CoChat
Sign Up
Cited by 2Renal Diseases and GlomerulopathiesVasculitis and related conditionsChronic Kidney Disease and Diabetes

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

IgA nephropathy: an overview of the disease, its pathophysiology, and involvement of the gut-kidney axis

Open access
Cheung, Chee Kay, Mariani, Laura H.·2026·Kidney International Supplements
DOI 10.1016/j.kisu.2026.01.003PMC PMC13387150
Open this paper in CoChat — free account

Abstract

IgA nephropathy (IgAN) is the most common primary glomerular disease worldwide. Its incidence and prevalence vary widely, with estimates of annual incidence ranging from 0.06 to 10.5 per 100,000 per year in adults and children. IgAN represents an important cause of progressive kidney disease, leading to kidney failure in a large proportion of patients, and is associated with a wide spectrum of clinical symptoms, which negatively impact quality of life. Although the consequences of IgAN manifest in the kidney, multiple lines of evidence support a major role for the gut in the pathogenesis of IgAN, including genome-wide association studies that identify risk loci for IgAN that encode genes related to mucosal immunity, maintenance of the intestinal epithelial barrier, and inflammatory bowel disease. Further insights into the underlying disease pathogenesis have led to the development of a multihit model comprising 4 sequential "hits": (i) increased levels of galactose-deficient IgA1 in the systemic circulation, (ii) followed by binding of specific autoantibodies directed against galactose-deficient IgA1, which (iii) form pathogenic IgA-containing immune complexes that (iv) deposit within the glomerular mesangium of the kidney, triggering inflammation, damage, and progressive decline in kidney function. The purpose of this article is to provide an overview of IgAN, examining its epidemiology and clinical features, and the mechanisms underlying its pathophysiology.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.kisu.2026.01.003

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 131

  1. Berger, 1968, [Intercapillary deposits of IgA-IgG], J Urol Nephrol (Paris), 74, 694
  2. McGrogan, 2011, The incidence of primary glomerulonephritis worldwide: a systematic review of the literature, Nephrol Dial Transplant, 26, 414, 10.1093/ndt/gfq665 · DOI
  3. Cheung, 2025, The pathogenesis of IgA nephropathy and implications for treatment, Nat Rev Nephrol, 21, 9, 10.1038/s41581-024-00885-3 · DOI · Paper page
  4. Pitcher, 2023, Long-term outcomes in IgA nephropathy, Clin J Am Soc Nephrol, 18, 727, 10.2215/CJN.0000000000000135 · DOI
  5. Kiryluk, 2023, Global incidence of IgA nephropathy by race and ethnicity: a systematic review, Kidney360, 4, 1112, 10.34067/KID.0000000000000165 · DOI
  6. Willey, 2023, The incidence and prevalence of IgA nephropathy in Europe, Nephrol Dial Transplant, 38, 2340, 10.1093/ndt/gfad082 · DOI
  7. Shibano, 2016, Epidemiological survey and clinical investigation of pediatric IgA nephropathy, Clin Exp Nephrol, 20, 111, 10.1007/s10157-015-1129-8 · DOI
  8. Schena, 2018, Epidemiology of IgA nephropathy: a global perspective, Semin Nephrol, 38, 435, 10.1016/j.semnephrol.2018.05.013 · DOI
  9. Lee, 2023, Ethnicity and IgA nephropathy: worldwide differences in epidemiology, timing of diagnosis, clinical manifestations, management and prognosis, Clin Kidney J, 16, ii1, 10.1093/ckj/sfad199 · DOI
  10. Kiryluk, 2012, Geographic differences in genetic susceptibility to IgA nephropathy: GWAS replication study and geospatial risk analysis, PLoS Genet, 8, 10.1371/journal.pgen.1002765 · DOI
