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{{Minimal change disease}}
{{Minimal change disease}}
{{CMG}}; {{AE}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]
==Overview==
The exact pathogenesis of minimal change disease is not well-understood. T-cell dysfunction may mediate the pathogenesis of minimal change disease.<ref name="pmid4140273">{{cite journal| author=Shalhoub RJ| title=Pathogenesis of lipoid nephrosis: a disorder of T-cell function. | journal=Lancet | year= 1974 | volume= 2 | issue= 7880 | pages= 556-60 | pmid=4140273 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4140273  }} </ref>  Due to the remarkable observation of disease recurrence after transplantation and the resolution of renal disease in recipients of kidneys from donors with MCD, it has been suggested that the presence of circulatory compounds may be attributable to the disease.<ref name="pmid11518795">{{cite journal| author=Hoyer JR, Vernier RL, Najarian JS, Raij L, Simmons RL, Michael AF| title=Recurrence of idiopathic nephrotic syndrome after renal transplantation. 1972. | journal=J Am Soc Nephrol | year= 2001 | volume= 12 | issue= 9 | pages= 1994-2002 | pmid=11518795 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11518795  }} </ref><ref name="pmid376811">{{cite journal| author=Mauer SM, Hellerstein S, Cohn RA, Sibley RK, Vernier RL| title=Recurrence of steroid-responsive nephrotic syndrome after renal transplantation. | journal=J Pediatr | year= 1979 | volume= 95 | issue= 2 | pages= 261-4 | pmid=376811 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=376811  }} </ref><ref name="pmid7940721">{{cite journal| author=Ali AA, Wilson E, Moorhead JF, Amlot P, Abdulla A, Fernando ON et al.| title=Minimal-change glomerular nephritis. Normal kidneys in an abnormal environment? | journal=Transplantation | year= 1994 | volume= 58 | issue= 7 | pages= 849-52 | pmid=7940721 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7940721  }} </ref> Factors associated with the pathophysiology of minimal change disease include GPF from T cells,<ref name="pmid1787645">{{cite journal| author=Koyama A, Fujisaki M, Kobayashi M, Igarashi M, Narita M| title=A glomerular permeability factor produced by human T cell hybridomas. | journal=Kidney Int | year= 1991 | volume= 40 | issue= 3 | pages= 453-60 | pmid=1787645 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1787645  }} </ref><ref name="pmid1174637">{{cite journal| author=Lagrue G, Xheneumont S, Branellec A, Hirbec G, Weil B| title=A vascular permeability factor elaborated from lymphocytes. I. Demonstration in patients with nephrotic syndrome. | journal=Biomedicine | year= 1975 | volume= 23 | issue= 1 | pages= 37-40 | pmid=1174637 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1174637  }} </ref> hemopexin,<ref name="pmid10446937">{{cite journal| author=Cheung PK, Stulp B, Immenschuh S, Borghuis T, Baller JF, Bakker WW| title=Is 100KF an isoform of hemopexin? Immunochemical characterization of the vasoactive plasma factor 100KF. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 8 | pages= 1700-8 | pmid=10446937 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10446937  }} </ref><ref name="pmid18753258">{{cite journal| author=Lennon R, Singh A, Welsh GI, Coward RJ, Satchell S, Ni L et al.| title=Hemopexin induces nephrin-dependent reorganization of the actin cytoskeleton in podocytes. | journal=J Am Soc Nephrol | year= 2008 | volume= 19 | issue= 11 | pages= 2140-9 | pmid=18753258 | doi=10.1681/ASN.2007080940 | pmc=PMC2573012 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18753258  }} </ref> interleukin-(IL)13,<ref name="pmid17429054">{{cite journal| author=Lai KW, Wei CL, Tan LK, Tan PH, Chiang GS, Lee CG et al.