Glomerulosclerosis, Focal Segmental
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Subject Areas on Research
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A circulating antibody panel for pretransplant prediction of FSGS recurrence after kidney transplantation.
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A glomerular transcriptomic landscape of apolipoprotein L1 in Black patients with focal segmental glomerulosclerosis.
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A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis.
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A novel missense mutation of Wilms' Tumor 1 causes autosomal dominant FSGS.
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ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation.
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APOL1 genotype-associated morphologic changes among patients with focal segmental glomerulosclerosis.
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APOL1 variants increase risk for FSGS and HIVAN but not IgA nephropathy.
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Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis.
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Blockade of the natriuretic peptide clearance receptor attenuates proteinuria in a mouse model of focal segmental glomerulosclerosis.
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Cells of renin lineage are progenitors of podocytes and parietal epithelial cells in experimental glomerular disease.
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Clinical and genetic heterogeneity in familial focal segmental glomerulosclerosis. International Collaborative Group for the Study of Familial Focal Segmental Glomerulosclerosis.
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Clinical and pathologic features of familial focal segmental glomerulosclerosis.
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Clinical trial of focal segmental glomerulosclerosis in children and young adults.
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Clinical trials treating focal segmental glomerulosclerosis should measure patient quality of life.
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Collapsing glomerulopathy associated with inherited mitochondrial injury.
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Comparing Kidney Health Outcomes in Children, Adolescents, and Adults With Focal Segmental Glomerulosclerosis.
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CureGN Study Rationale, Design, and Methods: Establishing a Large Prospective Observational Study of Glomerular Disease.
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Current views on collapsing glomerulopathy.
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De novo TRIM8 variants impair its protein localization to nuclear bodies and cause developmental delay, epilepsy, and focal segmental glomerulosclerosis.
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Design of the Nephrotic Syndrome Study Network (NEPTUNE) to evaluate primary glomerular nephropathy by a multidisciplinary approach.
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Evaluation of recurrent glomerulonephritis in kidney allografts.
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Exclusion of homozygous PLCE1 (NPHS3) mutations in 69 families with idiopathic and hereditary FSGS.
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Focal segmental glomerulosclerosis associated with nephrotic syndrome in cholesterol atheroembolism: clinicopathological correlations.
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Focal segmental glomerulosclerosis--epidemiology aspects in children and adults.
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Focal segmental glomerulosclerosis: a need for caution in live-related renal transplantation.
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Global glomerulosclerosis with nephrotic syndrome; the clinical importance of age adjustment.
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Gq signaling causes glomerular injury by activating TRPC6.
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Graft loss due to recurrent focal segmental glomerulosclerosis in renal transplant recipients in the United States.
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HIV-associated nephropathy: clinical presentation, pathology, and epidemiology in the era of antiretroviral therapy.
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Idiopathic collapsing focal segmental glomerulosclerosis: a clinicopathologic study.
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Inaxaplin for Proteinuric Kidney Disease in Persons with Two APOL1 Variants.
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Inverted formin 2 mutations with variable expression in patients with sporadic and hereditary focal and segmental glomerulosclerosis.
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Kidney Biopsy Features Most Predictive of Clinical Outcomes in the Spectrum of Minimal Change Disease and Focal Segmental Glomerulosclerosis.
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Linkage of a gene causing familial focal segmental glomerulosclerosis to chromosome 11 and further evidence of genetic heterogeneity.
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Losing their footing: Rac1 signaling causes podocyte detachment and FSGS.
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Management of idiopathic childhood nephrotic syndrome in sub-Saharan Africa: Ibadan consensus statement.
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Modulation of podocyte phenotype in collapsing glomerulopathies.
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Mutations in the gene that encodes the F-actin binding protein anillin cause FSGS.
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Open-Label Clinical Trials of Oral Pulse Dexamethasone for Adults with Idiopathic Nephrotic Syndrome.
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Pathogenesis and therapy of focal segmental glomerulosclerosis: an update.
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Podocyte biology in segmental sclerosis and progressive glomerular injury.
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Podocyte effacement closely links to suPAR levels at time of posttransplantation focal segmental glomerulosclerosis occurrence and improves with therapy.
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Precision nephrology identified tumor necrosis factor activation variability in minimal change disease and focal segmental glomerulosclerosis.
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Prevalence of Cardiovascular Disease Risk Factors in Childhood Glomerular Diseases.
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Progressive glomerulosclerosis and enhanced renal accumulation of basement membrane components in mice transgenic for human immunodeficiency virus type 1 genes.
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Proteinuria in pediatric renal transplant recipients during the first 60 post-transplant days.
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Quantification of Glomerular Structural Lesions: Associations With Clinical Outcomes and Transcriptomic Profiles in Nephrotic Syndrome.
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Race and glomerulonephritis in patients with and without hepatosplenic Schistosomiasis mansoni.
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Rapid Progression of Focal Segmental Glomerulosclerosis in Patients with High-Risk APOL1 Genotypes.
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Rare hereditary COL4A3/COL4A4 variants may be mistaken for familial focal segmental glomerulosclerosis.
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Recurrence of nephrotic syndrome following kidney transplantation is associated with initial native kidney biopsy findings.
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Regarding Maas's editorial letter on serum suPAR levels.
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Renal disease in type I glycogen storage disease.
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Renal involvement in type I glycogen storage disease.
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Spectrum of disease in familial focal and segmental glomerulosclerosis.
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TRPC Channels in Proteinuric Kidney Diseases.
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The Application of Digital Pathology to Improve Accuracy in Glomerular Enumeration in Renal Biopsies.
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The Human FSGS-Causing ANLN R431C Mutation Induces Dysregulated PI3K/AKT/mTOR/Rac1 Signaling in Podocytes.
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The author replies.
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The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy.
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Therapeutic targets in focal and segmental glomerulosclerosis.
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Type I glycogen storage disease: kidney involvement, pathogenesis and its treatment.
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Ultrastructural Characterization of Proteinuric Patients Predicts Clinical Outcomes.
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Unexpected role of TRPC6 channel in familial nephrotic syndrome: does it have clinical implications?
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Keywords of People