  11. Yeo, 2019, Is immunoglobulin A nephropathy different in different ethnic populations?, Nephrology (Carlton), 24, 885, 10.1111/nep.13592 · DOI
  12. Kiryluk, 2023, Genome-wide association analyses define pathogenic signaling pathways and prioritize drug targets for IgA nephropathy, Nat Genet, 55, 1091, 10.1038/s41588-023-01422-x · DOI
  13. Pattrapornpisut, 2021, IgA nephropathy: core curriculum 2021, Am J Kidney Dis, 78, 429, 10.1053/j.ajkd.2021.01.024 · DOI
  14. Selvaskandan, 2020, Monitoring immune responses in IgA nephropathy: biomarkers to guide management, Front Immunol, 11, 10.3389/fimmu.2020.572754 · DOI
  15. Cheung, 2024, The use of albuminuria or proteinuria for risk prediction in IgAN, Nephrol Dial Transplant, 40, 1, 10.1093/ndt/gfae151 · DOI
  16. 2026, Jain K, Rizk DV. The expanding role of biomarkers in the management of IgA nephropathy, Kidney Int Suppl, 15, 37, 10.1016/j.kisu.2026.01.004 · DOI · Paper page
  17. Barbour, 2016, The MEST score provides earlier risk prediction in lgA nephropathy, Kidney Int, 89, 167, 10.1038/ki.2015.322 · DOI
  18. Cattran, 2009, The Oxford classification of IgA nephropathy: rationale, clinicopathological correlations, and classification, Kidney Int, 76, 534, 10.1038/ki.2009.243 · DOI
  19. Roberts, 2009, The Oxford classification of IgA nephropathy: pathology definitions, correlations, and reproducibility, Kidney Int, 76, 546, 10.1038/ki.2009.168 · DOI
  20. Trimarchi, 2017, Oxford classification of IgA nephropathy 2016: an update from the IgA Nephropathy Classification Working Group, Kidney Int, 91, 1014, 10.1016/j.kint.2017.02.003 · DOI
  21. Haas, 2020, Consensus definitions for glomerular lesions by light and electron microscopy: recommendations from a working group of the Renal Pathology Society, Kidney Int, 98, 1120, 10.1016/j.kint.2020.08.006 · DOI
  22. 2021, KDIGO 2021 clinical practice guideline for the management of glomerular diseases, Kidney Int, 100, S1
  23. Suzuki, 2021, The phenotypic difference of IgA nephropathy and its race/gender-dependent molecular mechanisms, Kidney360, 2, 1339, 10.34067/KID.0002972021 · DOI
  24. Fraser, 2016, Chronic kidney disease: identification and management in primary care, Pragmat Obs Res, 7, 21
  25. Kwon, 2021, A systematic literature review of the epidemiology, health-related quality of life impact, and economic burden of immunoglobulin A nephropathy, J Health Econ Outcomes Res, 8, 36, 10.36469/jheor.2021.26129 · DOI
  26. Selewski, 2018, Clinical characteristics and treatment patterns of children and adults with IgA nephropathy or IgA vasculitis: findings from the CureGN study, Kidney Int Rep, 3, 1373, 10.1016/j.ekir.2018.07.021 · DOI
  27. Le, 2012, Long-term renal survival and related risk factors in patients with IgA nephropathy: results from a cohort of 1155 cases in a Chinese adult population, Nephrol Dial Transplant, 27, 1479, 10.1093/ndt/gfr527 · DOI
  28. Coppo, 2014, Validation of the Oxford classification of IgA nephropathy in cohorts with different presentations and treatments, Kidney Int, 86, 828, 10.1038/ki.2014.63 · DOI
  29. Faucon, 2025, Albuminuria predicts kidney events in IgA nephropathy, Nephrol Dial Transplant, 40, 465, 10.1093/ndt/gfae085 · DOI
  30. Hastings, 2018, Life expectancy for patients from the southeastern United States with IgA nephropathy, Kidney Int Rep, 3, 99, 10.1016/j.ekir.2017.08.008 · DOI
  31. Jarrick, 2019, Mortality in IgA nephropathy: a nationwide population-based cohort study, J Am Soc Nephrol, 30, 8660, 10.1681/ASN.2018101017 · DOI
