Glomerulosclerosis, Focal Segmental
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Subject Areas on Research
- A circulating antibody panel for pretransplant prediction of FSGS recurrence after kidney transplantation.
- A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis.
- A novel missense mutation of Wilms' Tumor 1 causes autosomal dominant FSGS.
- APOL1 variants increase risk for FSGS and HIVAN but not IgA nephropathy.
- Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis.
- Cells of renin lineage are progenitors of podocytes and parietal epithelial cells in experimental glomerular disease
- Clinical and genetic heterogeneity in familial focal segmental glomerulosclerosis. International Collaborative Group for the Study of Familial Focal Segmental Glomerulosclerosis.
- Clinical and pathologic features of familial focal segmental glomerulosclerosis.
- Clinical trial of focal segmental glomerulosclerosis in children and young adults.
- Clinical trials treating focal segmental glomerulosclerosis should measure patient quality of life.
- Collapsing glomerulopathy associated with inherited mitochondrial injury.
- Current views on collapsing glomerulopathy.
- Design of the Nephrotic Syndrome Study Network (NEPTUNE) to evaluate primary glomerular nephropathy by a multidisciplinary approach.
- Exclusion of homozygous PLCE1 (NPHS3) mutations in 69 families with idiopathic and hereditary FSGS.
- Focal segmental glomerulosclerosis associated with nephrotic syndrome in cholesterol atheroembolism: clinicopathological correlations.
- Focal segmental glomerulosclerosis: a need for caution in live-related renal transplantation.
- Global glomerulosclerosis with nephrotic syndrome; the clinical importance of age adjustment.
- Gq signaling causes glomerular injury by activating TRPC6.
- Graft loss due to recurrent focal segmental glomerulosclerosis in renal transplant recipients in the United States.
- HIV-associated nephropathy: clinical presentation, pathology, and epidemiology in the era of antiretroviral therapy.
- Idiopathic collapsing focal segmental glomerulosclerosis: a clinicopathologic study.
- Inverted formin 2 mutations with variable expression in patients with sporadic and hereditary focal and segmental glomerulosclerosis.
- Linkage of a gene causing familial focal segmental glomerulosclerosis to chromosome 11 and further evidence of genetic heterogeneity.
- Losing their footing: Rac1 signaling causes podocyte detachment and FSGS.
- Modulation of podocyte phenotype in collapsing glomerulopathies.
- Mutations in the gene that encodes the F-actin binding protein anillin cause FSGS.
- Outcome of living donor renal allograft survival in children with focal segmental glomerulosclerosis.
- Pathogenesis and therapy of focal segmental glomerulosclerosis: an update.
- Podocyte biology in segmental sclerosis and progressive glomerular injury.
- Podocyte effacement closely links to suPAR levels at time of posttransplantation focal segmental glomerulosclerosis occurrence and improves with therapy.
- Progressive glomerulosclerosis and enhanced renal accumulation of basement membrane components in mice transgenic for human immunodeficiency virus type 1 genes.
- Rare hereditary COL4A3/COL4A4 variants may be mistaken for familial focal segmental glomerulosclerosis.
- Regarding Maas's editorial letter on serum suPAR levels.
- Spectrum of disease in familial focal and segmental glomerulosclerosis.
- The Application of Digital Pathology to Improve Accuracy in Glomerular Enumeration in Renal Biopsies.
- The author replies.
- The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy.
- Therapeutic targets in focal and segmental glomerulosclerosis.
- Unexpected role of TRPC6 channel in familial nephrotic syndrome: does it have clinical implications?
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Keywords of People
- Middleton, John Paul, Associate Professor of Medicine, Medicine, Nephrology