| title=Overexpression of interleukin-13 induces minimal-change-like nephropathy in rats. | journal=J Am Soc Nephrol | year= 2007 | volume= 18 | issue= 5 | pages= 1476-85 | pmid=17429054 | doi=10.1681/ASN.2006070710 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17429054  }} </ref> cardiotrophin-like cytokine (CLC)-1,<ref name="pmid20966123">{{cite journal| author=McCarthy ET, Sharma M, Savin VJ| title=Circulating permeability factors in idiopathic nephrotic syndrome and focal segmental glomerulosclerosis. | journal=Clin J Am Soc Nephrol | year= 2010 | volume= 5 | issue= 11 | pages= 2115-21 | pmid=20966123 | doi=10.2215/CJN.03800609 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20966123  }} </ref>, and vascular endothelial growth factor (VEGF).<ref name="pmid22033283">{{cite journal| author=Parikh SM| title=Circulating mediators of focal segmental glomerulosclerosis: soluble urokinase plasminogen activator receptor in context. | journal=Am J Kidney Dis | year= 2012 | volume= 59 | issue= 3 | pages= 336-9 | pmid=22033283 | doi=10.1053/j.ajkd.2011.09.011 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22033283  }} </ref>
==Pathophysiology==
==Pathophysiology==
The exact pathogenesis of minimal change disease is not well-understood. Shalhoub and colleagues were the first to propose the T-cell dysfunction may mediate the pathogenesis of minimal change disease.<ref name="pmid4140273">{{cite journal| author=Shalhoub RJ| title=Pathogenesis of lipoid nephrosis: a disorder of T-cell function. | journal=Lancet | year= 1974 | volume= 2 | issue= 7880 | pages= 556-60 | pmid=4140273 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4140273  }} </ref> T cells seems to release pro-inflammatory cytokines that ultimately damage the polyanion barrier of the renal glomerulus and subsequent heavy proteinuria.<ref name="pmid17195422">{{cite journal| author=Saha TC, Singh H| title=Minimal change disease: a review. | journal=South Med J | year= 2006 | volume= 99 | issue= 11 | pages= 1264-70 | pmid=17195422 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17195422  }} </ref> When measured, CD8 lymphocytes increased and CD4 lymphocytes decreased in relapses of disease, emphasizing the role of an abnormal T cell response in MCD.<ref name="pmid1762295">{{cite journal| author=Fiser RT, Arnold WC, Charlton RK, Steele RW, Childress SH, Shirkey B| title=T-lymphocyte subsets in nephrotic syndrome. | journal=Kidney Int | year= 1991 | volume= 40 | issue= 5 | pages= 913-6 | pmid=1762295 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1762295  }} </ref>
The exact pathogenesis of minimal change disease is not well-understood. T-cell dysfunction may mediate the pathogenesis of minimal change disease.<ref name="pmid4140273">{{cite journal| author=Shalhoub RJ| title=Pathogenesis of lipoid nephrosis: a disorder of T-cell function. | journal=Lancet | year= 1974 | volume= 2 | issue= 7880 | pages= 556-60 | pmid=4140273 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4140273  }} </ref> T cells release pro-inflammatory cytokines that ultimately damage the polyanion barrier of the renal glomerulus and subsequently lead to heavy proteinuria.<ref name="pmid17195422">{{cite journal| author=Saha TC, Singh H| title=Minimal change disease: a review. | journal=South Med J | year= 2006 | volume= 99 | issue= 11 | pages= 1264-70 | pmid=17195422 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17195422  }} </ref> When measured, CD8 lymphocytes increased and CD4 lymphocytes decreased in relapses of disease, emphasizing the role of an abnormal T cell response in MCD.<ref name="pmid1762295">{{cite journal| author=Fiser RT, Arnold WC, Charlton RK, Steele RW, Childress SH, Shirkey B| title=T-lymphocyte subsets in nephrotic syndrome. | journal=Kidney Int | year= 1991 | volume= 40 | issue= 5 | pages= 913-6 | pmid=1762295 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1762295  }} </ref>