  32. Barbour, 2022, Application of the International IgA Nephropathy Prediction Tool one or two years post-biopsy, Kidney Int, 102, 160, 10.1016/j.kint.2022.02.042 · DOI
  33. Barbour, 2019, Evaluating a new international risk-prediction tool in IgA nephropathy, JAMA Intern Med, 179, 942, 10.1001/jamainternmed.2019.0600 · DOI
  34. 2026, Canetta PA, Reich HN. Management of IgA nephropathy and the expanding role of immunomodulation, Kidney Int Suppl, 15, 14, 10.1016/j.kisu.2026.01.002 · DOI
  35. Peruzzi, 2024, IgAN across the age spectrum: the pediatric perspective, Semin Nephrol, 44, 10.1016/j.semnephrol.2025.151569 · DOI
  36. Su, 2024, Are children with IgA nephropathy different from adult patients?, Pediatr Nephrol, 39, 2403, 10.1007/s00467-024-06361-1 · DOI
  37. Sausukpaiboon, 2022, Clinical manifestations and pathological correlation of immunoglobulin A nephropathy in children, BMC Nephrol, 23, 366, 10.1186/s12882-022-03002-3 · DOI
  38. Rovin, 2025, KDIGO 2025 clinical practice guideline for the management of immunoglobulin A nephropathy (IgAN) and immunoglobulin A vasculitis (IgAV), Kidney Int, 108, S1, 10.1016/j.kint.2025.04.004 · DOI · Paper page
  39. Barbour, 2021, Updating the International IgA Nephropathy Prediction Tool for use in children, Kidney Int, 99, 1439, 10.1016/j.kint.2020.10.033 · DOI
  40. Liu, 2024, Predictive role of Oxford Classification for prognosis in children with IgA nephropathy: a systematic review and meta-analysis, Ren Fail, 46, 10.1080/0886022X.2024.2411846 · DOI
  41. Kiryluk, 2014, Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens, Nat Genet, 46, 1187, 10.1038/ng.3118 · DOI
  42. Fan, 2018, The influence of environmental factors on clinical pathological changes of patients with immunoglobulin A nephropathy from different areas of China, Ren Fail, 40, 597, 10.1080/0886022X.2018.1532907 · DOI
  43. Kohan, 2023, Targeting the endothelin A receptor in IgA nephropathy, Kidney Int Rep, 8, 2198, 10.1016/j.ekir.2023.07.023 · DOI
  44. Sanchez-Rodriguez, 2021, GWAS-based discoveries in IgA nephropathy, membranous nephropathy, and steroid-sensitive nephrotic syndrome, Clin J Am Soc Nephrol, 16, 458, 10.2215/CJN.14031119 · DOI
  45. Cheung, 2015, Gluten and IgA nephropathy: you are what you eat?, Kidney Int, 88, 215, 10.1038/ki.2015.149 · DOI
  46. Barratt, 2020, Why target the gut to treat IgA nephropathy?, Kidney Int Rep, 5, 1620, 10.1016/j.ekir.2020.08.009 · DOI
  47. Selvaskandan, 2022, Immunological drivers of IgA nephropathy: exploring the mucosa-kidney link, Int J Immunogenet, 49, 8, 10.1111/iji.12561 · DOI
  48. Hogg, 1988, IgA nephropathy: clinical features and natural history--a pediatric perspective, Am J Kidney Dis, 12, 358, 10.1016/S0272-6386(88)80024-6 · DOI
  49. Wang, 2012, Comparison of clinicopathological features between children and adults with IgA nephropathy, Pediatr Nephrol, 27, 1293, 10.1007/s00467-012-2139-3 · DOI
  50. Kawalec, 2022, Gut microbiota alterations and primary glomerulonephritis in children: a review, Int J Mol Sci, 24, 574, 10.3390/ijms24010574 · DOI
  51. Rehnberg, 2021, Inflammatory bowel disease is more common in patients with IgA nephropathy and predicts progression of ESKD: a Swedish population-based cohort study, J Am Soc Nephrol, 32, 411, 10.1681/ASN.2020060848 · DOI
  52. Serino, 2012, Abnormal miR-148b expression promotes aberrant glycosylation of IgA1 in IgA nephropathy, J Am Soc Nephrol, 23, 814, 10.1681/ASN.2011060567 · DOI
  53. Hu, 2015, Increased miR-374b promotes cell proliferation and the production of aberrant glycosylated IgA1 in B cells of IgA nephropathy, FEBS Lett, 589, 4019, 10.1016/j.febslet.2015.10.033 · DOI
