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Title:
The effect of renal hyperfiltration on urinary inflammatory cytokines/chemokines in patients with uncomplicated type 1 diabetes mellitus | Diabetologia
Description:
Aims/hypothesis High intraglomerular pressure causes renal inflammation in experimental models of diabetes. Our objective was to determine whether renal hyperfiltration, a surrogate for intraglomerular hypertension, is associated with increased excretion of urinary cytokines/chemokines in patients with type 1 diabetes mellitus. Methods Blood pressure, renal haemodynamic function (inulin and para-aminohippurate clearances for glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), respectively) and urine samples were obtained during clamped euglycaemia in individuals with type 1 diabetes with either hyperfiltration (GFR determined using inulin [GFRINULIN] ≥135 ml min−1 1.73 m−2, n = 28) or normofiltration (n = 21) and healthy control individuals (n = 18). Results Baseline clinical characteristics, dietary sodium and protein intake and blood pressure levels were similar in the diabetic and healthy control groups. In addition, HbA1c levels were similar in the two diabetic groups. As expected baseline GFR was higher in hyperfilterers than either normofiltering diabetic patients or healthy control patients (165 ± 9 vs 113 ± 2 and 116 ± 4 ml min−1 1.73 m−2, respectively, p < 0.01). ERPF and renal blood flow were also comparatively higher and renal vascular resistance was lower in hyperfiltering patients (p < 0.01). Hyperfiltering diabetic patients had higher excretion rates for eotaxin, IFNα2, macrophage-derived chemokine, platelet-derived growth factor (PDGF)-AA, PDGF-AB/BB and granulocyte-macrophage colony-stimulating factor (p ≤ 0.01). Urinary monocyte chemoattractant protein (MCP)-1 and RANTES (regulated on activation, normal T expressed and secreted) excretion was also higher in hyperfiltering vs normofiltering diabetic individuals (p < 0.01) and fibroblast growth factor-2, MCP-3 and CD40K excretion was elevated in hyperfiltering diabetic individuals vs healthy controls (p < 0.01). Conclusions/interpretation Renal hyperfiltration is associated with increased urinary excretion of inflammatory cytokines/chemokines in patients with uncomplicated type 1 diabetes.
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Keywords {🔍}
diabetes, renal, urinary, article, type, pubmed, google, scholar, patients, cas, hyperfiltration, excretion, diabetic, mcp, cytokineschemokines, nephropathy, inulin, urine, participants, cherney, study, function, dmh, pressure, cytokinechemokine, disease, blood, factors, effect, filtration, gfrinulin, factor, early, toronto, uncomplicated, mellitus, protein, levels, group, university, kidney, data, intraglomerular, increased, glomerular, humans, inflammatory, scholey, rate, gfr,
Topics {✒️}
granulocyte-macrophage colony-stimulating factor granulocyte–macrophage colony-stimulating factor platelet-derived growth factor endogenous renin–angiotensin system urinary cytokine/chemokine assay urinary cytokine/chemokine excretion /userguides/tech1/proto_mpxhcyto-60k renin-angiotensin system activation macrophage inflammatory protein-1α human-cultured mesangial cells minimise false-positive results potentially high-risk group urinary inflammatory cytokines/chemokines including urinary cytokines/chemokines macrophage-derived chemokine renal physiology laboratory hyperglycaemia-induced neurohormonal activation fibroblast growth factor-2 end-stage renal disease controlled dietary preparation privacy choices/manage cookies increased urinary excretion translational physiology experiments inflammation/fibrosis full access temperature-controlled room electronic supplementary material established diabetes mellitus cherney dz related subjects increased sodium–glucose monocyte chemoattractant protein high dietary protein monocyte chemoattractant protein-3 monocyte chemoattractant protein-1 glomerular filtration rate inflammatory mediators correlates recent clinic visits pre-clinical stage renal tubular secretion kidney angiotensin ii renal vascular resistance pre-clinical biomarkers renal hyperfiltration related renal blood flow high intraglomerular pressure inflammatory cytokines/chemokines antidiabetic combination strategies late follicular phase urinary cytokines/chemokines
Questions {❓}
- Magee GM, Bilous RW, Cardwell CR, Hunter SJ, Kee F, Fogarty DG (2009) Is hyperfiltration associated with the future risk of developing diabetic nephropathy?
- Thomas MC, Moran JL, Harjutsalo V et al (2012) Hyperfiltration in type 1 diabetes: does it exist and does it matter for nephropathy?
