–449

    PubMed  CAS  Google Scholar 

  6. Boute N, Gribouval O, Roselli S, Benessy F, Lee H, Fuchshuber A, Dahan K, Gubler MC, Niaudet P, Antignac C (2000) NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome. Nat Genet 24:349–354

    Article  PubMed  CAS  Google Scholar 

  7. Kestila M, Lenkkeri U, Mannikko M, Lamerdin J, McCready P, Putaala H, Ruotsalainen V, Morita T, Nissinen M, Herva R, Kashtan CE, Peltonen L, Holmberg C, Olsen A, Tryggvason K (1998) Positionally cloned gene for a novel glomerular protein–nephrin–is mutated in congenital nephrotic syndrome. Mol Cell 1:575–582

    Article  PubMed  CAS  Google Scholar 

  8. Hinkes BG, Mucha B, Vlangos CN, Gbadegesin R, Liu J, Hasselbacher K, Hangan D, Ozaltin F, Zenker M, Hildebrandt F (2007) Nephrotic syndrome in the first year of life: two thirds of cases are caused by mutations in 4 genes (NPHS1, NPHS2, WT1, and LAMB2). Pediatrics 119:e907–e919

    Article  PubMed  Google Scholar 

  9. Wartiovaara J, Ofverstedt LG, Khoshnoodi J, Zhang J, Makela E, Sandin S, Ruotsalainen V, Cheng RH, Jalanko H, Skoglund U, Tryggvason K (2004) Nephrin strands contribute to a porous slit diaphragm scaffold as revealed by electron tomography. J Clin Invest 114:1475–1483

    PubMed  CAS  Google Scholar 

  10. Huber TB, Simons M, Hartleben B, Sernetz L, Schmidts M, Gundlach E, Saleem MA, Walz G, Benzing T (2003) Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains. Hum Mol Genet 12:3397–3405

    Article  PubMed  CAS  Google Scholar 

  11. Patrakka J, Tryggvason K (2007) Nephrin—a unique structural and signaling protein of the kidney filter. Trends Mol Med 13:396–403

    Article  PubMed  CAS  Google Scholar 

  12. Huber TB, Benzing T (2005) The slit diaphragm: a signaling platform to regulate podocyte function. Curr Opin Nephrol Hypertens 14:211–216

    Article  PubMed  Google Scholar 

  13. Garg P, Verma R, Nihalani D, Johnstone DB, Holzman LB (2007) Neph1 cooperates with nephrin to transduce a signal that induces actin polymerization. Mol Cell Biol 27:8698–8712

    Article  PubMed  CAS  Google Scholar 

  14. Jones N, Blasutig IM, Eremina V, Ruston JM, Bladt F, Li H, Huang H, Larose L, Li SS, Takano T, Quaggin SE, Pawson T (2006) Nck adaptor proteins link nephrin to the actin cytoskeleton of kidney podocytes. Nature 440:818–823

    Article  PubMed  CAS  Google Scholar 

  15. Verma R, Kovari I, Soofi A, Nihalani D, Patrie K, Holzman LB (2006) Nephrin ectodomain engagement results in Src kinase activation, nephrin phosphorylation, Nck recruitment, and actin polymerization. J Clin Invest 116:1346–1359

    Article  PubMed  CAS  Google Scholar 

  16. Huber TB, Hartleben B, Kim J, Schmidts M, Schermer B, Keil A, Egger L, Lecha RL, Borner C, Pavenstadt H, Shaw AS, Walz G, Benzing T (2003) Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT-dependent signaling. Mol Cell Biol 23:4917–4928

    Article  PubMed  CAS  Google Scholar 

  17. Zhu J, Sun N, Aoudjit L, Li H, Kawachi H, Lemay S, Takano T (2008) Nephrin mediates actin reorganization via phosphoinositide 3-kinase in podocytes. Kidney Int 73:556–566

    Article  PubMed  CAS  Google Scholar 

  18. Asanuma K, Kim K, Oh J, Giardino L, Chabanis S, Faul C, Reiser J, Mundel P (2005) Synaptopodin regulates the actin-bundling activity of alpha-actinin in an isoform-specific manner. J Clin Invest 115:1188–1198

    PubMed  CAS  Google Scholar 

  19. Harita Y, Kurihara H, Kosako H, Tezuka T, Sekine T, Igarashi T, Ohsawa I, Ohta S, Hattori S (2009) Phosphorylation of nephrin triggers Ca2+ signaling by recruitment and activation of phospholipase C-{gamma}1. J Biol Chem 284:8951–8962