  54. Serino, 2015, Role of let-7b in the regulation of N-acetylgalactosaminyltransferase 2 in IgA nephropathy, Nephrol Dial Transplant, 30, 1132, 10.1093/ndt/gfv032 · DOI
  55. Pawluczyk, 2021, A pilot study to predict risk of IgA nephropathy progression based on miR-204 expression, Kidney Int Rep, 6, 2179, 10.1016/j.ekir.2021.05.018 · DOI
  56. Kerr, 1990, The structure and function of human IgA, Biochem J, 271, 285, 10.1042/bj2710285 · DOI
  57. Scinicariello, 2001, Intraspecies heterogeneity of immunoglobulin alpha-chain constant region genes in rhesus macaques, Immunology, 103, 441, 10.1046/j.1365-2567.2001.01251.x · DOI
  58. Suzuki, 2021, IgA glycosylation and immune complex formation in IgAN, Semin Immunopathol, 43, 669, 10.1007/s00281-021-00883-8 · DOI
  59. Ohyama, 2020, Analysis of O-glycoforms of the IgA1 hinge region by sequential deglycosylation, Sci Rep, 10, 671, 10.1038/s41598-020-57510-z · DOI
  60. Gharavi, 2008, Aberrant IgA1 glycosylation is inherited in familial and sporadic IgA nephropathy, J Am Soc Nephrol, 19, 1008, 10.1681/ASN.2007091052 · DOI
  61. Xu, 2021, Mass spectrometry-based screening identifies circulating immunoglobulinA-alpha1-microglobulin complex as potential biomarker in immunoglobulin A nephropathy, Nephrol Dial Transplant, 36, 782, 10.1093/ndt/gfaa352 · DOI
  62. Roberts, 2024, IgA nephropathy: emerging mechanisms of disease, Indian J Nephrol, 34, 297, 10.25259/ijn_425_23 · DOI
  63. Feehally, 1986, Sequential study of the IgA system in relapsing IgA nephropathy, Kidney Int, 30, 924, 10.1038/ki.1986.274 · DOI
  64. Gesualdo, 2021, The mucosal immune system and IgA nephropathy, Semin Immunopathol, 43, 657, 10.1007/s00281-021-00871-y · DOI
  65. Bemark, 2024, Gut-associated lymphoid tissue: a microbiota-driven hub of B cell immunity, Trends Immunol, 45, 211, 10.1016/j.it.2024.01.006 · DOI
  66. Hirano, 2019, Association between tonsillectomy and outcomes in patients with immunoglobulin A nephropathy, JAMA Netw Open, 2, 10.1001/jamanetworkopen.2019.4772 · DOI
  67. Feehally, 2016, Tonsillectomy in a European cohort of 1,147 patients with IgA nephropathy, Nephron, 132, 15, 10.1159/000441852 · DOI
  68. Seikrit, 2021, The immune landscape of IgA induction in the gut, Semin Immunopathol, 43, 627, 10.1007/s00281-021-00879-4 · DOI
  69. Sanchez-Russo, 2022, The gut and kidney crosstalk in immunoglobulin A nephropathy, Kidney360, 3, 1630, 10.34067/KID.0002382022 · DOI
  70. Cerutti, 2008, The regulation of IgA class switching, Nat Rev Immunol, 8, 421, 10.1038/nri2322 · DOI
  71. Cheung, 2023, The role of BAFF and APRIL in IgA nephropathy: pathogenic mechanisms and targeted therapies, Front Nephrol, 3
  72. Cheung, 2024, Targeting APRIL in the treatment of IgA nephropathy, Clin J Am Soc Nephrol, 19, 394, 10.2215/CJN.0000000000000338 · DOI
  73. Cheung, 2024, Targeting APRIL in the treatment of glomerular diseases, Kidney Int, 106, 806, 10.1016/j.kint.2024.08.012 · DOI
  74. Zheng, 2017, Expression profile of BAFF in peripheral blood from patients of IgA nephropathy: correlation with clinical features and Streptococcus pyogenes infection, Mol Med Rep, 15, 1925, 10.3892/mmr.2017.6190 · DOI
  75. Sallustio, 2021, High levels of gut-homing immunoglobulin A+ B lymphocytes support the pathogenic role of intestinal mucosal hyperresponsiveness in immunoglobulin A nephropathy patients, Nephrol Dial Transplant, 36, 452, 10.1093/ndt/gfaa264 · DOI
