Immunoglobulin a nephropathy with mild renal lesions: a call in the forest for physicians and nephrologists

2001 ◽  
Vol 110 (6) ◽  
pp. 499-500 ◽  
Author(s):  
Francesco Paolo Schena
Author(s):  
Francesco Paolo Schena ◽  
Michele Rossini ◽  
Daniela Isabel Abbrescia ◽  
Gianluigi Zaza

AbstractKidney biopsy is the cornerstone for the diagnosis of immunoglobulin A nephropathy (IgAN). The immunofluorescence technique evidences the IgA deposits in the glomeruli; the routine histology shows degree of active and chronic renal lesions. The spectrum of renal lesions is highly variable, ranging from minor or no detectable lesions to diffuse proliferative or crescentic lesions. Over the past three decades, renal transcriptomic studies have been performed on fresh or frozen renal tissue, and formalin-fixed paraffin-embedded kidney tissue specimens obtained from archival histological repositories. This paper aims to describe (1) the transcriptomic profiles of the kidney biopsy and (2) the potential urinary biomarkers that can be used to monitor the follow-up of IgAN patients. The use of quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), microarrays and RNA-sequencing (RNA-seq) techniques on renal tissue and separated compartments of the nephron such as glomeruli and tubule-interstitium has clarified many aspects of the renal damage in IgAN. Recently, the introduction of the single-cell RNA-seq techniques has overcome the limitations of the previous methods, making that it is possible to study the whole renal tissue without the dissection of the nephron segments; it also allows better analysis of the cell-specific gene expression involved in cell differentiation. These gene products could represent effective candidates for urinary biomarkers for clinical decision making. Finally, some of these molecules may be the targets of old drugs, such as corticosteroids, renin–angiotensin–aldosterone blockers, and new drugs such as monoclonal antibodies. In the era of personalized medicine and precision therapy, high-throughput technologies may better characterize different renal patterns of IgAN and deliver targeted treatments to individual patients.


2019 ◽  
Vol 74 (5) ◽  
pp. 744-758 ◽  
Author(s):  
Yuxi Wang ◽  
Zhizhi Hu ◽  
Jianliang Wu ◽  
Pengge Wang ◽  
Qian Yang ◽  
...  

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.


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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