CarrollL. Through the Looking-Glass, and What Alice Found There, London: Macmillan and Company, 1871.
2.
LewisEJSchwartzMM. Pathology of lupus nephritis. Lupus2005; 14: 31–38.
3.
Lupus nephritis. In: ChurgJBernsteinJGlassockR (eds). In: Renal disease: classification and atlas of glomerular diseases, New York: Igaku-Shoin, 1995, pp. 151–180.
4.
WeeningJJD’AgatiVDSchwartzMM. The classification of glomerulonephritis in systemic lupus erythematosus revisited. J Am Soc Nephrol2004; 15: 241–250.
5.
BeharaVYWhittierWLKorbetSMSchwartzMMMartensMLewisEJ. Pathogenetic features of severe segmental lupus nephritis. Nephrol Dial Transplant2010; 25: 153–159.
6.
HillGSDelahousseMNochyDBarietyJ. Class IV-S versus class IV-G lupus nephritis: Clinical and morphologic differences suggesting different pathogenesis. Kidney Int2005; 68: 2288–2297.
SchwartzMMKorbetSMKatzRSLewisEJ. Evidence of concurrent immunopathological mechanisms determining the pathology of severe lupus nephritis. Lupus2009; 18: 149–158.
10.
DooleyMClinical manifestations of lupus nephritis. In: LewisESchwartzMMKorbetSMChanT (eds). Lupus nephritis, New York, USA: Oxford University Press, 2011, pp. 1–34.
11.
HanTSSchwartzMMLewisEJ. Association of glomerular podocytopathy and nephrotic proteinuria in mesangial lupus nephritis. Lupus2006; 15: 71–75.
12.
KraftSWSchwartzMMKorbetSMLewisEJ. Glomerular podocytopathy in patients with systemic lupus erythematosus. J Am Soc Nephrol2005; 16: 175–179.
13.
LewisEJLupus podocytopathy. In: LewisEJSchwartzMMKorbetSMChanT (eds). Lupus nephritis, New York, USA: Oxford University Press, 2011, pp. 199–210.
14.
WangYYuFSongDWangSXZhaoMH. Podocyte involvement in lupus nephritis based on the 2003 ISN/RPS system: A large cohort study from a single centre. Rheumatology (Oxford)2014; 53: 1235–1244.
15.
DesaiNCimbalukDLewisEJWhittierWL. Proteinuria in membranous lupus nephritis: The pathology is in the podocyte. Lupus2013; 22: 461–468.
WeiCMollerCCAltintasMM. Modification of kidney barrier function by the urokinase receptor. Nat Med2008; 14: 55–63.
18.
WeiCElHSLiJ. Circulating urokinase receptor as a cause of focal segmental glomerulosclerosis. Nat Med2011; 17: 952–960.
19.
AlachkarNWeiCArendLJ. Podocyte effacement closely links to suPAR levels at time of posttransplantation focal segmental glomerulosclerosis occurrence and improves with therapy. Transplantation2013; 96: 649–656.
20.
ZhangBShiWMaJ. The calcineurin-NFAT pathway allows for urokinase receptor-mediated beta3 integrin signaling to cause podocyte injury. J Mol Med (Berl)2012; 90: 1407–1420.
21.
Maile LA, Busby WH, Gollahon KA, et al. Blocking ligand occupancy of the alphaVbeta3 integrin inhibits the development of nephropathy in diabetic pigs. Endocrinology. 155: 4665–4675.
22.
MoysiadisDKPerysinakiGSBertsiasG. Early treatment with glucocorticoids or cyclophosphamide retains the slit diaphragm proteins nephrin and podocin in experimental lupus nephritis. Lupus2012; 21: 1196–1207.
23.
PerysinakiGSMoysiadisDKBertsiasG. Podocyte main slit diaphragm proteins, nephrin and podocin, are affected at early stages of lupus nephritis and correlate with disease histology. Lupus2011; 20: 781–791.
24.
DelvilleMSigdelTKWeiC. A circulating antibody panel for pretransplant prediction of FSGS recurrence after kidney transplantation. Sci Transl Med2014; 6: 256ra136–256ra136.
25.
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. 26: 133–147.