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The impact of primary immunodeficiency on the severity of chronic rhinosinusitis.
Am J Otolaryngol
December 2024
Department of Otolaryngology-Head & Neck Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. Electronic address:
Article Synopsis
- The study investigates the impact of primary IgA and/or IgG immunodeficiencies on the severity of chronic rhinosinusitis (CRS) among patients at a Boston medical center.
- Results indicate that patients with these immunodeficiencies have a higher prevalence of CRS (12%) compared to those with normal levels (5%).
- However, the immunodeficient group does not show statistically significant differences in acute rhinosinusitis episodes or the need for surgical interventions compared to the normal group.
Atrasentan in Patients with IgA Nephropathy.
N Engl J Med
October 2024
From the Department of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands (H.J.L.H.); the National Health and Medical Research Council Clinical Trials Centre, University of Sydney, Sydney (M.J.); the Division of Nephrology, University of Utah Health, Salt Lake City (D.E.K.); Stanford University, Stanford, CA (R.A.L.); the University of British Columbia, Vancouver, Canada (A. Levin); Mount Elizabeth Novena Hospital, Singapore (A. Liew); Peking University First Hospital, Beijing (H.Z.); Chinook Therapeutics, Seattle (T.G.); Novartis, East Hanover, NJ (A. Lodha, Y.W.); Novartis, Basel, Switzerland (R.R.); and the University of Leicester, Leicester, United Kingdom (J.B.).
Background: Patients with IgA nephropathy and severe proteinuria have a high lifetime risk of kidney failure. The efficacy and safety of the selective endothelin type A receptor antagonist atrasentan in reducing proteinuria in patients with IgA nephropathy are incompletely understood.
Methods: We are conducting a phase 3, multinational, double-blind, randomized, controlled trial involving adults with biopsy-proven IgA nephropathy, a total urinary protein excretion of at least 1 g per day, and an estimated glomerular filtration rate of at least 30 ml per minute per 1.
Immunoglobulin A nephropathy is not what it used to be!
Intern Med J
November 2024
Nephrology and Transplantation Unit, John Hunter Hospital, Newcastle, New South Wales, Australia.
Immunoglobulin A (IgA) nephropathy is the most common primary glomerulonephritis worldwide and thought to be a benign disease. Recent literature review would suggest otherwise, with outcomes remaining generally poor. Few patients do not progress to kidney failure in their lifetime even in population groups previously thought to be low risk.
View Article and Find Full Text PDFMy lifetime in IgA nephropathy: An unexpected journey.
Nephrology (Carlton)
September 2024
Division of Nephrology, Department of Medicine, University of Alabama at Birmingham Heersink School of Medicine, Birmingham, Alabama, USA.
The pathogenesis of IgA nephropathy and implications for treatment.
Nat Rev Nephrol
January 2025
Mayer IgA Nephropathy Laboratories, Department of Cardiovascular Sciences, University of Leicester, Leicester, UK.
IgA nephropathy (IgAN) is a common form of primary glomerulonephritis and represents an important cause of chronic kidney disease globally, with observational studies indicating that most patients are at risk of developing kidney failure within their lifetime. Several research advances have provided insights into the underlying disease pathogenesis, framed by a multi-hit model whereby an increase in circulating IgA1 that lacks galactose from its hinge region - probably derived from the mucosal immune system - is followed by binding of specific IgG and IgA antibodies, generating immune complexes that deposit within the glomeruli, which triggers inflammation, complement activation and kidney damage. Although treatment options are currently limited, new therapies are rapidly emerging that target different pathways, cells and mediators involved in the disease pathogenesis, including B cell priming in the gut mucosa, the cytokines APRIL and BAFF, plasma cells, complement activation and endothelin pathway activation.
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