    Article  PubMed  CAS  Google Scholar 

  20. Liu XL, Kilpelainen P, Hellman U, Sun Y, Wartiovaara J, Morgunova E, Pikkarainen T, Yan K, Jonsson AP, Tryggvason K (2005) Characterization of the interactions of the nephrin intracellular domain. FEBS J 272:228–243

    Article  PubMed  CAS  Google Scholar 

  21. Hartleben B, Schweizer H, Lubben P, Bartram MP, Moller CC, Herr R, Wei C, Neumann-Haefelin E, Schermer B, Zentgraf H, Kerjaschki D, Reiser J, Walz G, Benzing T, Huber TB (2008) Neph-Nephrin proteins bind the Par3-Par6-atypical protein kinase C (aPKC) complex to regulate podocyte cell polarity. J Biol Chem 283:23033–23038

    Article  PubMed  CAS  Google Scholar 

  22. Huber TB, Hartleben B, Winkelmann K, Schneider L, Becker JU, Leitges M, Walz G, Haller H, Schiffer M (2009) Loss of podocyte aPKClambda/iota causes polarity defects and nephrotic syndrome. J Am Soc Nephrol 20:798–806

    Article  PubMed  CAS  Google Scholar 

  23. Shono A, Tsukaguchi H, Yaoita E, Nameta M, Kurihara H, Qin XS, Yamamoto T, Doi T (2007) Podocin participates in the assembly of tight junctions between foot processes in nephrotic podocytes. J Am Soc Nephrol 18:2525–2533

    Article  PubMed  CAS  Google Scholar 

  24. Huber TB, Schermer B, Benzing T (2007) Podocin organizes ion channel-lipid supercomplexes: implications for mechanosensation at the slit diaphragm. Nephron Exp Nephrol 106:e27–e31

    Article  PubMed  CAS  Google Scholar 

  25. Huber TB, Kottgen M, Schilling B, Walz G, Benzing T (2001) Interaction with podocin facilitates nephrin signaling. J Biol Chem 276:41543–41546

    Article  PubMed  CAS  Google Scholar 

  26. Li H, Lemay S, Aoudjit L, Kawachi H, Takano T (2004) SRC-family kinase Fyn phosphorylates the cytoplasmic domain of nephrin and modulates its interaction with podocin. J Am Soc Nephrol 15:3006–3015

    Article  PubMed  Google Scholar 

  27. Reiser J, Polu KR, Moller CC, Kenlan P, Altintas MM, Wei C, Faul C, Herbert S, Villegas I, Avila-Casado C, McGee M, Sugimoto H, Brown D, Kalluri R, Mundel P, Smith PL, Clapham DE, Pollak MR (2005) TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function. Nat Genet 37:739–744

    Article  PubMed  CAS  Google Scholar 

  28. Winn MP, Conlon PJ, Lynn KL, Farrington MK, Creazzo T, Hawkins AF, Daskalakis N, Kwan SY, Ebersviller S, Burchette JL, Pericak-Vance MA, Howell DN, Vance JM, Rosenberg PB (2005) A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis. Science 308:1801–1804

    Article  PubMed  CAS  Google Scholar 

  29. Zhu B, Chen N, Wang ZH, Pan XX, Ren H, Zhang W, Wang WM (2008) Identification and functional analysis of a novel TRPC6 mutation associated with late onset familial focal segmental glomerulosclerosis in Chinese patients. Mutat Res 664:84–90

    PubMed  Google Scholar 

  30. Kaplan JM, Kim SH, North KN, Rennke H, Correia LA, Tong HQ, Mathis BJ, Rodriguez-Perez JC, Allen PG, Beggs AH, Pollak MR (2000) Mutations in ACTN4, encoding alpha-actinin-4, cause familial focal segmental glomerulosclerosis. Nat Genet 24:251–256

    Article  PubMed  CAS  Google Scholar 

  31. Kim JM, Wu H, Green G, Winkler CA, Kopp JB, Miner JH, Unanue ER, Shaw AS (2003) CD2-associated protein haploinsufficiency is linked to glomerular disease susceptibility. Science 300:1298–1300

    Article  PubMed  CAS  Google Scholar 

  32. Clapham DE (2007) Calcium signaling. Cell 131:1047–1058

    Article  PubMed  CAS  Google Scholar 

  33. Spassova MA, Hewavitharana T, Xu W, Soboloff J, Gill DL (2006) A common mechanism underlies stretch activation and receptor activation of TRPC6 channels. Proc Natl Acad Sci USA 103:16586–16591

    Article  PubMed  CAS  Google Scholar 

  34. Hisatsune C, Kuroda Y, Nakamura K, Inoue T, Nakamura T, Michikawa T, Mizutani A, Mikoshiba K (2004) Regulation of TRPC6 channel activity by tyrosine phosphorylation. J Biol Chem 279:18887–18894

