Systemic corticosteroids and mucosal-associated lymphoid tissue-targeted therapy in immunoglobulin A nephropathy: insight from the NEFIGAN study

2019 ◽  
Vol 35 (8) ◽  
pp. 1291-1294
Author(s):  
Rosanna Coppo ◽  
Christophe Mariat
Keyword(s):  
Targeted Therapy ◽  
Lymphoid Tissue ◽  
Immunoglobulin A ◽  
Immunoglobulin A Nephropathy ◽  
Systemic Corticosteroids

scholarly journals The mucosal immune system and IgA nephropathy

2021 ◽  
Author(s):  
Loreto Gesualdo ◽  
Vincenzo Di Leo ◽  
Rosanna Coppo
Keyword(s):  
Immune Response ◽  
Mucosal Immunity ◽  
Lymphoid Tissue ◽  
Genetic Factors ◽  
Immunoglobulin A ◽  
Mucosal Immune Response ◽  
Immunoglobulin A Nephropathy ◽  
Food Antigen ◽  
The Relationship

Abstract The precise pathogenesis of immunoglobulin A nephropathy (IgAN) is still not clearly established but emerging evidence confirms a pivotal role for mucosal immunity. This review focuses on the key role of mucosa-associated lymphoid tissue (MALT) in promoting the onset of the disease, underlying the relationship among microbiota, genetic factors, food antigen, infections, and mucosal immune response. Finally, we evaluate potential therapies targeting microbes and mucosa hyperresponsiveness in IgAN patients.

scholarly journals Role of Palatine Tonsil and Epipharyngeal Lymphoid Tissue in the Development of Glomerular Active Lesions (Glomerular vasculitis) in Immunoglobulin A Nephropathy

2022 ◽  
Vol 23 (2) ◽  
pp. 727
Author(s):  
Osamu Hotta ◽  
Norio Ieiri ◽  
Masaaki Nagai ◽  
Ayaki Tanaka ◽  
Yasuaki Harabuchi
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Lymphoid Tissue ◽  
Immunoglobulin A ◽  
Chronic Phase ◽  
Basement Membranes ◽  
Palatine Tonsil ◽  
Glomerular Sclerosis ◽  
Future Research ◽  
Immunoglobulin A Nephropathy

Hematuria is an essential symptom of immunoglobulin A nephropathy (IgAN). Although the etiology of hematuria in IgAN has not been fully elucidated, it is thought that the rupture of the glomerular basement membranes caused by intra-capillary leukocyte influx, so-called glomerular vasculitis, is the pathological condition responsible for severe hematuria. Glomerular vasculitis are active lesions that exist in the glomeruli of acute phase IgAN and it is important because it is suspected to make the transition to segmental glomerular sclerosis (SGS) as a repair scar lesion in the chronic phase, and the progression of SGS would eventually lead to glomerular obsolescence. Worsening of hematuria concomitant with acute pharyngitis is common in patients with IgAN; therefore, elucidating the relationship between the immune system of Waldeyer’s ring, including the palatine tonsil and epipharyngeal lymphoid tissue, and the glomerular vasculitis may lead to understanding the nature of IgAN. The epipharynx is an immunologically activated site even under normal conditions, and enhanced activation of innate immunity is likely to occur in response to airborne infection. Hyperactivation of innate immunity via upregulation of Toll-like receptors in the interfollicular area of the palatine tonsil and epipharyngeal lymphoid tissue, followed by enhanced fractalkine/CX3CR1 interactions, appears to play an important role in the development of glomerular vasculitis in IgAN. As latent but significant epipharyngitis is present in most patients with IgAN, it is plausible that acute upper respiratory infection may contribute as a trigger for the innate epipharyngeal immune system, which is already upregulated in a chronically inflamed environment. Given that epipharyngitis and its effects on IgAN are not fully understood, we propose that the so-called “epipharynx–kidney axis” may provide an important focus for future research.

scholarly journals The epipharynx-kidney axis triggers glomerular vasculitis in immunoglobulin A nephropathy

2019 ◽  
Vol 67 (4-5) ◽  
pp. 304-309 ◽  
Author(s):  
Osamu Hotta ◽  
Takashi Oda
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Lymphoid Tissue ◽  
Immunoglobulin A ◽  
Underlying Mechanism ◽  
Innate Immune ◽  
Immunoglobulin A Nephropathy ◽  
Macroscopic Hematuria ◽  
Acute Pharyngitis ◽  
Airborne Infection

AbstractMacroscopic hematuria concomitant with acute pharyngitis is a characteristic feature of immunoglobulin A nephropathy (IgAN). Although the underlying mechanism of worsening hematuria has not been fully elucidated, activation of the innate immune system of nasopharynx-associated lymphoid tissue is thought to play an important role. The epipharynx is an immunologically activated site even under normal conditions, and enhanced activation of innate immunity is likely to occur in response to airborne infection. As latent but significant epipharyngitis presents in most IgAN patients, it is plausible that acute pharyngitis due to airway infection may contribute as a trigger of the epipharyngeal innate immune system, which is already upregulated in the chronically inflamed environment. The aim of this review was to discuss the mechanism of epipharynx-kidney axis involvement in glomerular vasculitis responsible for the worsening of hematuria in IgAN.

