Physician
Nephrology
Dr. Wayne A. Border, MD
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Wayne Border is an expert in the field of Nephrology. He graduated from Washington University School of Medicine in St. Louis. Wayne Border has written publications. He has 101 publications published with PubMed. The lastest publication is: 'Increased levels of transforming growth factor-beta in HIV-associated nephropathy.'
Publications
- Targeting reduction of proteinuria in glomerulonephritis: Maximizing the antifibrotic effect of valsartan by protecting podocytes.
- Receptor-mediated nonproteolytic activation of prorenin and induction of TGF-β1 and PAI-1 expression in renal mesangial cells.
- Combining angiotensin II blockade and renin receptor inhibition results in enhanced antifibrotic effect in experimental nephritis.
- Infusion of angiotensin-(1-7) reduces glomerulosclerosis through counteracting angiotensin II in experimental glomerulonephritis.
- Mechanisms underlying the antifibrotic properties of noninhibitory PAI-1 (PAI-1R) in experimental nephritis.
- Receptor-dependent prorenin activation and induction of PAI-1 expression in vascular smooth muscle cells.
- Aldosterone and TGF-beta1 synergistically increase PAI-1 and decrease matrix degradation in rat renal mesangial and fibroblast cells.
- A PAI-1 mutant, PAI-1R, slows progression of diabetic nephropathy.
- Functional renin receptors in renal mesangial cells.
- Curcumin blocks fibrosis in anti-Thy 1 glomerulonephritis through up-regulation of heme oxygenase 1.
- Combining TGF-beta inhibition and angiotensin II blockade results in enhanced antifibrotic effect.
- Curcumin blocks multiple sites of the TGF-beta signaling cascade in renal cells.
- TGF-beta isoforms in renal fibrogenesis.
- Genes expressed by the kidney, but not by bone marrow-derived cells, underlie the genetic predisposition to progressive glomerulosclerosis after mesangial injury.
- A mutant, noninhibitory plasminogen activator inhibitor type 1 decreases matrix accumulation in experimental glomerulonephritis.
- L-arginine supplementation accelerates renal fibrosis and shortens life span in experimental lupus nephritis.
- Angiotensin II and progressive renal insufficiency.
- Clinical and antibody responses after influenza immunization in systemic lupus erythematosus.
- Henoch-Schönlein purpura: simultaneous demonstration of IgA deposits in involved skin, intestine, and kidney.
- In situ formation of subepithelial immune complexes in the rabbit glomerulus: requirement of a cationic antigen.
- Antigenic changes as a determinant of immune complex localization in the rat glomerulus.
- IgA antibasement membrane nephritis with pulmonary hemorrhage.
- Circulating immune complexes in rats with autologous immune complex nephritis.
- Antitubular basement-membrane antibodies in methicillin-associated interstitial nephritis.
- Crescentic glomerulonephritis: immune vs. nonimmune mechanisms.
- Hypersensitivity phenomena and the kidney: role of drugs and environmental agents.
- Immune complex detection in glomerular diseases.
- Circulating immune complexes in adults with idiopathic nephrotic syndrome. Collaborative Study of the Adult Idiopathic Nephrotic Syndrome.
- Detection of circulating immune complexes in patients with glomerulonephritis.
- Extracellular matrix/growth factor interactions.
- Integrins.
- Gallium citrate Ga 67 scanning in acute renal failure.
- Role of immunoglobulin class in mediation of experimental mesangial glomerulonephritis.
- The 260-kDa transforming growth factor (TGF)-beta binding protein in rat glomeruli is a complex comprised of 170- and 85-kDa TGF-beta binding proteins.
- Nephritic factor: Description of a new quantitative assay and findings in glomerulonephritis.
- Induction of membranous nephropathy in rabbits by administration of an exogenous cationic antigen.
- Electrical charge. Its role in the pathogenesis and prevention of experimental membranous nephropathy in the rabbit.
- Extracellular matrix and glomerular disease.
- From serum sickness to cytokines: advances in understanding the molecular pathogenesis of kidney disease.
- Transforming growth factor-beta in disease: the dark side of tissue repair.
- Cytokines and L-arginine in renal injury and repair.
- Transforming growth factor-beta and the pathogenesis of glomerular diseases.
- Role of transforming growth factor beta and decorin in controlling fibrosis.
- Failure of angiotensin converting enzyme inhibition to affect the course of chronic puromycin aminonucleoside nephropathy.
- Molecular and cellular biological techniques in the study of glomerular diseases.
- Failure of heparin to affect two types of experimental glomerulonephritis in rabbits.
- Suppression of experimental glomerulonephritis by antiserum against transforming growth factor beta 1.
- Role of proteoglycans and cytoskeleton in the effects of TGF-beta 1 on renal proximal tubule cells.
- Distinguishing minimal-change disease from mesangial disorders.
