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Gene Review

IGAN1  -  IgA nephropathy

Homo sapiens

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Disease relevance of IGAN

  • We have evaluated its role in both initiation and/or progression of primary immunoglobulin A (IgA) nephropathy (IGAN) in a case-control study involving a prospective cohort of 318 IGAN patients and a matched group of 294 controls [1].
  • The aim of this open prospective trial was to evaluate the efficacy and safety of low-dose immunoglobulin therapy in moderate IGAN and HSP with permanent proteinuria [2].
  • IGAN patients with macroscopical hematuria (macro-H) differ from the other IGAN patients in 9 aspects: history, HLA-DR, Gm-allotypes, actuarial kidney survival, initial creatinine clearance, initial proteinuria, initial microhematuria, age at presentation and light microscopy of the renal biopsy [3].
  • We review the literature on the association of IGAN with psoriasis and discuss the likely pathogenetic linkage [4].
  • Fourteen patients with moderate IGAN [idiopathic IGAN: n = 11; chronic idiopathic HSP: n = 3] and permanent albuminuria were treated with polyvalent IMIG (16.5%) for 9 months (0.35 ml/kg once a week for 1 month, followed by 0.35 ml/kg every 15 days for a further 8 months) [2].

Psychiatry related information on IGAN


High impact information on IGAN


Chemical compound and disease context of IGAN


Biological context of IGAN

  • The d32-CCR5 polymorphism played a significant role in the progression of primary IGAN, with the nl/nl genotype being an independent protective factor for late progression towards ESRF/dialysis [1].
  • The d32 allele frequency was not different in patients (11.0%) vs controls (8.3%), indicating no significant influence on IGAN initiation [1].
  • IGAN patients had the highest graft survival rate [16].
  • No single HLA haplotype or antigen was found in all the patients with IgA nephropathy [17].
  • In addition, dysfunction of the ASGR or altered N-linked glycosylation, but not O-glycans, that affects recognition by this receptor may account for the elevated serum IgA seen in liver disease and IgA nephropathy [18].

Anatomical context of IGAN


Associations of IGAN with chemical compounds

  • Circulating immune complexes (CIC) containing IgA and C3 were elevated in 48% of IgA nephropathy patients; IgA1 was the predominant subclass [24].
  • Role of the deletion of polymorphism of the angiotensin converting enzyme gene in the progression and therapeutic responsiveness of IgA nephropathy [25].
  • In this study, among patients with biopsy-proven IgA nephropathy, 53 patients in whom creatinine clearance had been monitored over 5 yr were recruited for study [25].
  • Circulating immune complexes in IgA nephropathy consist of IgA1 with galactose-deficient hinge region and antiglycan antibodies [26].
  • INTERPRETATION: A 6-month course of steroid treatment protected against deterioration in renal function in IgA nephropathy with no notable adverse effects during follow-up [27].

Physical interactions of IGAN

  • We report here an additional significant association between IgA nephropathy and an SNP located in the gene encoding immunoglobulin micro-binding protein 2 (IGHMBP2) at chromosome 11q13.2-q13 [28].
  • However, studying the functional aberration in the human IgA, CD89, and CD71 complex formation in pathogenesis of IgA nephropathy is hard [29].
  • The presence of fibronectin in the circulating aggregates may play an important role in the preferential deposition of nephritogenic IgA-containing immune complexes in the mesangium of patients with IgA nephropathy [30].
  • We studied serum IgA as antibodies to dietary antigens (Ag), as lectin-binding molecules, and as conglutinin-binding immune complexes (IgAIC) in people from geographical areas in which IgA nephropathy (IgAGN) is particularly frequent [31].

