1.- Altarescu G, Elstein D. Fabry disease in an oligosymptomatic male. IMAJ, 2011, 13: 191–192

2.- Tondel C, Bostad L, Kampevold K, Egil B, Houge G, Svartad E. Agalsidase benefits renal histology in young patients with Fabry Disease. J Am Soc Nephrol. 2013; 25: 137-148

3.- Warnock DG. Fabry Disease. Renal aspects of Fabry Disease. Nephrology. 2003; 1(6):802-807

4.- Politei JM, Cabello JF, Villalobos J, Valadez G, Loaeza A, Linares A, Martins AM. Enfermedad de Fabry: Nuevos conceptos en su historia natural, evolución y tratamiento, en relación a los hallazgos del Registro Fabry. Nefrologia, Diálisis y Transplante. 2009; 29(4):145-152

5.- Villalobos J, Politei JM, Martins AM, Cabrera G, Amartino H, Lemay R, Ospina S. Fabry Disease in Latin America: data from the Fabry Registry. JIMD Rep. 2013; 8: 91-99

6.- Keating GM. Simpson D. Agalsidase Beta: a review of its use in the management of Fabry disease. Drugs. 2007; 67 (3): 435-455

7.- Montero N, Soler MJ, Pascual MJ, Barrios C, Márquez E, Rodríguez E, Berrada A, et al. Correlación entre el cociente proteína/creatinina en orina esporádica y las proteínas en orina de 24 horas. Nefrologia. 2012; 32(4):494-501

8.- Carrol M, Temte J. Proteinuria in Adults: A Diagnostic Approach. Am FamPhysician. 2000; 62 (6):1333-1341

9.- Gubler MC, Lenoir G, Grünfeld JP, Ulmann A, Droz D, Habib R. Early renal changes in hemizygous and heterozygous patients with Fabry´s disease. KidneyInt. 1978; 13:223-235

10.- Torra R, Ballarín J. La enfermedad de Fabry. Nefrologia. 2003; 23 (1):84-89

11.- Babelova A, Jausen F, Sander K, Löhn M, Schäfer L, Fork C, Ruetten H , et al. Activation of Rac-1 y RhoA contributes to podocytes injury in chronic kidney disease. PLoS ONE. 2013; 8(11): e80328

12.- Ortiz A, Marrón B, Ramos A. El destino de los podocitos en las nefropatías proteinuricas. Nefrologia. 2002; 23 (5):425-430

13.- Li Y, Kang YS, Dai C, Kiss LP, Wen X, Liu Y. Epithelial to mesenchymal transition is a potential leading to podocytes dysfunction and proteinuria. Am J Med. 2008; 172(2): 299-308

14.- Doné SC,Takemoto M,He L ,Sun Y ,Hultenby K ,Betsholtz C,Tryggvason K. Nephrin is involved in podocyte maturation but not survival during glomerular development. KidneyInt. 2008; 73:697–704

15.- Reidy K, Susztak K. Epithelial-Mesenchymal transition and podocyte loss in diabetic kidney disease. AmJKidneyDis. 2009; 54 (4): 590-599

16.- Chen S, Meng XF, Zhang C. Role of NADPH oxidase-mediated reactive oxygen species in podocyte injury. BiomedRes Int. 2013; ID 839761, 7 pages http://dx.doi.org/10.1155/2013/839761

17.- Suzuki T, Matsusaka T, Nakayama M, Asano T, Watnabe T, Ichicawa I, Nagata M. Genetic podocyte linage reveals progressive podocytopenia with parietal cell hyperplasia in a murine model of cellular/collapsing focal segmental glomerulosclerosis. J Path. 2009;174, (5):1675-1682.

18.- Barisoni L, Kriz W, Mundel P, D´Agasti V. The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis ans HIV-associated nephropathy. J Am Soc Nephrol 1999; 10:51-61

19.- Pippin JW, Durvasula R, Petermann A, Hiromura K, Couser WG, Shankland SJ,. DNA damage is a novel response to sublytic complement C5b-9-induced injury in podocytes. J Clin Invest 2003; 111:877-885.

20.-Biancini GB, Vanzin CS, Rodriguez DB, Deon M, Ribas GS, Barschak AG, Manfredini V, et al. Globotriaosylceramide is correlated with oxidative stress and inflammation in Fabry patients treated with enzyme replacement therapy. Biochim BiophysActa. 2012;1822: 226-232

21.- Brignull L M, Czimmerer Z, Saidi H, Daniel B, Villela I, Bartlett N, Johnston S, Meira L, Nagy L, Nohturfft. Reprogramming of lysosomal gene expression by interleukin-4 and Stat 6 . BMC Genomics 2013; 14:853

22.- Lu Y, Hao Bai-Xia, Graeff R, Wong CWM, Wu T, Yue J. Two pore channel 2 (TPC2) inhibits autophagosomal-lysosomal fusion by alkalinizing lysosomal pH. J Bio Chem 2013; 288 (33): 24247–24263.

23.- Liebau MC., Braun F, Hopker K, Weitbrecht C, Bartels V, Muller RU¨ ller, Brodesser S, et al. Dysregulated autophagy contributes to podocyte damage in Fabry’s Disease PLoS ONE 2013;8(5): e63506

24.- Vernon PJ. and Tang D. Eat-Me: Autophagy, Phagocytosis, and Reactive Oxygen Species Signaling.Antioxid Redox Signal.2013;18(6):677-91

25.- Shen JS, Meng XL, Moore DF, Quirk JM, Shayman JA, Schiffmann R, Kaneski CR. Globotriaosylceramide induces oxidative stress and up-regulates cell adhesion molecule expression in Fabry disease endotelial cells. Mol Genet Metab. 2008; 95(3):163–168, doi:10.1016/j.ymgme.06.016.

26.- Sanchez-Niño M, Sans A, Carrasco S, Saleem M, Mathieson P, Valdivielso J, et al. Globotriaosylsphingosine actions on human glomerular podocytes: implications for Fabry nephropathy. Nephrol. Dial. Transplant. (2011) 26 (6): 1797-1802.

27.- Prabakaran T, Nielsen R, Larsen JV, Sørensen SS, Feldt-Rasmussen U, Saleem MA, Petersen CM et al. Receptor-mediated endocytosis of α-galactosidase A in human podocytes in Fabry disease. PLoS ONE.2011; 6(9):e25065

28.- Zhang A, Huang S. Progress in Pathogenesis of Proteinuria. Int J Nephrol 2012; 2012 Article ID 314251, 14 pages, http://dx.doi.org/10.1155/2012/314251