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headline:The effect of renal hyperfiltration on urinary inflammatory cytokines/chemokines in patients with uncomplicated type 1 diabetes mellitus
description:High intraglomerular pressure causes renal inflammation in experimental models of diabetes. Our objective was to determine whether renal hyperfiltration, a surrogate for intraglomerular hypertension, is associated with increased excretion of urinary cytokines/chemokines in patients with type 1 diabetes mellitus. Blood pressure, renal haemodynamic function (inulin and para-aminohippurate clearances for glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), respectively) and urine samples were obtained during clamped euglycaemia in individuals with type 1 diabetes with either hyperfiltration (GFR determined using inulin [GFRINULIN] ≥135 ml min−1 1.73 m−2, n = 28) or normofiltration (n = 21) and healthy control individuals (n = 18). Baseline clinical characteristics, dietary sodium and protein intake and blood pressure levels were similar in the diabetic and healthy control groups. In addition, HbA1c levels were similar in the two diabetic groups. As expected baseline GFR was higher in hyperfilterers than either normofiltering diabetic patients or healthy control patients (165 ± 9 vs 113 ± 2 and 116 ± 4 ml min−1 1.73 m−2, respectively, p < 0.01). ERPF and renal blood flow were also comparatively higher and renal vascular resistance was lower in hyperfiltering patients (p < 0.01). Hyperfiltering diabetic patients had higher excretion rates for eotaxin, IFNα2, macrophage-derived chemokine, platelet-derived growth factor (PDGF)-AA, PDGF-AB/BB and granulocyte-macrophage colony-stimulating factor (p ≤ 0.01). Urinary monocyte chemoattractant protein (MCP)-1 and RANTES (regulated on activation, normal T expressed and secreted) excretion was also higher in hyperfiltering vs normofiltering diabetic individuals (p < 0.01) and fibroblast growth factor-2, MCP-3 and CD40K excretion was elevated in hyperfiltering diabetic individuals vs healthy controls (p < 0.01). Renal hyperfiltration is associated with increased urinary excretion of inflammatory cytokines/chemokines in patients with uncomplicated type 1 diabetes.
datePublished:2013-02-15T00:00:00Z
dateModified:2013-02-15T00:00:00Z
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Renal hyperfiltration
Type 1 diabetes
Urine cytokines/chemokines
Internal Medicine
Metabolic Diseases
Human Physiology
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headline:The effect of renal hyperfiltration on urinary inflammatory cytokines/chemokines in patients with uncomplicated type 1 diabetes mellitus
description:High intraglomerular pressure causes renal inflammation in experimental models of diabetes. Our objective was to determine whether renal hyperfiltration, a surrogate for intraglomerular hypertension, is associated with increased excretion of urinary cytokines/chemokines in patients with type 1 diabetes mellitus. Blood pressure, renal haemodynamic function (inulin and para-aminohippurate clearances for glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), respectively) and urine samples were obtained during clamped euglycaemia in individuals with type 1 diabetes with either hyperfiltration (GFR determined using inulin [GFRINULIN] ≥135 ml min−1 1.73 m−2, n = 28) or normofiltration (n = 21) and healthy control individuals (n = 18). Baseline clinical characteristics, dietary sodium and protein intake and blood pressure levels were similar in the diabetic and healthy control groups. In addition, HbA1c levels were similar in the two diabetic groups. As expected baseline GFR was higher in hyperfilterers than either normofiltering diabetic patients or healthy control patients (165 ± 9 vs 113 ± 2 and 116 ± 4 ml min−1 1.73 m−2, respectively, p < 0.01). ERPF and renal blood flow were also comparatively higher and renal vascular resistance was lower in hyperfiltering patients (p < 0.01). Hyperfiltering diabetic patients had higher excretion rates for eotaxin, IFNα2, macrophage-derived chemokine, platelet-derived growth factor (PDGF)-AA, PDGF-AB/BB and granulocyte-macrophage colony-stimulating factor (p ≤ 0.01). Urinary monocyte chemoattractant protein (MCP)-1 and RANTES (regulated on activation, normal T expressed and secreted) excretion was also higher in hyperfiltering vs normofiltering diabetic individuals (p < 0.01) and fibroblast growth factor-2, MCP-3 and CD40K excretion was elevated in hyperfiltering diabetic individuals vs healthy controls (p < 0.01). Renal hyperfiltration is associated with increased urinary excretion of inflammatory cytokines/chemokines in patients with uncomplicated type 1 diabetes.
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Renal hyperfiltration
Type 1 diabetes
Urine cytokines/chemokines
Internal Medicine
Metabolic Diseases
Human Physiology
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