    Article  PubMed  CAS  Google Scholar 

  35. Faul C, Donnelly M, Merscher-Gomez S, Chang YH, Franz S, Delfgaauw J, Chang JM, Choi HY, Campbell KN, Kim K, Reiser J, Mundel P (2008) The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A. Nat Med 14:931–938

    Article  PubMed  CAS  Google Scholar 

  36. Schlondorff J, Del Camino D, Carrasquillo R, Lacey V, Pollak MR (2009) TRPC6 mutations associated with focal segmental glomerulosclerosis cause constitutive activation of NFAT-dependent transcription. Am J Physiol Cell Physiol 296:C558–C569

    Article  PubMed  CAS  Google Scholar 

  37. Möller CC, Flesche J, Reiser J (2009) Sensitizing the Slit Diaphragm with TRPC6 ion channels. J Am Soc Nephrol 20:950–953

    Google Scholar 

  38. Winn MP (2008) 2007 Young Investigator Award: TRP'ing into a new era for glomerular disease. J Am Soc Nephrol 19:1071–1075

    Article  PubMed  CAS  Google Scholar 

  39. Graham S, Ding M, Sours-Brothers S, Yorio T, Ma JX, Ma R (2007) Downregulation of TRPC6 protein expression by high glucose, a possible mechanism for the impaired Ca2+ signaling in glomerular mesangial cells in diabetes. Am J Physiol Renal Physiol 293:F1381–F1390

    Article  PubMed  CAS  Google Scholar 

  40. Moller CC, Wei C, Altintas MM, Li J, Greka A, Ohse T, Pippin JW, Rastaldi MP, Wawersik S, Schiavi S, Henger A, Kretzler M, Shankland SJ, Reiser J (2007) Induction of TRPC6 channel in acquired forms of proteinuric kidney disease. J Am Soc Nephrol 18:29–36

    Article  PubMed  CAS  Google Scholar 

  41. Hinkes B, Wiggins RC, Gbadegesin R, Vlangos CN, Seelow D, Nurnberg G, Garg P, Verma R, Chaib H, Hoskins BE, Ashraf S, Becker C, Hennies HC, Goyal M, Wharram BL, Schachter AD, Mudumana S, Drummond I, Kerjaschki D, Waldherr R, Dietrich A, Ozaltin F, Bakkaloglu A, Cleper R, Basel-Vanagaite L, Pohl M, Griebel M, Tsygin AN, Soylu A, Muller D, Sorli CS, Bunney TD, Katan M, Liu J, Attanasio M, O'Toole JF, Hasselbacher K, Mucha B, Otto EA, Airik R, Kispert A, Kelley GG, Smrcka AV, Gudermann T, Holzman LB, Nurnberg P, Hildebrandt F (2006) Positional cloning uncovers mutations in PLCE1 responsible for a nephrotic syndrome variant that may be reversible. Nat Genet 38:1397–1405

    Article  PubMed  CAS  Google Scholar 

  42. Gbadegesin R, Hinkes BG, Hoskins BE, Vlangos CN, Heeringa SF, Liu J, Loirat C, Ozaltin F, Hashmi S, Ulmer F, Cleper R, Ettenger R, Antignac C, Wiggins RC, Zenker M, Hildebrandt F (2008) Mutations in PLCE1 are a major cause of isolated diffuse mesangial sclerosis (IDMS). Nephrol Dial Transplant 23:1291–1297

    Article  PubMed  CAS  Google Scholar 

  43. Gilbert RD, Turner CL, Gibson J, Bass PS, Haq MR, Cross E, Bunyan DJ, Collins AR, Tapper WJ, Needell JC, Dell B, Morton NE, Temple IK, Robinson DO (2009) Mutations in phospholipase C epsilon 1 are not sufficient to cause diffuse mesangial sclerosis. Kidney Int 75:415–419

    Article  PubMed  CAS  Google Scholar 

  44. Wing MR, Bourdon DM, Harden TK (2003) PLC-epsilon: a shared effector protein in Ras-, Rho-, and G alpha beta gamma-mediated signaling. Mol Interv 3:273–280

    Article  PubMed  CAS  Google Scholar 

  45. Dietrich A, Gudermann T (2007) Trpc6. Handbook Exp Pharmacol 179:125–141

    Article  CAS  Google Scholar 

  46. Chaib H, Hoskins BE, Ashraf S, Goyal M, Wiggins RC, Hildebrandt F (2008) Identification of BRAF as a new interactor of PLCepsilon1, the protein mutated in nephrotic syndrome type 3. Am J Physiol Renal Physiol 294:F93–F99

