Publications by authors named "William G Couser"

Primary membranous nephropathy is an autoimmune disease usually associated with antibody to phospholipase A2 receptor (anti-PLA2R). The study by Meyer-Schwesinger et al. describes the first mouse model induced using a PLA2R system to study the pathogenicity of anti-PLA2R.

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Primary Membranous Nephropathy.

Clin J Am Soc Nephrol

June 2017

Membranous nephropathy (MN) is a unique glomerular lesion that is the most common cause of idiopathic nephrotic syndrome in nondiabetic white adults. About 80% of cases are renal limited (primary MN, PMN) and 20% are associated with other systemic diseases or exposures (secondary MN). This review focuses only on PMN.

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This review updates current concepts of the genetic risk factors, etiologic events, nephtitogenic responses and treatment of the major immunologically mediated types of glomerulonephritis (GN). These include post-infectious GN, IgA nephropathy, anti-glomerular basement membrane (GBM) antibody disease, ANCA-associated vasculitis (AAV) and lupus nephritis. Although the etiology(s) of most GNs remain undefined, many are now believed to be initiated by environmental insults, particularly infectious processes, that trigger host responses in genetically susceptible individuals which lead to GN.

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O'Sullivan et al. describe glomerular localization of myeloperoxidase (MPO) in anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) and correlate the amount of deposition with severity of injury. MPO is the antigen against which anti-MPO ANCAs are directed, the antigen to which pathogenic T cells that can induce antibody-independent AAV are directed, and MPO can induce glomerular injury directly by interacting with H2O2 and a halide to halogenate glomerular structures.

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Twelve March 2015 will mark the 10th anniversary of World Kidney Day (WKD), an initiative of the International Society of Nephrology and the International Federation of Kidney Foundations. Since its inception in 2006, WKD has become the most successful effort ever mounted to raise awareness among decision-makers and the general public about the importance of kidney disease. Each year WKD reminds us that kidney disease is common, harmful and treatable.

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Glomerulonephritis (GN) due to infective endocarditis (IE) is well documented, but most available data are based on old autopsy series. To update information, we now present the largest biopsy-based clinicopathologic series on IE-associated GN. The study group included 49 patients (male-to-female ratio of 3.

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Despite major advances in understanding genetic predispositions ('first hits'), pathogenic immune responses, and the mediators of tissue injury in glomerulonephritis (GN), there remains a dearth of knowledge about the etiologic events, or 'second hits', which trigger these diseases. This paper reviews evidence that infections initiate most forms of GN through numerous simultaneous and/or sequential pathways that begin with activation of the innate immune response and lead to autoimmunity. These pathways include immune dysregulation, adjuvant or bystander effects, epitope spreading, molecular mimicry, epitope conformational changes, and antigen complementarity that, in genetically susceptible individuals, result in the nephritogenic autoimmune responses that underlie GN.

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Objective: To assess the prevalence of microalbuminuria and kidney dysfunction in low-income countries and in the USA.

Design: Cross-sectional study of screening programmes in five countries.

Setting: Screening programmes in Nepal, Bolivia, the USA (National Health and Nutrition Examination Survey (NHANES) 2005-2008) Bangladesh and Georgia.

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In the past 25 years the International Society of Nephrology has sponsored 545 physicians from 83 developing countries to undertake nephrology training in renal units in the developed world. Data collected biennially from past fellows have demonstrated a very positive impact of the program on individual trainees and their home institutions. Many of the trainees have gone on to leadership positions in their home institutions, countries, and regions.

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Genetically modified immune responses to infections and self-antigens initiate most forms of GN by generating pathogen- and danger-associated molecular patterns that stimulate Toll-like receptors and complement. These innate immune responses activate circulating monocytes and resident glomerular cells to release inflammatory mediators and initiate adaptive, antigen-specific immune responses that collectively damage glomerular structures. CD4 T cells are needed for B cell-driven antibody production that leads to immune complex formation in glomeruli, complement activation, and injury induced by both circulating inflammatory and resident glomerular effector cells.

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Noncommunicable diseases (NCDs) are the most common causes of premature death and morbidity and have a major impact on health-care costs, productivity, and growth. Cardiovascular disease, cancer, diabetes, and chronic respiratory disease have been prioritized in the Global NCD Action Plan endorsed by the World Health Assembly, because they share behavioral risk factors amenable to public-health action and represent a major portion of the global NCD burden. Chronic kidney disease (CKD) is a key determinant of the poor health outcomes of major NCDs.

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World Kidney Day is observed on March 10 every year and in 2011 the 6th annual event is going to be celebrated under the joint sponsorers - International Society of Nephrology and the International Federation of Kidney Foundations. The presence of chronic kidney disease significantly increases the risk of a cardiovascular event in both diabetes and hypertension. Proteinuria is always a marker of kidney disease.

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