Plasma CXCL16 May Predict Renal Inflammation and the Progression of Immunoglobulin a Nephropathy

2019 ◽  
Author(s):  
Ran Luo ◽  
Yi-Chun Chen ◽  
Dan Chang ◽  
Ting-Ting Liu ◽  
Yue-Qiang Li ◽  
...  
Keyword(s):  
Immunoglobulin A ◽  
Immunoglobulin A Nephropathy ◽  
Renal Inflammation

Immunostaining of galactose-deficient IgA1 by KM55 is not specific for immunoglobulin A nephropathy

2020 ◽  
Vol 217 ◽  
pp. 108483 ◽  
Author(s):  
Lu Zhao ◽  
Liang Peng ◽  
Danyi Yang ◽  
Shi Chen ◽  
Zhixin Lan ◽  
...  
Keyword(s):  
Immunoglobulin A ◽  
Immunoglobulin A Nephropathy

Non-visible haematuria in a military setting

2018 ◽  
Vol 104 (3) ◽  
pp. 177-182
Author(s):  
D O’Brien ◽  
K Houlberg
Keyword(s):  
Basement Membrane ◽  
Immunoglobulin A ◽  
Armed Forces ◽  
Common Finding ◽  
Immunoglobulin A Nephropathy ◽  
Hereditary Nephritis ◽  
Military Recruits ◽  
Thin Basement Membrane Disease ◽  
Medical Examinations

AbstractAsymptomatic non-visible haematuria is a common finding at routine military medical examinations. This article briefly reviews the possible causes, which include malignancy, structural causes, exertion haematuria, hereditary nephritis, thin basement membrane disease (TBMD), immunoglobulin A nephropathy (IgAN), tuberculosis (TB) and schistosomiasis. This paper discusses how these conditions may affect potential military recruits as well as currently serving members of the Armed Forces, and offers a general approach to the management of a patient with non-visible haematuria.

Podocytopathy in the mesangial proliferative immunoglobulin A nephropathy: new insights into the mechanisms of damage and progression

2019 ◽  
Vol 34 (8) ◽  
pp. 1280-1285 ◽  
Author(s):  
Hernán Trimarchi ◽  
Rosanna Coppo
Keyword(s):  
Mesangial Cells ◽  
Immunosuppressive Treatment ◽  
Immunoglobulin A ◽  
Primary Site ◽  
New Drugs ◽  
Immunoglobulin A Nephropathy ◽  
Inflammatory Reactions ◽  
Persistent Proteinuria ◽  
Mesangial Area ◽  
Function Loss

Abstract Immunoglobulin A nephropathy (IgAN) was defined as a mesangiopathic disease, since the primary site of deposition of IgA immune material is the mesangium, and proliferation of mesangial cells and matrix excess deposition are the first histopathologic lesions. However, the relentless silent progression of IgAN is mostly due to the development of persistent proteinuria, and recent studies indicate that a major role is played by previous damage of function and anatomy of podocytes. In IgAN, the podocytopathic changes are the consequence of initial alterations in the mesangial area with accumulation of IgA containing immune material. Podocytes are therefore affected by interactions of messages originally driven from the mesangium. After continuous insult, podocytes detach from the glomerular basement membrane. This podocytopathy favours not only the development of glomerular focal and segmental sclerosis, but also the progressive renal function loss. It is still debated whether these lesions can be prevented or cured by corticosteroid/immunosuppressive treatment. We aimed to review recent data on the mechanisms implicated in the podocytopathy present in IgAN, showing new molecular risk factors for progression of this disease. Moreover, these observations may indicate that the target for new drugs is not only focused on decreasing the activity of mesangial cells and inflammatory reactions in IgAN, but also on improving podocyte function and survival.

Brief Communication: Immunoglobulin A1 protease: A new therapeutic candidate for immunoglobulin A nephropathy

Nephrology ◽  
2010 ◽  
Vol 15 (5) ◽  
pp. 584-586 ◽  
Author(s):  
LIN-SHEN XIE ◽  
JUN HUANG ◽  
WEI QIN ◽  
JUN-MING FAN
Keyword(s):  
Immunoglobulin A ◽  
Immunoglobulin A Nephropathy
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