    Article  PubMed  CAS  Google Scholar 

  47. Zenker M, Aigner T, Wendler O, Tralau T, Muntefering H, Fenski R, Pitz S, Schumacher V, Royer-Pokora B, Wuhl E, Cochat P, Bouvier R, Kraus C, Mark K, Madlon H, Dotsch J, Rascher W, Maruniak-Chudek I, Lennert T, Neumann LM, Reis A (2004) Human laminin beta2 deficiency causes congenital nephrosis with mesangial sclerosis and distinct eye abnormalities. Hum Mol Genet 13:2625–2632

    Article  PubMed  CAS  Google Scholar 

  48. Zenker M, Tralau T, Lennert T, Pitz S, Mark K, Madlon H, Dotsch J, Reis A, Muntefering H, Neumann LM (2004) Congenital nephrosis, mesangial sclerosis, and distinct eye abnormalities with microcoria: an autosomal recessive syndrome. Am J Med Genet A 130A:138–145

    Article  PubMed  Google Scholar 

  49. Choi HJ, Lee BH, Kang JH, Jeong HJ, Moon KC, Ha IS, Yu YS, Matejas V, Zenker M, Choi Y, Cheong HI (2008) Variable phenotype of Pierson syndrome. Pediatr Nephrol 23:995–1000

    Article  PubMed  Google Scholar 

  50. Hasselbacher K, Wiggins RC, Matejas V, Hinkes BG, Mucha B, Hoskins BE, Ozaltin F, Nurnberg G, Becker C, Hangan D, Pohl M, Kuwertz-Broking E, Griebel M, Schumacher V, Royer-Pokora B, Bakkaloglu A, Nurnberg P, Zenker M, Hildebrandt F (2006) Recessive missense mutations in LAMB2 expand the clinical spectrum of LAMB2-associated disorders. Kidney Int 70:1008–1012

    Article  PubMed  CAS  Google Scholar 

  51. Kagan M, Cohen AH, Matejas V, Vlangos C, Zenker M (2008) A milder variant of Pierson syndrome. Pediatr Nephrol 23:323–327

    Article  PubMed  Google Scholar 

  52. Matejas V, Al-Gazali L, Amirlak I, Zenker M (2006) A syndrome comprising childhood-onset glomerular kidney disease and ocular abnormalities with progressive loss of vision is caused by mutated LAMB2. Nephrol Dial Transplant 21:3283–3286

    Article  PubMed  CAS  Google Scholar 

  53. Tunggal P, Smyth N, Paulsson M, Ott MC (2000) Laminins: structure and genetic regulation. Microsc Res Tech 51:214–227

    Article  PubMed  CAS  Google Scholar 

  54. Yurchenco PD, Amenta PS, Patton BL (2004) Basement membrane assembly, stability and activities observed through a developmental lens. Matrix Biol 22:521–538

    Article  PubMed  CAS  Google Scholar 

  55. Miner JH, Yurchenco PD (2004) Laminin functions in tissue morphogenesis. Annu Rev Cell Dev Biol 20:255–284

    Article  PubMed  CAS  Google Scholar 

  56. Miner JH, Patton BL (1999) Laminin-11. Int J Biochem Cell Biol 31:811–816

    Article  PubMed  CAS  Google Scholar 

  57. Sachs N, Kreft M, van den Bergh Weerman MA, Beynon AJ, Peters TA, Weening JJ, Sonnenberg A (2006) Kidney failure in mice lacking the tetraspanin CD151. J Cell Biol 175:33–39

    Article  PubMed  CAS  Google Scholar 

  58. Karamatic Crew V, Burton N, Kagan A, Green CA, Levene C, Flinter F, Brady RL, Daniels G, Anstee DJ (2004) CD151, the first member of the tetraspanin (TM4) superfamily detected on erythrocytes, is essential for the correct assembly of human basement membranes in kidney and skin. Blood 104:2217–2223

    Article  PubMed  CAS  Google Scholar 

  59. Noakes PG, Miner JH, Gautam M, Cunningham JM, Sanes JR, Merlie JP (1995) The renal glomerulus of mice lacking s-laminin/laminin beta 2: nephrosis despite molecular compensation by laminin beta 1. Nat Genet 10:400–406

    Article  PubMed  CAS  Google Scholar 

  60. Kanasaki K, Kanda Y, Palmsten K, Tanjore H, Lee SB, Lebleu VS, Gattone VH Jr, Kalluri R (2008) Integrin beta1-mediated matrix assembly and signaling are critical for the normal development and function of the kidney glomerulus. Dev Biol 313:584–593

