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glomerulonephritis/hypoxia
L'enllaç es desa al porta-retalls
Pàgina 1 des de 61 resultats
Hypoxia-inducible factor-1alpha is involved in the attenuation of experimentally induced rat glomerulonephritis.
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OBJECTIVE
Among various kidney disease models, there are few rat glomerulonephritis (GN) models that develop in a short time, and with mainly glomerular lesions. Hypoxia-inducible factor (HIF)-1alpha is a transcriptional factor that induces genes supporting cell survival, but the involvement of
Arteriolar hyalinosis and arterial hypertension as possible surrogate markers of reduced interstitial blood flow and hypoxia in glomerulonephritis.
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BACKGROUND
In glomerulonephritis the final common pathway to end-stage renal disease (ESRD) is tubulo-interstitial damage (TID) whose main determinants are proteinuria and hypoxia consequent to haemodynamic and vascular alterations that reduce interstitial blood flow. Since oxygen tension is
Hypoperfusion of peritubular capillaries induces chronic hypoxia before progression of tubulointerstitial injury in a progressive model of rat glomerulonephritis.
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Chronic hypoxia likely plays a pivotal role in chronic renal disease, but the specifics of its involvement remain unclear. To elucidate how chronic hypoxia occurs and whether hypoxia participates in the progression of renal disease, the authors established an irreversible glomerulonephritis model
Analysis of relative expression level of VEGF ( vascular endothelial growth factor ), HIF-1α ( hypoxia inducible factor 1α ) and CTGF ( connective tissue growth factor ) genes in chronic glomerulonephritis (CGN) patients.
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Analysis of gene expression in renal tissue is considered to be a diagnostic tool predicting the clinical course of glomerulonephritis. The present study quantified the relative transcript levels of VEGF, CTGF and HIF-1α in renal tissue to establish their relationship with some clinical
[Spirographic data concerning oxygen deficiency in patients with chronic glomerulonephritis].
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[Oxygen deficiency in patients with chronic glomerulonephritis].
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Serious pulmonary hemorrhage, glomerulonephritis, and massive steroid therapy.
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A patient suffered from acute glomerulonephritis with modest renal impairment and life-threatening pulmonary hemorrhage. The pulmonary hemorrhage caused severe hypoxia that necessitated artificial ventilation. As a last resort, 1 g/day of methylprednisolone was administered intravenously. Rapid
Effects of chronic hypoxia on renal PDGF-A, PDGF-B, and VEGF gene expression in rats.
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There is evidence from in vitro studies to suggest that the genes of platelet-derived growth factor (PDGF), and vascular endothelial growth factor (VEGF) are, like the erythropoietin gene, regulated by oxygen tension. Hypoxia-induced stimulation of, for example, PDGF or VEGF might be
Effects of hypoxia on growth factor expression in the rat kidney in vivo.
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There is accumulating evidence from in vitro studies suggesting that the genes of endothelin-1, PDGF, and VEGF are, like the erythropoietin gene, regulated by oxygen tension and by divalent cations. Hypoxia-induced stimulation of, such as endothelin-1, PDGF or VEGF might be involved in the
Dysfunction of erythropoietin-producing interstitial cells in the kidneys of ICR-derived glomerulonephritis (ICGN) mice.
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Anemia is a major secondary symptom in chronic renal disorder (CRD), but the precise cause of insufficient production of erythropoietin (EPO) remains unclear owing to the controversial localization of EPO-producing cells in the kidneys. The ICR-derived glomerulonephritis (ICGN) mouse, a new
Erythropoietin-producing cells in the liver of ICR-derived glomerulonephritis (ICGN) mice.
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The ICR-derived glomerulonephritis (ICGN) mouse is an appropriate model for anemia associated with chronic renal disorder (CRD). Insufficient renal production of erythropoietin (EPO) induces the anemia associated with CRD. EPO mRNA is expressed in both kidneys and liver of progressing-stage ICGN
ANCA-negative glomerulonephritis associated with nonasthmatic Churg-Strauss syndrome.
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A 36-year-old white male with a history of allergic rhinitis and sinusitis presented to the emergency room with abdominal pain and diarrhea. Physical examination revealed fever, hypoxemia and a maculopapular rash. Laboratory tests showed proteinuria, hematuria, leukocytosis, eosinophilia
Expression of transforming growth factor-beta1 and hypoxia-inducible factor-1alpha in renal transplantation.
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Chronic allograft nephropathy (CAN) includes pathologic changes of interstitial fibrosis, tubular atrophy, and fibrous intimal thickening. Transforming growth factor (TGF)-beta1 is a fibrogenic cytokine involved in renal allograft fibrosis. Hypoxia-inducible factor (HIF)-1alpha is induced as an
Regulation of hypoxia-inducible factor 2-a is essential for integrity of the glomerular barrier.
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Deletion of the von Hippel-Lindau tumor suppressor (Vhl) gene from renal podocytes of mice (podVhl KO) leads to rapidly progressive glomerulonephritis (RPGN), a clinical syndrome characterized by rapid loss of renal function and crescents on renal biopsy. Genomic profiling of glomeruli isolated from
Factor inhibiting HIF limits the expression of hypoxia-inducible genes in podocytes and distal tubular cells.
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The two hypoxia-inducible factors (HIF-1α and HIF-2α) are transcription factors that regulate the response to hypoxia. Recently, the factor inhibiting HIF (FIH1) was identified as a molecular oxygen-dependent dioxygenase that blunts the transcriptional activity of HIF and has also been implicated in
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