Due to the remarkable observation of disease recurrence after transplantation and the resolution of renal disease in recipients of kidneys from donors with MCD, researchers have proposed the presence of circulatory compounds that may be attributable to the disease.<ref name="pmid11518795">{{cite journal| author=Hoyer JR, Vernier RL, Najarian JS, Raij L, Simmons RL, Michael AF| title=Recurrence of idiopathic nephrotic syndrome after renal transplantation. 1972. | journal=J Am Soc Nephrol | year= 2001 | volume= 12 | issue= 9 | pages= 1994-2002 | pmid=11518795 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11518795  }} </ref><ref name="pmid376811">{{cite journal| author=Mauer SM, Hellerstein S, Cohn RA, Sibley RK, Vernier RL| title=Recurrence of steroid-responsive nephrotic syndrome after renal transplantation. | journal=J Pediatr | year= 1979 | volume= 95 | issue= 2 | pages= 261-4 | pmid=376811 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=376811  }} </ref><ref name="pmid7940721">{{cite journal| author=Ali AA, Wilson E, Moorhead JF, Amlot P, Abdulla A, Fernando ON et al.| title=Minimal-change glomerular nephritis. Normal kidneys in an abnormal environment? | journal=Transplantation | year= 1994 | volume= 58 | issue= 7 | pages= 849-52 | pmid=7940721 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7940721  }} </ref> In guinea pigs , glomerular permeability factor (GPF), a possible lymphokine that has an activity similar to TNF, is produced by T cells.<ref name="pmid1174637">{{cite journal| author=Lagrue G, Xheneumont S, Branellec A, Hirbec G, Weil B| title=A vascular permeability factor elaborated from lymphocytes. I. Demonstration in patients with nephrotic syndrome. | journal=Biomedicine | year= 1975 | volume= 23 | issue= 1 | pages= 37-40 | pmid=1174637 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1174637  }} </ref> Products secreted from T cell hybridomas from patients with MCD were contributory to the induction of significant proteinuria in rats.<ref name="pmid1787645">{{cite journal| author=Koyama A, Fujisaki M, Kobayashi M, Igarashi M, Narita M| title=A glomerular permeability factor produced by human T cell hybridomas. | journal=Kidney Int | year= 1991 | volume= 40 | issue= 3 | pages= 453-60 | pmid=1787645 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1787645  }} </ref> Hemopexin, a plasma glycoprotein and an acute phase reactant in humans, seems to enhance the role of GPF and further promote proteinuria through the glomerular basement membrane.<ref name="pmid10446937">{{cite journal| author=Cheung PK, Stulp B, Immenschuh S, Borghuis T, Baller JF, Bakker WW| title=Is 100KF an isoform of hemopexin? Immunochemical characterization of the vasoactive plasma factor 100KF. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 8 | pages= 1700-8 | pmid=10446937 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10446937  }} </ref>
Due to the remarkable observation of disease recurrence after transplantation and the resolution of renal disease in recipients of kidneys from donors with MCD, it has been suggested that the presence of circulatory compounds may be attributable to the disease.<ref name="pmid11518795">{{cite journal| author=Hoyer JR, Vernier RL, Najarian JS, Raij L, Simmons RL, Michael AF| title=Recurrence of idiopathic nephrotic syndrome after renal transplantation. 1972. | journal=J Am Soc Nephrol | year= 2001 | volume= 12 | issue= 9 | pages= 1994-2002 | pmid=11518795 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11518795  }} </ref><ref name="pmid376811">{{cite journal| author=Mauer SM, Hellerstein S, Cohn RA, Sibley RK, Vernier RL| title=Recurrence of steroid-responsive nephrotic syndrome after renal transplantation. | journal=J Pediatr | year= 1979 | volume= 95 | issue= 2 | pages= 261-4 | pmid=376811 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=376811  }} </ref><ref name="pmid7940721">{{cite journal| author=Ali AA, Wilson E, Moorhead JF, Amlot P, Abdulla A, Fernando ON et al.| title=Minimal-change glomerular nephritis. Normal kidneys in an abnormal environment? | journal=Transplantation | year= 1994 | volume= 58 | issue= 7 | pages= 849-52 | pmid=7940721 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7940721  }} </ref> In guinea pigs , glomerular permeability factor (GPF), a possible lymphokine that has an activity similar to TNF, is produced by T cells.<ref name="pmid1174637">{{cite journal| author=Lagrue G, Xheneumont S, Branellec A, Hirbec G, Weil B| title=A vascular permeability factor elaborated from lymphocytes. I. Demonstration in patients with nephrotic syndrome. | journal=Biomedicine | year= 1975 | volume= 23 | issue= 1 | pages= 37-40 | pmid=1174637 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1174637  }} </ref> Products secreted from T cell hybridomas from patients with MCD were contributory to the induction of significant proteinuria in rats.<ref name="pmid1787645">{{cite journal| author=Koyama A, Fujisaki M, Kobayashi M, Igarashi M, Narita M| title=A glomerular permeability factor produced by human T cell hybridomas. | journal=Kidney Int | year= 1991 | volume= 40 | issue= 3 | pages= 453-60 | pmid=1787645 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1787645  }} </ref> Hemopexin, a plasma glycoprotein and an acute phase reactant in humans, seems to enhance the role of GPF and further promote proteinuria through the glomerular basement membrane.<ref name="pmid10446937">{{cite journal| author=Cheung PK, Stulp B, Immenschuh S, Borghuis T, Baller JF, Bakker WW| title=Is 100KF an isoform of hemopexin? Immunochemical characterization of the vasoactive plasma factor 100KF. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 8 | pages= 1700-8 | pmid=10446937 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10446937  }} </ref>




