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We are analyzing https://link.springer.com/article/10.1007/s00125-004-1542-0.

Title:
Aldosterone escape during blockade of the renin–angiotensin–aldosterone system in diabetic nephropathy is associated with enhanced decline in glomerular filtration rate | Diabetologia
Description:
It has been suggested that aldosterone plays a role in the initiation and progression of renal disease independently of arterial blood pressure and plasma angiotensin II levels. We evaluated the influence of plasma aldosterone levels on progression of diabetic nephropathy during long-term blockade of the renin–angiotensin–aldosterone system. A total of 63 hypertensive patients with type 1 diabetes and diabetic nephropathy were treated with losartan, 100 mg once daily, for a mean follow-up period of 35 months. Plasma aldosterone, GFR, albuminuria and 24-h blood pressure were determined at baseline and at regular intervals during the study. Patients were divided according to their increasing or decreasing levels of plasma aldosterone during long-term losartan treatment in an escape group (n=26) and a non-escape group (n=37). In the escape group, aldosterone levels increased from (geometric mean [95% CI]) 57 pg/ml (43–76 pg/ml) at 2 months, to 102 pg/ml (78–134 pg/ml) at the end of the study (p<0.01). The corresponding levels in the non-escape group were 83 pg/ml (69–102 pg/ml) and 49 pg/ml (40–60 pg/ml; p<0.01). The median rate of decline in GFR was 5.0 ml¡min−1¡year−1 (range 0.4–15.9 ml¡min−1¡year−1) in the escape group, compared with 2.4 ml¡min−1¡year−1 (−1.6 to 11.0 ml¡min−1¡year−1) in the non-escape group (p<0.005). The increase in plasma aldosterone correlated with the rate of decline in GFR (r 2=0.19, p<0.001), corresponding to a decline in GFR of 1.5 ml¡min−1¡year−1 for every two-fold increase in plasma aldosterone. Pre-treatment and treatment values of plasma aldosterone were not related to albuminuria or to changes in albuminuria during the study. Our data suggest that aldosterone escape during long-term blockade of the renin–angiotensin–aldosterone system is associated with an enhanced decline in GFR in patients with type 1 diabetes and diabetic nephropathy.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Fitness & Wellness
  • Science

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What CMS is link.springer.com built with?

Custom-built

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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 can't see how the site brings in money.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

aldosterone, plasma, patients, escape, pgml, study, gfr, decline, levels, treatment, diabetes, group, diabetic, nephropathy, blockade, rate, mlminyear, blood, pressure, albuminuria, groups, type, months, baseline, article, longterm, losartan, end, angii, table, cas, pubmed, google, scholar, data, increase, reninangiotensinaldosterone, system, nonescape, raas, renin, phenomenon, privacy, cookies, enhanced, suggested, angiotensin, compared, related, combination,

Topics {✒️}

renin–angiotensin–aldosterone system angiotensin-converting enzyme inhibitors long-term raas blockade long-term renoprotective effects long-term clinical trials angiotensin-converting enzyme grant/research support long-term arb treatment chronic heart failure long-term losartan treatment renal disease independently calcium channel blockers privacy choices/manage cookies angiotensin ii coronary heart disease ace insertion/deletion genotype long-term blockade glomerular filtration rate receptor antagonists regression dilution bias elevated aldosterone levels incomplete raas blockade coat-a-count ace dd genotype aldosterone levels increased aldosterone levels decreased developed aldosterone escape develop aldosterone escape european economic area lower circulating level plasma aldosterone levels renal vascular responses aldosterone escape phenomenon conditions privacy policy recent clinical trials left ventricular dysfunction additional antihypertensive treatment 10 mm hg corresponds alpha-blocking agent escape phenomenon occurs pre-treatment levels progressive renal dysfunction table 2 plasma aldosterone urinary aldosterone excretion plasma aldosterone correlated 0 ml·min−1·year−1 9 ml·min−1·year−1 4 ml·min−1·year−1 5 ml·min−1·year−1 82 ml·min−1·year−1