  76. Han, 2016, The role of TNF superfamily member 13 in the progression of IgA nephropathy, J Am Soc Nephrol, 27, 3430, 10.1681/ASN.2015060677 · DOI
  77. Xin, 2013, Serum BAFF is elevated in patients with IgA nephropathy and associated with clinical and histopathological features, J Nephrol, 26, 683, 10.5301/jn.5000218 · DOI
  78. Smith, 2006, O-glycosylation of serum IgA1 antibodies against mucosal and systemic antigens in IgA nephropathy, J Am Soc Nephrol, 17, 3520, 10.1681/ASN.2006060658 · DOI
  79. Boyd, 2012, An update on the pathogenesis and treatment of IgA nephropathy, Kidney Int, 81, 833, 10.1038/ki.2011.501 · DOI
  80. Zhu, 2024, IgA nephropathy: gut microbiome regulates the production of hypoglycosilated IgA1 via the TLR4 signaling pathway, Nephrol Dial Transplant, 39, 1624, 10.1093/ndt/gfae052 · DOI
  81. Zhou, 2025, Immunoglobulin A nephropathy: molecular pathogenesis and targeted therapy, MedComm (2020), 6
  82. Chemouny, 2019, Modulation of the microbiota by oral antibiotics treats immunoglobulin A nephropathy in humanized mice, Nephrol Dial Transplant, 34, 1135, 10.1093/ndt/gfy323 · DOI
  83. Lauriero, 2021, Fecal microbiota transplantation modulates renal phenotype in the humanized mouse model of IgA nephropathy, Front Immunol, 12, 10.3389/fimmu.2021.694787 · DOI
  84. McCarthy, 2011, Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy, J Clin Invest, 121, 3991, 10.1172/JCI45563 · DOI
  85. Shah, 2021, The gut and blood microbiome in IgA nephropathy and healthy controls, Kidney360, 2, 1261, 10.34067/KID.0000132021 · DOI
  86. Zhong, 2020, Modifications of gut microbiota are associated with the severity of IgA nephropathy in the Chinese population, Int Immunopharmacol, 89, 10.1016/j.intimp.2020.107085 · DOI
  87. Papista, 2015, Gluten exacerbates IgA nephropathy in humanized mice through gliadin-CD89 interaction, Kidney Int, 88, 276, 10.1038/ki.2015.94 · DOI
  88. Harper, 1996, Increased dimeric IgA producing B cells in the bone marrow in IgA nephropathy determined by in situ hybridisation for J chain mRNA, J Clin Pathol, 49, 38, 10.1136/jcp.49.1.38 · DOI
  89. Cheung, 2022, Further evidence for the mucosal origin of pathogenic IgA in IgA nephropathy, J Am Soc Nephrol, 33, 873, 10.1681/ASN.2022020201 · DOI
  90. Nihei, 2023, Identification of IgA autoantibodies targeting mesangial cells redefines the pathogenesis of IgA nephropathy, Sci Adv, 9, 10.1126/sciadv.add6734 · DOI
  91. Currie, 2022, Immunoglobulin A nephropathy is characterized by anticommensal humoral immune responses, JCI Insight, 7, 10.1172/jci.insight.141289 · DOI
  92. Zachova, 2022, Galactose-deficient IgA1 B cells in the circulation of IgA nephropathy patients carry preferentially lambda light chains and mucosal homing receptors, J Am Soc Nephrol, 33, 908, 10.1681/ASN.2021081086 · DOI
  93. Gleeson, 2024, The gut microbiota posttranslationally modifies IgA1 in autoimmune glomerulonephritis, Sci Transl Med, 16, 10.1126/scitranslmed.adl6149 · DOI
  94. Wang, 2004, Dysregulated LIGHT expression on T cells mediates intestinal inflammation and contributes to IgA nephropathy, J Clin Invest, 113, 826, 10.1172/JCI20096 · DOI
  95. Lafayette, 2023, Efficacy and safety of a targeted-release formulation of budesonide in patients with primary IgA nephropathy (NefIgArd): 2-year results from a randomised phase 3 trial, Lancet, 402, 859, 10.1016/S0140-6736(23)01554-4 · DOI
  96. 2026, Norouzi S, Lafayette RA. Approved therapies in the IgA nephropathy armamentarium: a summary of the evidence, Kidney Int Suppl, 15, 24, 10.1016/j.kisu.2026.03.001 · DOI