Regulatory relationships of IGAN


Other interactions of IGAN


Analytical, diagnostic and therapeutic context of IGAN


  1. CC-chemokine receptor five gene polymorphism in primary IgA nephropathy: the 32 bp deletion allele is associated with late progression to end-stage renal failure with dialysis. Berthoux, F.C., Berthoux, P., Mariat, C., Thibaudin, L., Afiani, A., Linossier, M.T. Kidney Int. (2006) [Pubmed]
  2. Immunomodulation with low-dose immunoglobulins for moderate IgA nephropathy and Henoch-Schönlein purpura. Preliminary results of a prospective uncontrolled trial. Rostoker, G., Desvaux-Belghiti, D., Pilatte, Y., Petit-Phar, M., Philippon, C., Deforges, L., Terzidis, H., Intrator, L., André, C., Adnot, S. Nephron (1995) [Pubmed]
  3. Subentities within adult primary IgA-nephropathy. Beukhof, J.R., Ockhuizen, T., Halie, L.M., Westra, J., Beelen, J.M., Donker, A.J., Hoedemaeker, P.J., van der Hem, G.K. Clin. Nephrol. (1984) [Pubmed]
  4. IgA nephropathy in psoriasis. Ahuja, T.S., Funtanilla, M., de Groot, J.J., Velasco, A., Badalamenti, J., Wilson, S. American journal of nephrology. (1998) [Pubmed]
  5. Transplant IgA nephropathy: déjà vu again? Hogg, R. Kidney Int. (2001) [Pubmed]
  6. IgA nephropathy in alcohol abuse. An animal model. Smith, S.M., Yu, G.S., Tsukamoto, H. Lab. Invest. (1990) [Pubmed]
  7. IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22-23. Gharavi, A.G., Yan, Y., Scolari, F., Schena, F.P., Frasca, G.M., Ghiggeri, G.M., Cooper, K., Amoroso, A., Viola, B.F., Battini, G., Caridi, G., Canova, C., Farhi, A., Subramanian, V., Nelson-Williams, C., Woodford, S., Julian, B.A., Wyatt, R.J., Lifton, R.P. Nat. Genet. (2000) [Pubmed]
  8. Apoptosis and loss of renal tissue in polycystic kidney diseases. Woo, D. N. Engl. J. Med. (1995) [Pubmed]
  9. A controlled trial of fish oil in IgA nephropathy. Mayo Nephrology Collaborative Group. Donadio, J.V., Bergstralh, E.J., Offord, K.P., Spencer, D.C., Holley, K.E. N. Engl. J. Med. (1994) [Pubmed]
  10. Thin-basement-membrane nephropathy in adults with persistent hematuria. Tiebosch, A.T., Frederik, P.M., van Breda Vriesman, P.J., Mooy, J.M., van Rie, H., van de Wiel, T.W., Wolters, J., Zeppenfeldt, E. N. Engl. J. Med. (1989) [Pubmed]
  11. Association of angiotensinogen gene T235 variant with progression of immunoglobin A nephropathy in Caucasian patients. Pei, Y., Scholey, J., Thai, K., Suzuki, M., Cattran, D. J. Clin. Invest. (1997) [Pubmed]
  12. Mycophenolate mofetil for systemic vasculitis and IgA nephropathy. Nowack, R., Birck, R., van der Woude, F.J. Lancet (1997) [Pubmed]
  13. Controlled prospective trial of prednisolone and cytotoxics in progressive IgA nephropathy. Ballardie, F.W., Roberts, I.S. J. Am. Soc. Nephrol. (2002) [Pubmed]
  14. Expression of nephrin in pediatric kidney diseases. Patrakka, J., Ruotsalainen, V., Ketola, I., Holmberg, C., Heikinheimo, M., Tryggvason, K., Jalanko, H. J. Am. Soc. Nephrol. (2001) [Pubmed]
  15. Immunohistochemical evidence for an increased oxidative stress and carbonyl modification of proteins in diabetic glomerular lesions. Suzuki, D., Miyata, T., Saotome, N., Horie, K., Inagi, R., Yasuda, Y., Uchida, K., Izuhara, Y., Yagame, M., Sakai, H., Kurokawa, K. J. Am. Soc. Nephrol. (1999) [Pubmed]
  16. The long-term effect of primary disease on cadaver-donor renal transplant recipients. Hirata, M., Terasaki, P.I. Clinical transplants. (1993) [Pubmed]