- Changes in heparan sulfate correlate with increased glomerular permeability.
- Transforming growth factor-beta 1 induces extracellular matrix formation in glomerulonephritis.
- Dietary protein restriction rapidly reduces transforming growth factor beta 1 expression in experimental glomerulonephritis.
- Enalapril and low protein reverse chronic puromycin aminonucleoside nephropathy.
- Transforming growth factor-beta in glomerular injury.
- Increased expression of transforming growth factor-beta in renal disease.
- Targeting TGF-beta for treatment of disease.
- Transforming growth factor-beta and extracellular matrix deposition in the kidney.
- Transforming growth factor beta in tissue fibrosis.
- Gene therapy by skeletal muscle expression of decorin prevents fibrotic disease in rat kidney.
- Cytokines in kidney disease: the role of transforming growth factor-beta.
- Role of TGF-beta 1 in experimental glomerulonephritis.
- Transforming growth factor-beta in human glomerular injury.
- Maximizing hemodynamic-independent effects of angiotensin II antagonists in fibrotic diseases.
- Natural inhibitor of transforming growth factor-beta protects against scarring in experimental kidney disease.
- Effect of maximal reduction of angiotensin in renal fibrosis: bad news-good news from a pediatric mouse.
- Transforming growth factor-beta regulates production of proteoglycans by mesangial cells.
- Production of extracellular matrix by glomerular epithelial cells is regulated by transforming growth factor-beta 1.
- Evidence that TGF-beta should be a therapeutic target in diabetic nephropathy.
- Transforming growth factor beta in diabetic nephropathy.
- Fibrosis linked to TGF-beta in yet another disease.
- In vivo interactions of TGF-beta and extracellular matrix.
- Nitric oxide mediates immunologic injury to kidney mesangium in experimental glomerulonephritis.
- TGF-beta: a cytokine mediator of glomerulosclerosis and a target for therapeutic intervention.
- L-arginine may mediate the therapeutic effects of low protein diets.
- Expression of transforming growth factor beta is elevated in human and experimental diabetic nephropathy.
- Elevated expression of transforming growth factor-beta and proteoglycan production in experimental glomerulonephritis. Possible role in expansion of the mesangial extr...
- Coordinated expression of beta 1 integrins and transforming growth factor-beta-induced matrix proteins in glomerulonephritis.
- Gene therapy by transforming growth factor-beta receptor-IgG Fc chimera suppressed extracellular matrix accumulation in experimental glomerulonephritis.
- Angiotensin II in renal fibrosis: should TGF-beta rather than blood pressure be the therapeutic target?
- Increased levels of transforming growth factor-beta in HIV-associated nephropathy.
- Interactions of transforming growth factor-beta and angiotensin II in renal fibrosis.
- L-arginine metabolism in immune-mediated glomerulonephritis in the rat.
- From rats to man: a perspective on dietary L-arginine supplementation in human renal disease.
- Dual effects of angiotensin II on the plasminogen/plasmin system in rat mesangial cells.
- Transforming growth factor-beta and angiotensin II: the missing link from glomerular hyperfiltration to glomerulosclerosis?
- Targeting TGF-beta overexpression: maximizing the antifibrotic actions of angiotensin II blockade in anti-Thy1 glomerulonephritis.
- Perspectives on blockade of TGFbeta overexpression.
- Angiotensin II, TGF-beta and renal fibrosis.
- Role of transforming growth factor-beta 1 in experimental chronic cyclosporine nephropathy.
- Transforming growth factor-beta and matrix protein expression in acute and chronic rejection of human renal allografts.
- Antagonists of transforming growth factor-beta: a novel approach to treatment of glomerulonephritis and prevention of glomerulosclerosis.
- TGF-beta in kidney fibrosis: a target for gene therapy.
- Expression of transforming growth factor-beta isoforms in human glomerular diseases.
- Glomerular matrix accumulation is linked to inhibition of the plasmin protease system.
- Angiotensin II stimulates extracellular matrix protein synthesis through induction of transforming growth factor-beta expression in rat glomerular mesangial cells.
- Targeting TGF-beta overexpression in renal disease: maximizing the antifibrotic action of angiotensin II blockade.
- Sustained expression of TGF-beta 1 underlies development of progressive kidney fibrosis.
- t-PA promotes glomerular plasmin generation and matrix degradation in experimental glomerulonephritis.
- Angiotensin II blockade and low-protein diet produce additive therapeutic effects in experimental glomerulonephritis.
- L-Arginine supplementation increases mesangial cell injury and subsequent tissue fibrosis in experimental glomerulonephritis.
Schools
Washington University St Louis
North Carolina Memorial Hospital
Doctors Specialties
- Nephrology
Accepted Insurances
Education
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University of North Carolina Hospitals -
Washington University School of Medicine in St. Louis
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