Primary glomerulonephritis: A review of important recent discoveries

Floege, Jürgen

doi:10.1016/j.krcp.2013.06.004

Cited by 12 publications

(13 citation statements)

References 70 publications

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“…2,24 Until now, there are no practical biomarkers reflecting immunologic disease activity in primary IgAN, such as anti-phospholipase A2 receptor antibody in idiopathic membranous nephropathy. 2,24 Until now, there are no practical biomarkers reflecting immunologic disease activity in primary IgAN, such as anti-phospholipase A2 receptor antibody in idiopathic membranous nephropathy.…”

Section: Discussionmentioning

confidence: 99%

“…IgA nephropathy is regarded as a type of autoimmune disease through the interaction between an intrinsic antigen and circulating antibodies. 2,24 Until now, there are no practical biomarkers reflecting immunologic disease activity in primary IgAN, such as anti-phospholipase A2 receptor antibody in idiopathic membranous nephropathy. Proteinuria level, renal function and pathologic parameters can be the consequences of the disease process rather than true causative markers of disease activity.…”

Section: Discussionmentioning

confidence: 99%

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First‐year GFR slope and long‐term renal outcome in IgA nephropathy

Lee

Shin

Park

et al. 2018

Eur J Clin Investigation

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

First‐year GFR slope and long‐term renal outcome in IgA nephropathy

Lee

Shin

Park

et al. 2018

Eur J Clin Investigation

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“…This property is known as immunoregulation and is of paramount importance, not only for the kidneys but also for the whole organism. Failures on the immunoregulation may lead either to the development of autoimmune diseases that can impair renal function, such as systemic lupus erythematosus (SLE), whose renal involvement is a severe type of GN called lupus nephritis or to the vulnerability to opportunistic infections, leading to repeated episodes of pyelonephritis and/or immune-mediated GN due to the accumulation of antigen-antibody complexes in the glomerular filtration barrier (GFB) [12].…”

Section: The Immune System and Kidney Diseasementioning

confidence: 99%

“…There are a number of different kinds of GN, which differ one from the other by the type of local renal infiltrating cells, by the presence and subtyping of autoantibodies, by the accumulation of complement system components, by the specific antigens that starts the renal local immune response, and also by some differential clinical and laboratorial features, including proteinuria, hematuria, and edema [12]. Although GN is an important cause of CKD, the molecular and cellular mechanisms involved in their onset and progression are beyond the scope of this revision, since GN is considered an immune-mediated kidney condition.…”

Section: Introductionmentioning

confidence: 99%

Inflammation in Nonimmune-Mediated Chronic Kidney Disease

Fanelli¹,

Noreddin²,

Nunes³

2018

Chronic Kidney Disease - From Pathophysiology to Clinical Improvements

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Regardless of its etiology, chronic kidney disease (CKD) is characterized by proteinuria, serum creatinine retention, glomerulosclerosis (GS), and tubulointerstitial damage. Notably, the last one has been correlated more closely with the evolution to kidney failure than the extent of glomerular injury. Tubulointerstitial inflammation comprises the activation of tubular epithelial cells, which release inflammatory mediators and chemokines promoting the influx of leukocytes in the renal parenchyma and the activation/proliferation of resident fibroblasts, leading to excessive production of extracellular matrix (EM), fibrosis, and renal function loss. Therefore, inflammation exerts a key role in the pathogenesis of CKD, although the mechanisms by which this process is activated and perpetuated, even when the initial insult is not immune-mediated, such as in the hypertensive nephrosclerosis, in the diabetic nephropathy, and in the crystal-induced renal disease, remain unclear. This chapter provides an overview on inflammation and CKD development not related to autoimmunity or caused by presence of foreign antigens. Cellular and molecular mechanisms involved in different pathways and its potential therapeutic targets to detain the progression of inflammation and fibrosis in CKD are also presented ahead as a contribution in this book.

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“…These include, but are not limited to, genetic predisposition, autoimmunity, malignancy, infections, and exposure to drugs. 1 , 4 , 5 GN can be categorized into renal disorders with the presence of proliferative changes (including IgA nephropathy [IgAN], lupus nephritis [LN], ANCA-associated vasculitis [AAV], idiopathic membranoproliferative GN [MPGN], antiglomerular basement membrane GN, and postinfectious GN) or absence of proliferative changes (including minimal change disease [MCD], focal and segmental glomerulosclerosis [FSGS], idiopathic membranous nephropathy [MGN], and steroid-responsive and steroid-resistant nephrotic syndrome). 6 The overarching goals in GN treatment are to improve quality of life for patients, prevent ESRD, and reduce burden to our health care system.…”

Section: Introductionmentioning

confidence: 99%

Prospects for Precision Medicine in Glomerulonephritis Treatment

Liu

Chun

2018

Can J Kidney Health Dis

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Background:Glomerulonephritis (GN) consists of a group of kidney diseases that are categorized based on shared histopathological features. The current classifications for GN make it difficult to distinguish the individual variability in presentation, disease progression, and response to treatment. GN is a significant cause of end-stage renal disease (ESRD), and improved therapies are desperately needed because current immunosuppressive therapies sometimes lack efficacy and can lead to significant toxicities. In recent years, the combination of high-throughput genetic approaches and technological advances has identified important regulators contributing to GN.Objectives:In this review, we summarize recent findings in podocyte biology and advances in experimental approaches that have opened the possibility of precision medicine in GN treatment. We provide an integrative basic science and clinical overview of new developments in GN research and the discovery of potential candidates for targeted therapies in GN.Findings:Advances in podocyte biology have identified many candidates for therapeutic targets and potential biomarkers of glomerular disease. The goal of precision medicine in GN is now being pursued with recent technological improvements in genetics, accessibility of biologic and clinical information with tissue biobanks, high-throughput analysis of large-scale data sets, and new human model systems such as kidney organoids.Conclusion:With advances in data collection, technologies, and experimental model systems, we now have vast tools available to pursue precision medicine in GN. We anticipate a growing number of studies integrating data from high-throughput analysis with the development of diagnostic tools and targeted therapies for GN in the near future.

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Primary glomerulonephritis: A review of important recent discoveries

Cited by 12 publications

References 70 publications

First‐year GFR slope and long‐term renal outcome in IgA nephropathy

First‐year GFR slope and long‐term renal outcome in IgA nephropathy

Inflammation in Nonimmune-Mediated Chronic Kidney Disease

Prospects for Precision Medicine in Glomerulonephritis Treatment

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