    Article  PubMed  CAS  Google Scholar 

  61. Jarad G, Cunningham J, Shaw AS, Miner JH (2006) Proteinuria precedes podocyte abnormalities inLamb2-/- mice, implicating the glomerular basement membrane as an albumin barrier. J Clin Invest 116:2272–2279

    Article  PubMed  CAS  Google Scholar 

  62. El-Aouni C, Herbach N, Blattner SM, Henger A, Rastaldi MP, Jarad G, Miner JH, Moeller MJ, St-Arnaud R, Dedhar S, Holzman LB, Wanke R, Kretzler M (2006) Podocyte-specific deletion of integrin-linked kinase results in severe glomerular basement membrane alterations and progressive glomerulosclerosis. J Am Soc Nephrol 17:1334–1344

    Article  PubMed  CAS  Google Scholar 

  63. Lehtonen S (2008) Connecting the interpodocyte slit diaphragm and actin dynamics: emerging role for the nephrin signaling complex. Kidney Int 73:903–905

    Article  PubMed  CAS  Google Scholar 

  64. Kao WH, Klag MJ, Meoni LA, Reich D, Berthier-Schaad Y, Li M, Coresh J, Patterson N, Tandon A, Powe NR, Fink NE, Sadler JH, Weir MR, Abboud HE, Adler SG, Divers J, Iyengar SK, Freedman BI, Kimmel PL, Knowler WC, Kohn OF, Kramp K, Leehey DJ, Nicholas SB, Pahl MV, Schelling JR, Sedor JR, Thornley-Brown D, Winkler CA, Smith MW, Parekh RS (2008) MYH9 is associated with nondiabetic end-stage renal disease in African Americans. Nat Genet 40:1185–1192

    Article  PubMed  CAS  Google Scholar 

  65. Kopp JB, Smith MW, Nelson GW, Johnson RC, Freedman BI, Bowden DW, Oleksyk T, McKenzie LM, Kajiyama H, Ahuja TS, Berns JS, Briggs W, Cho ME, Dart RA, Kimmel PL, Korbet SM, Michel DM, Mokrzycki MH, Schelling JR, Simon E, Trachtman H, Vlahov D, Winkler CA (2008) MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis. Nat Genet 40:1175–1184

    Article  PubMed  CAS  Google Scholar 

  66. Heath KE, Campos-Barros A, Toren A, Rozenfeld-Granot G, Carlsson LE, Savige J, Denison JC, Gregory MC, White JG, Barker DF, Greinacher A, Epstein CJ, Glucksman MJ, Martignetti JA (2001) Nonmuscle myosin heavy chain IIA mutations define a spectrum of autosomal dominant macrothrombocytopenias: May–Hegglin anomaly and Fechtner, Sebastian, Epstein, and Alport-like syndromes. Am J Hum Genet 69:1033–1045

    Article  PubMed  CAS  Google Scholar 

  67. Machuca E, Hummel A, Nevo F, Dantal J, Martinez F, Al-Sabban E, Baudouin V, Abel L, Grunfeld JP, Antignac C (2009) Clinical and epidemiological assessment of steroid-resistant nephrotic syndrome associated with the NPHS2 R229Q variant. Kidney Int 75:727–735

    Article  PubMed  CAS  Google Scholar 

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Acknowledgments

This work has been made possible through an International Society of Nephrology Fellowship awarded to E.M. and was supported by a grant from the Deutsche Forschungsgemeinschaft (SFB 423) to M.Z.

Conflict of interest statement

The authors declare that they have no conflict of interests.

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Authors and Affiliations

  1. Institute of Human Genetics, University Hospital Erlangen, University of Erlangen–Nuremberg, Schwabachanlage 10, 91054, Erlangen, Germany

    Martin Zenker

  2. Inserm, U574, Hôpital Necker-Enfants Malades, 75015, Paris, France

    Eduardo Machuca & Corinne Antignac

  3. Université Paris Descartes, Hôpital Necker-Enfants Malades, 75015, Paris, France

    Eduardo Machuca & Corinne Antignac

  4. Escuela de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile

    Eduardo Machuca

  5. Assistance Publique-Hôpitaux de Paris (AP-HP), Département de Génétique, Hôpital Necker-Enfants Malades, 75015, Paris, France

    Corinne Antignac

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Correspondence to Martin Zenker.

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Zenker, M., Machuca, E. & Antignac, C. Genetics of nephrotic syndrome: new insights into molecules acting at the glomerular filtration barrier. J Mol Med 87, 849–857 (2009). https://doi.org/10.1007/s00109-009-0505-9

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