scholarly journals Immunoglobulin A nephropathy. Quantitative immunohistomorphometry of the tonsillar plasma cells evidences an inversion of the immunoglobulin A versus immunoglobulin G secreting cell balance.

1983 ◽  
Vol 71 (5) ◽  
pp. 1342-1347 ◽  
Author(s):  
M C Bene ◽  
G Faure ◽  
B Hurault de Ligny ◽  
M Kessler ◽  
J Duheille
Nephrology ◽  
2010 ◽  
Vol 15 (8) ◽  
pp. 747-754 ◽  
Author(s):  
TAKAHITO MORIYAMA ◽  
ARI SHIMIZU ◽  
TAKASHI TAKEI ◽  
KEIKO UCHIDA ◽  
KAZUHO HONDA ◽  
...  

2019 ◽  
Vol 66 ◽  
pp. 13-18 ◽  
Author(s):  
Di Liu ◽  
Jing You ◽  
Yexin Liu ◽  
Xiaofang Tang ◽  
Xia Tan ◽  
...  

2019 ◽  
Author(s):  
Ran Luo ◽  
Yi-Chun Chen ◽  
Dan Chang ◽  
Ting-Ting Liu ◽  
Yue-Qiang Li ◽  
...  

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

2018 ◽  
Vol 104 (3) ◽  
pp. 177-182
Author(s):  
D O’Brien ◽  
K Houlberg

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.


2003 ◽  
Vol 71 (8) ◽  
pp. 4808-4814 ◽  
Author(s):  
Firdausi Qadri ◽  
Edward T. Ryan ◽  
A. S. G. Faruque ◽  
Firoz Ahmed ◽  
Ashraful Islam Khan ◽  
...  

ABSTRACT Gut-derived lymphocytes transiently migrate through the peripheral circulation before homing back to mucosal sites and can be detected using an ELISPOT-based antibody secreting cell (ASC) assay. Alternatively, transiently circulating lymphocytes may be cultured in vitro, and culture supernatants may be assayed for antigen-specific responses (antibody in lymphocyte supernatant [ALS] assay). The ALS assay has not been validated extensively in natural mucosal infection, nor has the ALS response been compared to the ASC assay and other cholera-specific immunological responses. Accordingly, we examined immune responses in 30 adult patients with acute cholera in Bangladesh, compared with 10 healthy controls, measuring ALS-immunoglobulin A (IgA), ASC-IgA, and serum and fecal IgA responses to two potent Vibrio cholerae immunogens, the nontoxic B subunit of cholera toxin (CtxB) and lipopolysaccharide (LPS) and a weaker V. cholerae immunogen, the mannose-sensitive hemagglutinin (MSHA). We found significant increases of anti-CtxB, anti-LPS, and anti-MSHA IgA in supernatants of lymphocytes cultured 7 days after onset of cholera using the ALS assay. We found that ALS and ASC responses correlated extremely well; both had comparable sensitivities as the vibriocidal responses, and both procedures were more sensitive than fecal IgA measurements. An advantage of the ALS assay for studying mucosal immune responses is the ability to freeze antibodies in supernatants for subsequent evaluation; like the ASC assay, the ALS assay can distinguish recent from remote mucosal infection, a distinction that may be difficult to make in endemic settings using other procedures.


2019 ◽  
Vol 34 (8) ◽  
pp. 1280-1285 ◽  
Author(s):  
Hernán Trimarchi ◽  
Rosanna Coppo

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.


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