  17. Familial IgA nephropathy. Evidence of an inherited mechanism of disease. Julian, B.A., Quiggins, P.A., Thompson, J.S., Woodford, S.Y., Gleason, K., Wyatt, R.J. N. Engl. J. Med. (1985) [Pubmed]
  18. The N-glycans determine the differential blood clearance and hepatic uptake of human immunoglobulin (Ig)A1 and IgA2 isotypes. Rifai, A., Fadden, K., Morrison, S.L., Chintalacharuvu, K.R. J. Exp. Med. (2000) [Pubmed]
  19. Identification of the transferrin receptor as a novel immunoglobulin (Ig)A1 receptor and its enhanced expression on mesangial cells in IgA nephropathy. Moura, I.C., Centelles, M.N., Arcos-Fajardo, M., Malheiros, D.M., Collawn, J.F., Cooper, M.D., Monteiro, R.C. J. Exp. Med. (2001) [Pubmed]
  20. Dysregulated LIGHT expression on T cells mediates intestinal inflammation and contributes to IgA nephropathy. Wang, J., Anders, R.A., Wu, Q., Peng, D., Cho, J.H., Sun, Y., Karaliukas, R., Kang, H.S., Turner, J.R., Fu, Y.X. J. Clin. Invest. (2004) [Pubmed]
  21. Endothelin-1 mRNA expression by peripheral blood monocytes in IgA nephropathy. Nakamura, T., Ebihara, I., Shirato, I., Fukui, M., Tomino, Y., Koide, H. Lancet (1993) [Pubmed]
  22. Autoimmunity in IgA nephropathy. Ballardie, F.W., Brenchley, P.E., Williams, S., O'Donoghue, D.J. Lancet (1988) [Pubmed]
  23. Patients with IgA nephropathy have circulating anti-basement membrane antibodies reacting with structures common to collagen I, II, and IV. Cederholm, B., Wieslander, J., Bygren, P., Heinegård, D. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  24. Circulating immune complexes and immunoglobulin A rheumatoid factor in patients with mesangial immunoglobulin A nephropathies. Czerkinsky, C., Koopman, W.J., Jackson, S., Collins, J.E., Crago, S.S., Schrohenloher, R.E., Julian, B.A., Galla, J.H., Mestecky, J. J. Clin. Invest. (1986) [Pubmed]
  25. Role of the deletion of polymorphism of the angiotensin converting enzyme gene in the progression and therapeutic responsiveness of IgA nephropathy. Yoshida, H., Mitarai, T., Kawamura, T., Kitajima, T., Miyazaki, Y., Nagasawa, R., Kawaguchi, Y., Kubo, H., Ichikawa, I., Sakai, O. J. Clin. Invest. (1995) [Pubmed]
  26. Circulating immune complexes in IgA nephropathy consist of IgA1 with galactose-deficient hinge region and antiglycan antibodies. Tomana, M., Novak, J., Julian, B.A., Matousovic, K., Konecny, K., Mestecky, J. J. Clin. Invest. (1999) [Pubmed]
  27. Corticosteroids in IgA nephropathy: a randomised controlled trial. Pozzi, C., Bolasco, P.G., Fogazzi, G.B., Andrulli, S., Altieri, P., Ponticelli, C., Locatelli, F. Lancet (1999) [Pubmed]
  28. Association of a single-nucleotide polymorphism in the immunoglobulin mu-binding protein 2 gene with immunoglobulin A nephropathy. Ohtsubo, S., Iida, A., Nitta, K., Tanaka, T., Yamada, R., Ohnishi, Y., Maeda, S., Tsunoda, T., Takei, T., Obara, W., Akiyama, F., Ito, K., Honda, K., Uchida, K., Tsuchiya, K., Yumura, W., Ujiie, T., Nagane, Y., Miyano, S., Suzuki, Y., Narita, I., Gejyo, F., Fujioka, T., Nihei, H., Nakamura, Y. J. Hum. Genet. (2005) [Pubmed]
  29. IgA-CD89 complex in IgA nephropathy: a study on molecular function. Wiwanitkit, V. Renal failure. (2006) [Pubmed]
  30. Serum IgA-fibronectin aggregates in patients with IgA nephropathy and Henoch-Schönlein purpura: diagnostic value and pathogenic implications. The Glomerular Disease Collaborative Network. Jennette, J.C., Wieslander, J., Tuttle, R., Falk, R.J. Am. J. Kidney Dis. (1991) [Pubmed]
