Expression of response gene to complement-32 in renal tissue of children with immunoglobulin A nephropathy

2011 ◽  
Vol 45 (5) ◽  
pp. 371-376 ◽  
Author(s):  
Xiao-Ling Niu ◽  
Xin-Yu Kuang ◽  
Zhi-Gang Zhang ◽  
Xue-Guang Liu ◽  
Zhong-Hua Zhao ◽  
...  
2018 ◽  
Vol 34 (9) ◽  
pp. 1549-1558 ◽  
Author(s):  
Ran Luo ◽  
Shui-Ming Guo ◽  
Yue-Qiang Li ◽  
Yi Yang ◽  
Meng-Lan Li ◽  
...  

Abstract Background A recognized noninvasive biomarker to improve risk stratification of immunoglobulin A nephropathy (IgAN) patients is scarce. Fractalkine has been shown to play a key role in glomerular disease as chemoattractant, adhesion and even fibrosis factor. The current study assessed the possibility of plasma fractalkine as a novel biomarker in IgAN patients. Methods Plasma fractalkine was measured in 229 patients with renal biopsy consistent IgAN from 2012 to 2014, and clinical, pathological and prognostic relationships were analyzed. Results The plasma fractalkine levels in IgAN patients were significantly correlated with the creatinine level and 24-h urine protein by both univariate and multivariate analysis. Mesangial hypercellularity was still significantly correlated with the plasma fractalkine levels even after adjustment for other potential predictor variables by multivariate analysis. In addition, the counts of CD20+ B cells or CD68+ macrophage in renal biopsies of IgAN patients were significantly correlated with the plasma fractalkine levels, but not CD4+ and CD8+ T cells. Finally, we concluded that patients with higher plasma fractalkine levels had higher risk of poor renal outcome compared with those with lower plasma fractalkine levels. No association was observed between the CX3CR1 polymorphisms and clinical parameters including plasma fractalkine levels and prognosis. Recombinant fractalkine induced mesangial cells extracellular matrix synthesis and promoted the migration of microphage cells RAW264.7. Conclusions Plasma fractalkine levels were associated with creatinine level, 24-h urine protein, mesangial hypercellularity pathological damage, the CD68+ macrophage and CD20+ B cell infiltration in renal tissue and renal outcome in IgAN patients. Plasma fractalkine might be a potential prognosis novel predictor in Chinese patients with IgAN.


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.


1997 ◽  
Vol 25 (2) ◽  
pp. 71-80 ◽  
Author(s):  
Y Taniguchi ◽  
N Yorioka ◽  
T Masaki ◽  
K Yamashita ◽  
T Ito ◽  
...  

The role of transforming growth factor-β1 (TGF-β1) in human glomerulonephritis is still poorly understood. The relationship between expression of TGF-β1 protein or TGF-β1 mRNA and tissue damage was investigated using the enzyme–antibody and in situ hybridization method in frozen slices of renal tissue from 30 patients: 25 with glomerulonephritis (18 with immunoglobulin A nephropathy; two with focal glomerulosclerosis, one with membranous nephropathy, one with crescentic glomerulonephritis and three with lupus nephritis) and five control patients with minimal change disease. The expression of TGF-β1 mRNA was high in sclerotic and proliferative glomeruli, as well as in the tubular epithelial cells within tubulointerstitial lesions. There was significant correlation between the severity of tissue damage in immunoglobulin A nephropathy and the presence of TGF-β1protein and TGF-β1 mRNA. These findings suggest that TGF-β1 is involved in glomerulosclerosis and the development of tubulointerstitial lesions, indicating its potential importance in the progression and aggravation of immunoglobulin A nephropathy.


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.


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

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