Revision as of 15:32, 5 April 2015

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, Serge Korjian

Overview

The exact pathogenesis of minimal change disease is not well-understood. T-cell dysfunction may mediate the pathogenesis of minimal change disease.[1] Due to the remarkable observation of disease recurrence after transplantation and the resolution of renal disease in recipients of kidneys from donors with MCD, it has been suggested that the presence of circulatory compounds may be attributable to the disease.[2][3][4] Factors associated with the pathophysiology of minimal change disease include GPF from T cells,[5][6] hemopexin,[7][8] interleukin-(IL)13,[9] cardiotrophin-like cytokine (CLC)-1,[10], and vascular endothelial growth factor (VEGF).[11]

Pathophysiology

The exact pathogenesis of minimal change disease is not well-understood. T-cell dysfunction may mediate the pathogenesis of minimal change disease.[1] T cells release pro-inflammatory cytokines that ultimately damage the polyanion barrier of the renal glomerulus and subsequently lead to heavy proteinuria.[12] When measured, CD8 lymphocytes increased and CD4 lymphocytes decreased in relapses of disease, emphasizing the role of an abnormal T cell response in MCD.[13]

Due to the remarkable observation of disease recurrence after transplantation and the resolution of renal disease in recipients of kidneys from donors with MCD, it has been suggested that the presence of circulatory compounds may be attributable to the disease.[2][3][4] In guinea pigs , glomerular permeability factor (GPF), a possible lymphokine that has an activity similar to TNF, is produced by T cells.[6] Products secreted from T cell hybridomas from patients with MCD were contributory to the induction of significant proteinuria in rats.[5] Hemopexin, a plasma glycoprotein and an acute phase reactant in humans, seems to enhance the role of GPF and further promote proteinuria through the glomerular basement membrane.[7]


The following is a list that shows factors that have been shown to be associated with the pathogenesis of MCD:

  • GPF from T cells[5][6]
  • Hemopexin[7][8]
  • Interleukin-(IL)13[9]
  • Cardiotrophin-like cytokine (CLC)-1[10]
  • Angiopoietin-like 4 (Angpl4)[10]
  • Soluble urokinase plasminogen activator receptor (suPAR)[14]
  • Vascular endothelial growth factor (VEGF)[11]
  • Heparinase[11]
  • Sialidase[11]
  • C-mip intracellular protein[11]
  • CD80[11]
  • Beta-3 integrin 1[11]


In MCD, albumin excretion is significantly elevated with consequential hypoalbuminemia, increased protein catabolism, and hyperlipidemia that may be so extensive that cannot be compensated.[15][16] However, Carrie and colleagues showed that the fractional excretion of dextran was decreased in MCD patients, suggesting a probable decrease in the size of the glomerular pores.[15] A decrease in nephrin[17] and dystroglycan[18], two important podocyte proteins, and consequential slit-pore membrane obliteration between podocyte foot processes occur with effacement or fusion of the foot processes. However, recent data in 2004 showed that the degree of podocyte effacement does not seem to correlate with the degree of proteinuria.[19]