  31. IgA antibodies to dietary antigens and lectin-binding IgA in sera from Italian, Australian, and Japanese IgA nephropathy patients. Coppo, R., Amore, A., Roccatello, D., Gianoglio, B., Molino, A., Piccoli, G., Clarkson, A.R., Woodroffe, A.J., Sakai, H., Tomino, Y. Am. J. Kidney Dis. (1991) [Pubmed]
  32. Expression of PDGF and PDGF receptor mRNA in glomeruli in IgA nephropathy. Terada, Y., Yamada, T., Nakashima, O., Sasaki, S., Nonoguchi, H., Tomita, K., Marumo, F. J. Am. Soc. Nephrol. (1997) [Pubmed]
  33. Increased IL-10 production by stimulated whole blood cultures in primary IgA nephropathy. De Fijter, J.W., Daha, M.R., Schroeijers, W.E., van Es, L.A., Van Kooten, C. Clin. Exp. Immunol. (1998) [Pubmed]
  34. Expression and function of fibronectin receptors on peripheral mononuclear cells in IgA nephropathy. Namie, S., Ozono, Y., Harada, T., Hara, K. Nephrol. Dial. Transplant. (1995) [Pubmed]
  35. Increased excretion of tumor necrosis factor alpha and interleukin 1 beta in urine from patients with IgA nephropathy and Schönlein-Henoch purpura. Wu, T.H., Wu, S.C., Huang, T.P., Yu, C.L., Tsai, C.Y. Nephron (1996) [Pubmed]
  36. Interleukin-13 inhibits cytokine secretion by blood monocytes from patients with IgA nephropathy. Matsumoto, K. Nephron (1997) [Pubmed]
  37. Influence of the endothelial nitric oxide synthase polymorphism on the progression of autosomal dominant polycystic kidney disease and IgA nephropathy. Merta, M., Reiterová, J., Tesar, V., Stekrová, J., Viklický, O. Renal failure. (2002) [Pubmed]
  38. Engagement of transferrin receptor by polymeric IgA1: evidence for a positive feedback loop involving increased receptor expression and mesangial cell proliferation in IgA nephropathy. Moura, I.C., Arcos-Fajardo, M., Gdoura, A., Leroy, V., Sadaka, C., Mahlaoui, N., Lepelletier, Y., Vrtovsnik, F., Haddad, E., Benhamou, M., Monteiro, R.C. J. Am. Soc. Nephrol. (2005) [Pubmed]
  39. Role for interactions between IP-10/Mig and CXCR3 in proliferative glomerulonephritis. Romagnani, P., Beltrame, C., Annunziato, F., Lasagni, L., Luconi, M., Galli, G., Cosmi, L., Maggi, E., Salvadori, M., Pupilli, C., Serio, M. J. Am. Soc. Nephrol. (1999) [Pubmed]
  40. Influence of the endothelial nitric oxide synthase polymorphism on the progression of autosomal dominant polycystic kidney disease and IgA nephropathy. Merta, M., Reiterová, J., Tesar, V., Stekrová, J., Viklický, O. Renal failure. (2002) [Pubmed]
  41. Selective deposition of immunoglobulin A1 in immunoglobulin A nephropathy, anaphylactoid purpura nephritis, and systemic lupus erythematosus. Conley, M.E., Cooper, M.D., Michael, A.F. J. Clin. Invest. (1980) [Pubmed]
  42. A mesangium-predominant gene, megsin, is a new serpin upregulated in IgA nephropathy. Miyata, T., Nangaku, M., Suzuki, D., Inagi, R., Uragami, K., Sakai, H., Okubo, K., Kurokawa, K. J. Clin. Invest. (1998) [Pubmed]
  43. Expression of platelet-derived growth factor receptors in normal and diseased human kidney. An immunohistochemistry and in situ hybridization study. Gesualdo, L., Di Paolo, S., Milani, S., Pinzani, M., Grappone, C., Ranieri, E., Pannarale, G., Schena, F.P. J. Clin. Invest. (1994) [Pubmed]
  44. Polymorphisms in angiotensin-converting-enzyme gene and progression of IgA nephropathy. Harden, P.N., Geddes, C., Rowe, P.A., McIlroy, J.H., Boulton-Jones, M., Rodger, R.S., Junor, B.J., Briggs, J.D., Connell, J.M., Jardine, A.G. Lancet (1995) [Pubmed]
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