  97. Suzuki, 2011, The pathophysiology of IgA nephropathy, J Am Soc Nephrol, 22, 1795, 10.1681/ASN.2011050464 · DOI
  98. Xu, 2023, An update on the genetics of IgA nephropathy, J Clin Med, 13, 123, 10.3390/jcm13010123 · DOI
  99. Kiryluk, 2014, The genetics and immunobiology of IgA nephropathy, J Clin Invest, 124, 2325, 10.1172/JCI74475 · DOI
  100. Canetta, 2014, Glomerular diseases: emerging tests and therapies for IgA nephropathy, Clin J Am Soc Nephrol, 9, 617, 10.2215/CJN.07260713 · DOI
  101. Berthoux, 2012, Autoantibodies targeting galactose-deficient IgA1 associate with progression of IgA nephropathy, J Am Soc Nephrol, 23, 1579, 10.1681/ASN.2012010053 · DOI
  102. Maixnerova, 2019, Galactose-deficient IgA1 and the corresponding IgG autoantibodies predict IgA nephropathy progression, PLoS One, 14
  103. Suzuki, 2009, Aberrantly glycosylated IgA1 in IgA nephropathy patients is recognized by IgG antibodies with restricted heterogeneity, J Clin Invest, 119, 1668
  104. Coppo, 2017, Persistent microscopic hematuria as a risk factor for progression of IgA nephropathy: new floodlight on a nearly forgotten biomarker, J Am Soc Nephrol, 28, 2831, 10.1681/ASN.2017060639 · DOI
  105. Novak, 2005, IgA1-containing immune complexes in IgA nephropathy differentially affect proliferation of mesangial cells, Kidney Int, 67, 504, 10.1111/j.1523-1755.2005.67107.x · DOI
  106. Caravaca-Fontán, 2023, Targeting complement in IgA nephropathy, Clin Kidney J, 16, ii28, 10.1093/ckj/sfad198 · DOI
  107. Chiu, 2021, Alternative complement pathway is activated and associated with galactose-deficient IgA(1) antibody in IgA nephropathy patients, Front Immunol, 12, 10.3389/fimmu.2021.638309 · DOI
  108. Scionti, 2022, New insights into the pathogenesis and treatment strategies in IgA nephropathy, Glomerular Dis, 2, 15, 10.1159/000519973 · DOI
  109. Trimarchi, 2019, Podocytopathy in the mesangial proliferative immunoglobulin A nephropathy: new insights into the mechanisms of damage and progression, Nephrol Dial Transplant, 34, 1280, 10.1093/ndt/gfy413 · DOI
  110. Huang, 2023, Kidney fibrosis: from mechanisms to therapeutic medicines, Signal Transduct Target Ther, 8, 129, 10.1038/s41392-023-01379-7 · DOI
  111. Lai, 1996, Serologic study of immunoglobulin A-fibronectin aggregates in immunoglobulin A nephropathy, Am J Kidney Dis, 27, 622, 10.1016/S0272-6386(96)90095-5 · DOI
  112. Poppelaars, 2021, The contribution of complement to the pathogenesis of IgA nephropathy: are complement-targeted therapies moving from rare disorders to more common diseases?, J Clin Med, 10, 4715, 10.3390/jcm10204715 · DOI
  113. Cheung, 2023, The role of complement in glomerulonephritis-are novel therapies ready for prime time?, Nephrol Dial Transplant, 38, 1789, 10.1093/ndt/gfac296 · DOI
  114. Wu, 2021, Mesangial C3 deposition and serum C3 levels predict renal outcome in IgA nephropathy, Clin Exp Nephrol, 25, 641, 10.1007/s10157-021-02034-7 · DOI
  115. Kim, 2012, Decreased circulating C3 levels and mesangial C3 deposition predict renal outcome in patients with IgA nephropathy, PLoS One, 7
  116. Barratt, 2023, IgA nephropathy: the lectin pathway and implications for targeted therapy, Kidney Int, 104, 254, 10.1016/j.kint.2023.04.029 · DOI
  117. Medjeral-Thomas, 2018, Progressive IgA nephropathy is associated with low circulating mannan-binding lectin-associated serine protease-3 (MASP-3) and increased glomerular factor H-related protein-5 (FHR5) deposition, Kidney Int Rep, 3, 426, 10.1016/j.ekir.2017.11.015 · DOI