The loss of important proteins also includes immunoglobulin and complement proteins, such as factor B.[20] Concomitantly, serum concentrations of IgA and IgG were found to be low in patients with MCD.[21] In contrast, an elevation in serum concentration of IgM[21] and occasional glomerular IgM deposition[22] further underscore the hypothesis. This finding suggested that patients with MCD may have abnormal immunological capacity of immunoglobulin switching. The most likely etiology for switching defect may be a deficiency of thymic cell function.[21][12] In conclusion, patients with MCD are more susceptible to infections. Other significant components lost in urine include and thyroid-binding globulin[23], and iron and copper-binding transferrin.[24][25][26][27]

Loss of protein S and anti-thrombin III lead to excessive production of factors V and VIII, making minimal change disease a hypercoagulable state.[12]

References

  1. ↑ 1.0 1.1 Shalhoub RJ (1974). "Pathogenesis of lipoid nephrosis: a disorder of T-cell function". Lancet. 2 (7880): 556–60. PMID 4140273.
  2. ↑ 2.0 2.1 Hoyer JR, Vernier RL, Najarian JS, Raij L, Simmons RL, Michael AF (2001). "Recurrence of idiopathic nephrotic syndrome after renal transplantation. 1972". J Am Soc Nephrol. 12 (9): 1994–2002. PMID 11518795.
  3. ↑ 3.0 3.1 Mauer SM, Hellerstein S, Cohn RA, Sibley RK, Vernier RL (1979). "Recurrence of steroid-responsive nephrotic syndrome after renal transplantation". J Pediatr. 95 (2): 261–4. PMID 376811.
  4. ↑ 4.0 4.1 Ali AA, Wilson E, Moorhead JF, Amlot P, Abdulla A, Fernando ON; et al. (1994). "Minimal-change glomerular nephritis. Normal kidneys in an abnormal environment?". Transplantation. 58 (7): 849–52. PMID 7940721.
  5. ↑ 5.0 5.1 5.2 Koyama A, Fujisaki M, Kobayashi M, Igarashi M, Narita M (1991). "A glomerular permeability factor produced by human T cell hybridomas". Kidney Int. 40 (3): 453–60. PMID 1787645.
  6. ↑ 6.0 6.1 6.2 Lagrue G, Xheneumont S, Branellec A, Hirbec G, Weil B (1975). "A vascular permeability factor elaborated from lymphocytes. I. Demonstration in patients with nephrotic syndrome". Biomedicine. 23 (1): 37–40. PMID 1174637.
  7. ↑ 7.0 7.1 7.2 Cheung PK, Stulp B, Immenschuh S, Borghuis T, Baller JF, Bakker WW (1999). "Is 100KF an isoform of hemopexin? Immunochemical characterization of the vasoactive plasma factor 100KF". J Am Soc Nephrol. 10 (8): 1700–8. PMID 10446937.
  8. ↑ 8.0 8.1 Lennon R, Singh A, Welsh GI, Coward RJ, Satchell S, Ni L; et al. (2008). "Hemopexin induces nephrin-dependent reorganization of the actin cytoskeleton in podocytes". J Am Soc Nephrol. 19 (11): 2140–9. doi:10.1681/ASN.2007080940. PMC 2573012. PMID 18753258.
  9. ↑ 9.0 9.1 Lai KW, Wei CL, Tan LK, Tan PH, Chiang GS, Lee CG; et al. (2007). "Overexpression of interleukin-13 induces minimal-change-like nephropathy in rats". J Am Soc Nephrol. 18 (5): 1476–85. doi:10.1681/ASN.2006070710. PMID 17429054.
  10. ↑ 10.0 10.1 10.2 McCarthy ET, Sharma M, Savin VJ (2010). "Circulating permeability factors in idiopathic nephrotic syndrome and focal segmental glomerulosclerosis". Clin J Am Soc Nephrol. 5 (11): 2115–21. doi:10.2215/CJN.03800609. PMID 20966123.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 Parikh SM (2012). "Circulating mediators of focal segmental glomerulosclerosis: soluble urokinase plasminogen activator receptor in context". Am J Kidney Dis. 59 (3): 336–9. doi:10.1053/j.ajkd.2011.09.011. PMID 22033283.
