Clinical course of Immunoglobulin A nephropathy with crescents in a multi‐ethnic Southeast Asian cohort

Nephrology ◽  
2020 ◽  
Vol 25 (9) ◽  
pp. 708-713
Author(s):  
Cynthia C. Lim ◽  
Shashidhar Baikunje ◽  
Jason C. J. Choo ◽  
Puay H. Tan ◽  
Marjorie Foo ◽  
...  
Keyword(s):  
Clinical Course ◽  
Immunoglobulin A ◽  
Southeast Asian ◽  
Immunoglobulin A Nephropathy ◽  
Asian Cohort

Evaluating the Clinical Course and Prognostic Factors of Posttransplantation Immunoglobulin A Nephropathy

2008 ◽  
Vol 40 (7) ◽  
pp. 2349-2354 ◽  
Author(s):  
K. Kiattisunthorn ◽  
N. Premasathian ◽  
A. Wongwiwatana ◽  
P. Parichatikanond ◽  
B. Cheunsuchon ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Clinical Course ◽  
Immunoglobulin A ◽  
Immunoglobulin A Nephropathy

Immunoglobulin A nephropathy

2015 ◽  
Author(s):  
Kar Neng Lai ◽  
Sydney C. W. Tang
Keyword(s):  
Extracellular Matrix ◽  
Renal Failure ◽  
Clinical Presentation ◽  
Mesangial Cells ◽  
Clinical Course ◽  
Immunoglobulin A ◽  
Immunoglobulin A Nephropathy ◽  
Primary Glomerulonephritis ◽  
End Stage Renal Failure ◽  
End Stage

Immunoglobulin A (IgA) nephropathy is the most common primary glomerulonephritis. It runs a slow and sometimes relentless clinical course with consequent end-stage renal failure in 35–40% of patients 25–30 years after first clinical presentation. The pathology is characterized by deposition of macromolecular (polymeric) IgA1 in the glomerular mesangium, proliferation of mesangial cells, increased synthesis of extracellular matrix, and infiltration of macrophage, monocytes, and T cells.

Clinical course of immunoglobulin A nephropathy in children

1987 ◽  
Vol 110 (4) ◽  
pp. 555-560 ◽  
Author(s):  
Norishige Yoshikawa ◽  
Hiroshi Ito ◽  
Shochi Yoshiara ◽  
Chieko Nakahara ◽  
Katsuhiko Yoshiya ◽  
...  
Keyword(s):  
Clinical Course ◽  
Immunoglobulin A ◽  
Immunoglobulin A Nephropathy

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.

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