  118. Wang, 2024, The prognostic role of activation of the complement pathways in the progression of advanced IgA nephropathy to end-stage renal disease, BMC Nephrol, 25, 387, 10.1186/s12882-024-03832-3 · DOI
  119. Roos, 2006, Glomerular activation of the lectin pathway of complement in IgA nephropathy is associated with more severe renal disease, J Am Soc Nephrol, 17, 1724, 10.1681/ASN.2005090923 · DOI
  120. Espinosa, 2014, Association of C4d deposition with clinical outcomes in IgA nephropathy, Clin J Am Soc Nephrol, 9, 897, 10.2215/CJN.09710913 · DOI
  121. Segarra, 2018, Mesangial C4d deposits in early IgA nephropathy, Clin J Am Soc Nephrol, 13, 258, 10.2215/CJN.02530317 · DOI
  122. Jiang, 2021, Glomerular C4d deposition and kidney disease progression in IgA nephropathy: a systematic review and meta-analysis, Kidney Med, 3, 1014, 10.1016/j.xkme.2021.06.009 · DOI
  123. Chua, 2019, Complement-mediated microangiopathy in IgA nephropathy and IgA vasculitis with nephritis, Mod Pathol, 32, 1147, 10.1038/s41379-019-0259-z · DOI
  124. Nishiwaki, 2015, Absence of mesangial C1q deposition is associated with resolution of proteinuria and hematuria after tonsillectomy plus steroid pulse therapy for immunoglobulin a nephropathy, Nephron, 130, 1, 10.1159/000381217 · DOI
  125. Tan, 2021, A multicenter, prospective, observational study to determine association of mesangial C1q deposition with renal outcomes in IgA nephropathy, Sci Rep, 11, 5467, 10.1038/s41598-021-84715-7 · DOI
  126. De Miguel, 2016, Endothelin-1 and the kidney: new perspectives and recent findings, Curr Opin Nephrol Hypertens, 25, 35, 10.1097/MNH.0000000000000185 · DOI
  127. Kohan, 2014, Endothelin and endothelin antagonists in chronic kidney disease, Kidney Int, 86, 896, 10.1038/ki.2014.143 · DOI
  128. Smeijer, 2021, Endothelin receptor antagonists for the treatment of diabetic and nondiabetic chronic kidney disease, Curr Opin Nephrol Hypertens, 30, 456, 10.1097/MNH.0000000000000716 · DOI
  129. Lehrke, 2001, Renal endothelin-1 and endothelin receptor type B expression in glomerular diseases with proteinuria, J Am Soc Nephrol, 12, 2321, 10.1681/ASN.V12112321 · DOI
  130. Benigni, 2000, Tubulointerstitial disease mediators of injury: the role of endothelin, Nephrol Dial Transplant, 15, 50, 10.1093/ndt/15.suppl_6.50 · DOI
  131. 2026, Tang SCW, Reich HN. IgA nephropathy management: what does the future hold?, Kidney Int Suppl, 15, 47, 10.1016/j.kisu.2026.01.001 · DOI

Metadata

Authors
Cheung, C. K., & Mariani, L. H.
Affiliations
  • University of Leicester (GB)
  • University of Michigan (US)
Corresponding author
Cheung, Chee Kay
ORCID
Venue
Kidney International Supplements
Publisher
Elsevier BV
Published
2026-08
Volume
15
Issue
1
Pages
3-13
ISSN
2157-1716 (ISSN-L)
DOI
10.1016/j.kisu.2026.01.003
PMC
PMC13387150
OpenAlex
W7169779486
Cited by
2
References
1
Citations by year
2026: 2
FWCI
1.97
Type
journal article
Language
en
Open access
Licence
Locations
  • Kidney International Supplements (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
Oxford University Hospitals NHS Foundation Trust
Topics
  • Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
  • Health Sciences › Medicine › Rheumatology › Vasculitis and related conditions
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
Keywords
IgA nephropathy, primary glomerular disease, gut-kidney axis, pathophysiology, galactose-deficient IgA1, autoantibodies, immune complexes, mesangial deposition, mucosal immunity, intestinal epithelial barrier, inflammatory bowel disease, genetic susceptibility loci, renal failure, clinical features

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review