  12. ↑ 12.0 12.1 12.2 Saha TC, Singh H (2006). "Minimal change disease: a review". South Med J. 99 (11): 1264–70. PMID 17195422.
  13. ↑ Fiser RT, Arnold WC, Charlton RK, Steele RW, Childress SH, Shirkey B (1991). "T-lymphocyte subsets in nephrotic syndrome". Kidney Int. 40 (5): 913–6. PMID 1762295.
  14. ↑ Wei C, El Hindi S, Li J, Fornoni A, Goes N, Sageshima J; et al. (2011). "Circulating urokinase receptor as a cause of focal segmental glomerulosclerosis". Nat Med. 17 (8): 952–60. doi:10.1038/nm.2411. PMID 21804539.
  15. ↑ 15.0 15.1 Carrie BJ, Salyer WR, Myers BD (1981). "Minimal change nephropathy: an electrochemical disorder of the glomerular membrane". Am J Med. 70 (2): 262–8. PMID 6162382.
  16. ↑ GITLIN D, CORNWELL DG, NAKASATO D, ONCLEY JL, HUGHES WL, JANEWAY CA (1958). "Studies on the metabolism of plasma proteins in the nephrotic syndrome. II. The lipoproteins". J Clin Invest. 37 (2): 172–84. doi:10.1172/JCI103596. PMC 293074. PMID 13513748.
  17. ↑ Wernerson A, Dunér F, Pettersson E, Widholm SM, Berg U, Ruotsalainen V; et al. (2003). "Altered ultrastructural distribution of nephrin in minimal change nephrotic syndrome". Nephrol Dial Transplant. 18 (1): 70–6. PMID 12480962.
  18. ↑ Regele HM, Fillipovic E, Langer B, Poczewki H, Kraxberger I, Bittner RE; et al. (2000). "Glomerular expression of dystroglycans is reduced in minimal change nephrosis but not in focal segmental glomerulosclerosis". J Am Soc Nephrol. 11 (3): 403–12. PMID 10703664.
  19. ↑ van den Berg JG, van den Bergh Weerman MA, Assmann KJ, Weening JJ, Florquin S (2004). "Podocyte foot process effacement is not correlated with the level of proteinuria in human glomerulopathies". Kidney Int. 66 (5): 1901–6. doi:10.1111/j.1523-1755.2004.00964.x. PMID 15496161.
  20. ↑ Spika JS, Halsey NA, Fish AJ, Lum GM, Lauer BA, Schiffman G; et al. (1982). "Serum antibody response to pneumococcal vaccine in children with nephrotic syndrome". Pediatrics. 69 (2): 219–23. PMID 7058096.
  21. ↑ 21.0 21.1 21.2 Giangiacomo J, Cleary TG, Cole BR, Hoffsten P, Robson AM (1975). "Serum immunoglobulins in the nephrotic syndrome. A possible cause of minimal-change nephrotic syndrome". N Engl J Med. 293 (1): 8–12. doi:10.1056/NEJM197507032930103. PMID 1079322.
  22. ↑ Waldherr R, Gubler MC, Levy M, Broyer M, Habib R (1978). "The significance of pure diffuse mesangial proliferation in idiopathic nephrotic syndrome". Clin Nephrol. 10 (5): 171–9. PMID 365403.
  23. ↑ Afrasiabi MA, Vaziri ND, Gwinup G, Mays DM, Barton CH, Ness RL; et al. (1979). "Thyroid function studies in the nephrotic syndrome". Ann Intern Med. 90 (3): 335–8. PMID 106751.
  24. ↑ CARTWRIGHT GE, GUBLER CJ, WINTROBE MM (1954). "Studies on copper metabolism. XI. Copper and iron metabolism in the nephrotic syndrome". J Clin Invest. 33 (4): 685–98. doi:10.1172/JCI102939. PMC 1087284. PMID 13152208.
  25. ↑ RIFKIND D, KRAVETZ HM, KNIGHT V, SCHADE AL (1961). "Urinary excretion of iron-binding protein in the nephrotic syndrome". N Engl J Med. 265: 115–8. doi:10.1056/NEJM196107202650303. PMID 13741582.
  26. ↑ Ellis D (1977). "Anemia in the course of the nephrotic syndrome secondary to transferrin depletion". J Pediatr. 90 (6): 953–5. PMID 859066.
  27. ↑ Stec J, Podracká L, Pavkovceková O, Kollár J (1990). "Zinc and copper metabolism in nephrotic syndrome". Nephron. 56 (2): 186–7. PMID 2243574.

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