Questions {❓}

  • (2003) Long-term renoprotective effects of losartan in diabetic nephropathy: interaction with ACE insertion/deletion genotype?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Aldosterone escape during blockade of the renin–angiotensin–aldosterone system in diabetic nephropathy is associated with enhanced decline in glomerular filtration rate
         description:It has been suggested that aldosterone plays a role in the initiation and progression of renal disease independently of arterial blood pressure and plasma angiotensin II levels. We evaluated the influence of plasma aldosterone levels on progression of diabetic nephropathy during long-term blockade of the renin–angiotensin–aldosterone system. A total of 63 hypertensive patients with type 1 diabetes and diabetic nephropathy were treated with losartan, 100 mg once daily, for a mean follow-up period of 35 months. Plasma aldosterone, GFR, albuminuria and 24-h blood pressure were determined at baseline and at regular intervals during the study. Patients were divided according to their increasing or decreasing levels of plasma aldosterone during long-term losartan treatment in an escape group (n=26) and a non-escape group (n=37). In the escape group, aldosterone levels increased from (geometric mean [95% CI]) 57 pg/ml (43–76 pg/ml) at 2 months, to 102 pg/ml (78–134 pg/ml) at the end of the study (p<0.01). The corresponding levels in the non-escape group were 83 pg/ml (69–102 pg/ml) and 49 pg/ml (40–60 pg/ml; p<0.01). The median rate of decline in GFR was 5.0 ml¡min−1¡year−1 (range 0.4–15.9 ml¡min−1¡year−1) in the escape group, compared with 2.4 ml¡min−1¡year−1 (−1.6 to 11.0 ml¡min−1¡year−1) in the non-escape group (p<0.005). The increase in plasma aldosterone correlated with the rate of decline in GFR (r 2=0.19, p<0.001), corresponding to a decline in GFR of 1.5 ml¡min−1¡year−1 for every two-fold increase in plasma aldosterone. Pre-treatment and treatment values of plasma aldosterone were not related to albuminuria or to changes in albuminuria during the study. Our data suggest that aldosterone escape during long-term blockade of the renin–angiotensin–aldosterone system is associated with an enhanced decline in GFR in patients with type 1 diabetes and diabetic nephropathy.
         datePublished:2004-11-17T00:00:00Z
         dateModified:2004-11-17T00:00:00Z
         pageStart:1936
         pageEnd:1939
         sameAs:https://doi.org/10.1007/s00125-004-1542-0
         keywords:
            Aldosterone escape
            Angiotensin II receptor blockade
            Diabetes
            Diabetic nephropathy
            Renin–angiotensin–aldosterone system
            Internal Medicine
            Metabolic Diseases
            Human Physiology
         image:
         isPartOf:
            name:Diabetologia
            issn:
               1432-0428
               0012-186X
            volumeNumber:47
            type:
               Periodical
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                     address:
                        name:Steno Diabetes Center, Gentofte, Denmark
                        type:PostalAddress
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               type:Person
               name:S. Andersen
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                     name:Steno Diabetes Center
                     address:
                        name:Steno Diabetes Center, Gentofte, Denmark
                        type:PostalAddress
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                     name:Steno Diabetes Center
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                        name:Steno Diabetes Center, Gentofte, Denmark
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                     name:Steno Diabetes Center
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                        name:Steno Diabetes Center, Gentofte, Denmark
                        type:PostalAddress
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                     name:Steno Diabetes Center
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                        name:Steno Diabetes Center, Gentofte, Denmark
                        type:PostalAddress
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                     name:University of Aarhus
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                        name:Faculty of Health Science, University of Aarhus, Denmark
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ScholarlyArticle:
      headline:Aldosterone escape during blockade of the renin–angiotensin–aldosterone system in diabetic nephropathy is associated with enhanced decline in glomerular filtration rate
