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IgA nephropathy

E. Stamellou, C. Seikrit, SCW. Tang, P. Boor, V. Tesař, J. Floege, J. Barratt, R. Kramann

. 2023 ; 9 (1) : 67. [pub] 20231130

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články, přehledy

Perzistentní odkaz   https://www.medvik.cz/link/bmc24000579
E-zdroje Online Plný text

NLK ProQuest Central od 2015-01-01 do Před 1 rokem
Health & Medicine (ProQuest) od 2015-01-01 do Před 1 rokem

Odkazy

PubMed 38036542
DOI 10.1038/s41572-023-00476-9
Knihovny.cz E-zdroje

IgA nephropathy (IgAN), the most prevalent primary glomerulonephritis worldwide, carries a considerable lifetime risk of kidney failure. Clinical manifestations of IgAN vary from asymptomatic with microscopic or intermittent macroscopic haematuria and stable kidney function to rapidly progressive glomerulonephritis. IgAN has been proposed to develop through a 'four-hit' process, commencing with overproduction and increased systemic presence of poorly O-glycosylated galactose-deficient IgA1 (Gd-IgA1), followed by recognition of Gd-IgA1 by antiglycan autoantibodies, aggregation of Gd-IgA1 and formation of polymeric IgA1 immune complexes and, lastly, deposition of these immune complexes in the glomerular mesangium, leading to kidney inflammation and scarring. IgAN can only be diagnosed by kidney biopsy. Extensive, optimized supportive care is the mainstay of therapy for patients with IgAN. For those at high risk of disease progression, the 2021 KDIGO Clinical Practice Guideline suggests considering a 6-month course of systemic corticosteroid therapy; however, the efficacy of systemic steroid treatment is under debate and serious adverse effects are common. Advances in understanding the pathophysiology of IgAN have led to clinical trials of novel targeted therapies with acceptable safety profiles, including SGLT2 inhibitors, endothelin receptor blockers, targeted-release budesonide, B cell proliferation and differentiation inhibitors, as well as blockade of complement components.

Citace poskytuje Crossref.org

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