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We are analyzing https://link.springer.com/article/10.1007/s00125-013-2857-5.

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.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Education
  • Science

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We don't see any clear sign of profit-making.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com could be secretly minting cash, but we can't detect the process.

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?

Schema {🗺️}

WebPage:
      mainEntity:
         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 &lt; 0.01). ERPF and renal blood flow were also comparatively higher and renal vascular resistance was lower in hyperfiltering patients (p &lt; 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 &lt; 0.01) and fibroblast growth factor-2, MCP-3 and CD40K excretion was elevated in hyperfiltering diabetic individuals vs healthy controls (p &lt; 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
         pageStart:1166
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         sameAs:https://doi.org/10.1007/s00125-013-2857-5
         keywords:
            Renal hyperfiltration
            Type 1 diabetes
            Urine cytokines/chemokines
            Internal Medicine
            Metabolic Diseases
            Human Physiology
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ScholarlyArticle:
      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 &lt; 0.01). ERPF and renal blood flow were also comparatively higher and renal vascular resistance was lower in hyperfiltering patients (p &lt; 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 &lt; 0.01) and fibroblast growth factor-2, MCP-3 and CD40K excretion was elevated in hyperfiltering diabetic individuals vs healthy controls (p &lt; 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
      pageStart:1166
      pageEnd:1173
      sameAs:https://doi.org/10.1007/s00125-013-2857-5
      keywords:
         Renal hyperfiltration
         Type 1 diabetes
         Urine cytokines/chemokines
         Internal Medicine
         Metabolic Diseases
         Human Physiology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00125-013-2857-5/MediaObjects/125_2013_2857_Fig1_HTML.gif
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         name:Springer-Verlag
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            name:J. W. Scholey
            affiliation:
                  name:University Health Network
                  address:
                     name:Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Canada
                     type:PostalAddress
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            name:D. Daneman
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                  name:University of Toronto
                  address:
                     name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
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            type:Person
            name:F. H. Mahmud
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                  name:University of Toronto
                  address:
                     name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
                     type:PostalAddress
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            type:Person
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                  name:University of Toronto
                  address:
                     name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
                     type:PostalAddress
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            type:Person
            name:V. Lai
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                  name:University Health Network
                  address:
                     name:Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Canada
                     type:PostalAddress
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                  address:
                     name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
                     type:PostalAddress
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                     name:Eve Technologies, Calgary, Canada
                     type:PostalAddress
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                     type:PostalAddress
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                  name:University Health Network
                  address:
                     name:Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Canada
                     type:PostalAddress
                  type:Organization
            type:Person
            name:D. Z. I. Cherney
            affiliation:
                  name:University of Toronto
                  address:
                     name:Division of Nephrology, Toronto General Hospital, University Health Network, Banting and Best Diabetes Centre, University of Toronto, Toronto, Canada
                     type:PostalAddress
                  type:Organization
            email:[email protected]
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      name:Diabetologia
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               name:Division of Nephrology, Toronto General Hospital, University Health Network, Banting and Best Diabetes Centre, University of Toronto, Toronto, Canada
               type:PostalAddress
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      name:J. W. Scholey
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            address:
               name:Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Canada
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      name:D. Daneman
      affiliation:
            name:University of Toronto
            address:
               name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
               type:PostalAddress
            type:Organization
      name:F. H. Mahmud
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            name:University of Toronto
            address:
               name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
               type:PostalAddress
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      name:R. Dekker
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            name:University of Toronto
            address:
               name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
               type:PostalAddress
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            address:
               name:Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Canada
               type:PostalAddress
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      name:Y. Elia
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            name:University of Toronto
            address:
               name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
               type:PostalAddress
            type:Organization
      name:M. L. Fritzler
      affiliation:
            name:Eve Technologies
            address:
               name:Eve Technologies, Calgary, Canada
               type:PostalAddress
            type:Organization
      name:E. B. Sochett
      affiliation:
            name:University of Toronto
            address:
               name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
               type:PostalAddress
            type:Organization
      name:H. N. Reich
      affiliation:
            name:University Health Network
            address:
               name:Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Canada
               type:PostalAddress
            type:Organization
      name:D. Z. I. Cherney
      affiliation:
            name:University of Toronto
            address:
               name:Division of Nephrology, Toronto General Hospital, University Health Network, Banting and Best Diabetes Centre, University of Toronto, Toronto, Canada
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Division of Nephrology, Toronto General Hospital, University Health Network, Banting and Best Diabetes Centre, University of Toronto, Toronto, Canada
      name:Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Canada
      name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
      name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
      name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
      name:Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Canada
      name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
      name:Eve Technologies, Calgary, Canada
      name:Division of Pediatric Endocrinology, Hospital for Sick Children, University of Toronto, Toronto, Canada
      name:Division of Nephrology, Toronto General Hospital, University Health Network, Toronto, Canada
      name:Division of Nephrology, Toronto General Hospital, University Health Network, Banting and Best Diabetes Centre, University of Toronto, Toronto, Canada

External Links {🔗}(178)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

4.03s.