      description:It has been suggested that aldosterone plays a role in the initiation and progression of renal disease independently of arterial blood pressure and plasma angiotensin II levels. We evaluated the influence of plasma aldosterone levels on progression of diabetic nephropathy during long-term blockade of the renin–angiotensin–aldosterone system. A total of 63 hypertensive patients with type 1 diabetes and diabetic nephropathy were treated with losartan, 100 mg once daily, for a mean follow-up period of 35 months. Plasma aldosterone, GFR, albuminuria and 24-h blood pressure were determined at baseline and at regular intervals during the study. Patients were divided according to their increasing or decreasing levels of plasma aldosterone during long-term losartan treatment in an escape group (n=26) and a non-escape group (n=37). In the escape group, aldosterone levels increased from (geometric mean [95% CI]) 57 pg/ml (43–76 pg/ml) at 2 months, to 102 pg/ml (78–134 pg/ml) at the end of the study (p<0.01). The corresponding levels in the non-escape group were 83 pg/ml (69–102 pg/ml) and 49 pg/ml (40–60 pg/ml; p<0.01). The median rate of decline in GFR was 5.0 ml¡min−1¡year−1 (range 0.4–15.9 ml¡min−1¡year−1) in the escape group, compared with 2.4 ml¡min−1¡year−1 (−1.6 to 11.0 ml¡min−1¡year−1) in the non-escape group (p<0.005). The increase in plasma aldosterone correlated with the rate of decline in GFR (r 2=0.19, p<0.001), corresponding to a decline in GFR of 1.5 ml¡min−1¡year−1 for every two-fold increase in plasma aldosterone. Pre-treatment and treatment values of plasma aldosterone were not related to albuminuria or to changes in albuminuria during the study. Our data suggest that aldosterone escape during long-term blockade of the renin–angiotensin–aldosterone system is associated with an enhanced decline in GFR in patients with type 1 diabetes and diabetic nephropathy.
      datePublished:2004-11-17T00:00:00Z
      dateModified:2004-11-17T00:00:00Z
      pageStart:1936
      pageEnd:1939
      sameAs:https://doi.org/10.1007/s00125-004-1542-0
      keywords:
         Aldosterone escape
         Angiotensin II receptor blockade
         Diabetes
         Diabetic nephropathy
         Renin–angiotensin–aldosterone system
         Internal Medicine
         Metabolic Diseases
         Human Physiology
      image:
      isPartOf:
         name:Diabetologia
         issn:
            1432-0428
            0012-186X
         volumeNumber:47
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:K. J. Schjoedt
            affiliation:
                  name:Steno Diabetes Center
                  address:
                     name:Steno Diabetes Center, Gentofte, Denmark
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:S. Andersen
            affiliation:
                  name:Steno Diabetes Center
                  address:
                     name:Steno Diabetes Center, Gentofte, Denmark
                     type:PostalAddress
                  type:Organization
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            name:P. Rossing
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                  name:Steno Diabetes Center
                  address:
                     name:Steno Diabetes Center, Gentofte, Denmark
                     type:PostalAddress
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            name:L. Tarnow
            affiliation:
                  name:Steno Diabetes Center
                  address:
                     name:Steno Diabetes Center, Gentofte, Denmark
                     type:PostalAddress
                  type:Organization
            type:Person
            name:H.-H. Parving
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                  name:Steno Diabetes Center
                  address:
                     name:Steno Diabetes Center, Gentofte, Denmark
                     type:PostalAddress
                  type:Organization
                  name:University of Aarhus
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                     name:Faculty of Health Science, University of Aarhus, Denmark
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         name:Steno Diabetes Center, Gentofte, Denmark
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         name:Steno Diabetes Center, Gentofte, Denmark
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            name:Steno Diabetes Center
            address:
               name:Steno Diabetes Center, Gentofte, Denmark
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:S. Andersen
      affiliation:
            name:Steno Diabetes Center
            address:
               name:Steno Diabetes Center, Gentofte, Denmark
               type:PostalAddress
            type:Organization
      name:P. Rossing
      affiliation:
            name:Steno Diabetes Center
            address:
               name:Steno Diabetes Center, Gentofte, Denmark
               type:PostalAddress
            type:Organization
      name:L. Tarnow
      affiliation:
            name:Steno Diabetes Center
            address:
               name:Steno Diabetes Center, Gentofte, Denmark
               type:PostalAddress
            type:Organization
      name:H.-H. Parving
      affiliation:
            name:Steno Diabetes Center
            address:
               name:Steno Diabetes Center, Gentofte, Denmark
               type:PostalAddress
            type:Organization
            name:University of Aarhus
            address:
               name:Faculty of Health Science, University of Aarhus, Denmark
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Steno Diabetes Center, Gentofte, Denmark
      name:Steno Diabetes Center, Gentofte, Denmark
      name:Steno Diabetes Center, Gentofte, Denmark
      name:Steno Diabetes Center, Gentofte, Denmark
      name:Steno Diabetes Center, Gentofte, Denmark
      name:Faculty of Health Science, University of Aarhus, Denmark

External Links {🔗}(57)

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3.98s.