Effect of a Reduction in Uric Acid on Renal Outcomes During Losartan Treatment: A Post Hoc Analysis of the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial
Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore...
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| Published in | Hypertension (Dallas, Tex. 1979) Vol. 58; no. 1; pp. 2 - 7 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
American Heart Association, Inc
01.07.2011
Lippincott Williams & Wilkins |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore tested this hypothesis. In a post hoc analysis of 1342 patients with type 2 diabetes mellitus and nephropathy participating in the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial, we determined the relationship between month 6 change in SUA and renal endpoints, defined as a doubling of serum creatinine or end-stage renal disease. Baseline SUA was 6.7 mg/dL in placebo and losartan-treated subjects. During the first 6 months, losartan lowered SUA by −0.16 mg/dL (95% CI−0.30 to −0.01; P=0.031) as compared with placebo. The risk of renal events was decreased by 6% (95% CI10% to 3%) per 0.5-mg/dL decrement in SUA during the first 6 months. This effect was independent of other risk markers, including estimate glomerular filtration rate and albuminuria. Adjustment of the overall treatment effects for SUA attenuated losartanʼs renoprotective effect from 22% (95% CI6% to 35%) to 17% (95% CI1% to 31%), suggesting that approximately one fifth of losartanʼs renoprotective effect could be attributed to its effect on SUA. Losartan lowers SUA levels compared with placebo treatment in patients with type 2 diabetes mellitus and nephropathy. The degree of reduction in SUA is subsequently associated with the degree in long-term renal risk reduction and explains part of losartanʼs renoprotective effect. These findings support the view that SUA may be a modifiable risk factor for renal disease. |
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| AbstractList | Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore tested this hypothesis. In a post hoc analysis of 1342 patients with type 2 diabetes mellitus and nephropathy participating in the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial, we determined the relationship between month 6 change in SUA and renal endpoints, defined as a doubling of serum creatinine or end-stage renal disease. Baseline SUA was 6.7 mg/dL in placebo and losartan-treated subjects. During the first 6 months, losartan lowered SUA by -0.16 mg/dL (95% CI: -0.30 to -0.01; P=0.031) as compared with placebo. The risk of renal events was decreased by 6% (95% CI: 10% to 3%) per 0.5-mg/dL decrement in SUA during the first 6 months. This effect was independent of other risk markers, including estimate glomerular filtration rate and albuminuria. Adjustment of the overall treatment effects for SUA attenuated losartan's renoprotective effect from 22% (95% CI: 6% to 35%) to 17% (95% CI: 1% to 31%), suggesting that approximately one fifth of losartan's renoprotective effect could be attributed to its effect on SUA. Losartan lowers SUA levels compared with placebo treatment in patients with type 2 diabetes mellitus and nephropathy. The degree of reduction in SUA is subsequently associated with the degree in long-term renal risk reduction and explains part of losartan's renoprotective effect. These findings support the view that SUA may be a modifiable risk factor for renal disease. Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore tested this hypothesis. In a post hoc analysis of 1342 patients with type 2 diabetes mellitus and nephropathy participating in the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial, we determined the relationship between month 6 change in SUA and renal endpoints, defined as a doubling of serum creatinine or end-stage renal disease. Baseline SUA was 6.7 mg/dL in placebo and losartan-treated subjects. During the first 6 months, losartan lowered SUA by −0.16 mg/dL (95% CI−0.30 to −0.01; P=0.031) as compared with placebo. The risk of renal events was decreased by 6% (95% CI10% to 3%) per 0.5-mg/dL decrement in SUA during the first 6 months. This effect was independent of other risk markers, including estimate glomerular filtration rate and albuminuria. Adjustment of the overall treatment effects for SUA attenuated losartanʼs renoprotective effect from 22% (95% CI6% to 35%) to 17% (95% CI1% to 31%), suggesting that approximately one fifth of losartanʼs renoprotective effect could be attributed to its effect on SUA. Losartan lowers SUA levels compared with placebo treatment in patients with type 2 diabetes mellitus and nephropathy. The degree of reduction in SUA is subsequently associated with the degree in long-term renal risk reduction and explains part of losartanʼs renoprotective effect. These findings support the view that SUA may be a modifiable risk factor for renal disease. Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore tested this hypothesis. In a post hoc analysis of 1342 patients with type 2 diabetes mellitus and nephropathy participating in the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial, we determined the relationship between month 6 change in SUA and renal endpoints, defined as a doubling of serum creatinine or end-stage renal disease. Baseline SUA was 6.7 mg/dL in placebo and losartan-treated subjects. During the first 6 months, losartan lowered SUA by −0.16 mg/dL (95% CI: −0.30 to −0.01; P =0.031) as compared with placebo. The risk of renal events was decreased by 6% (95% CI: 10% to 3%) per 0.5-mg/dL decrement in SUA during the first 6 months. This effect was independent of other risk markers, including estimate glomerular filtration rate and albuminuria. Adjustment of the overall treatment effects for SUA attenuated losartan's renoprotective effect from 22% (95% CI: 6% to 35%) to 17% (95% CI: 1% to 31%), suggesting that approximately one fifth of losartan's renoprotective effect could be attributed to its effect on SUA. Losartan lowers SUA levels compared with placebo treatment in patients with type 2 diabetes mellitus and nephropathy. The degree of reduction in SUA is subsequently associated with the degree in long-term renal risk reduction and explains part of losartan's renoprotective effect. These findings support the view that SUA may be a modifiable risk factor for renal disease. Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore tested this hypothesis. In a post hoc analysis of 1342 patients with type 2 diabetes mellitus and nephropathy participating in the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial, we determined the relationship between month 6 change in SUA and renal endpoints, defined as a doubling of serum creatinine or end-stage renal disease. Baseline SUA was 6.7 mg/dL in placebo and losartan-treated subjects. During the first 6 months, losartan lowered SUA by -0.16 mg/dL (95% CI: -0.30 to -0.01; P=0.031) as compared with placebo. The risk of renal events was decreased by 6% (95% CI: 10% to 3%) per 0.5-mg/dL decrement in SUA during the first 6 months. This effect was independent of other risk markers, including estimate glomerular filtration rate and albuminuria. Adjustment of the overall treatment effects for SUA attenuated losartan's renoprotective effect from 22% (95% CI: 6% to 35%) to 17% (95% CI: 1% to 31%), suggesting that approximately one fifth of losartan's renoprotective effect could be attributed to its effect on SUA. Losartan lowers SUA levels compared with placebo treatment in patients with type 2 diabetes mellitus and nephropathy. The degree of reduction in SUA is subsequently associated with the degree in long-term renal risk reduction and explains part of losartan's renoprotective effect. These findings support the view that SUA may be a modifiable risk factor for renal disease.Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore tested this hypothesis. In a post hoc analysis of 1342 patients with type 2 diabetes mellitus and nephropathy participating in the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial, we determined the relationship between month 6 change in SUA and renal endpoints, defined as a doubling of serum creatinine or end-stage renal disease. Baseline SUA was 6.7 mg/dL in placebo and losartan-treated subjects. During the first 6 months, losartan lowered SUA by -0.16 mg/dL (95% CI: -0.30 to -0.01; P=0.031) as compared with placebo. The risk of renal events was decreased by 6% (95% CI: 10% to 3%) per 0.5-mg/dL decrement in SUA during the first 6 months. This effect was independent of other risk markers, including estimate glomerular filtration rate and albuminuria. Adjustment of the overall treatment effects for SUA attenuated losartan's renoprotective effect from 22% (95% CI: 6% to 35%) to 17% (95% CI: 1% to 31%), suggesting that approximately one fifth of losartan's renoprotective effect could be attributed to its effect on SUA. Losartan lowers SUA levels compared with placebo treatment in patients with type 2 diabetes mellitus and nephropathy. The degree of reduction in SUA is subsequently associated with the degree in long-term renal risk reduction and explains part of losartan's renoprotective effect. These findings support the view that SUA may be a modifiable risk factor for renal disease. |
| Author | Parving, Hans-Henrik Lambers Heerspink, Hiddo J. Laverman, Goos D. Cooper, Mark E. Miao, Yan Brenner, Barry M. Grobbee, Diederick E. Ottenbros, Stefan A. Shahinfar, Shahnaz de Zeeuw, Dick |
| AuthorAffiliation | From the Department of Clinical Pharmacology (Y.M., S.A.O., D.d.Z., H.J.L.H.) and Division of Nephrology, Department of Internal Medicine (G.D.L.), University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; Brigham and Womenʼs Hospital and Harvard School of Medicine (B.M.B.), Boston, MA; Baker IDI Heart and Diabetes Research Institute (M.E.C.), Melbourne, Australia; Department of Medical Endocrinology (H.-H.P.), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; Faculty of Health Sciences (H.-H.P.), Aarhus University, Aarhus, Denmark; Julius Center for Health Science and Primary Care (D.E.G.), University Medical Center Utrecht, Utrecht, The Netherlands; Sshahinfar Consulting (S.S.), Children Hospital of Philadelphia, Philadelphia, PA |
| AuthorAffiliation_xml | – name: From the Department of Clinical Pharmacology (Y.M., S.A.O., D.d.Z., H.J.L.H.) and Division of Nephrology, Department of Internal Medicine (G.D.L.), University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; Brigham and Womenʼs Hospital and Harvard School of Medicine (B.M.B.), Boston, MA; Baker IDI Heart and Diabetes Research Institute (M.E.C.), Melbourne, Australia; Department of Medical Endocrinology (H.-H.P.), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; Faculty of Health Sciences (H.-H.P.), Aarhus University, Aarhus, Denmark; Julius Center for Health Science and Primary Care (D.E.G.), University Medical Center Utrecht, Utrecht, The Netherlands; Sshahinfar Consulting (S.S.), Children Hospital of Philadelphia, Philadelphia, PA |
| Author_xml | – sequence: 1 givenname: Yan surname: Miao fullname: Miao, Yan organization: From the Department of Clinical Pharmacology (Y.M., S.A.O., D.d.Z., H.J.L.H.) and Division of Nephrology, Department of Internal Medicine (G.D.L.), University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; Brigham and Womenʼs Hospital and Harvard School of Medicine (B.M.B.), Boston, MA; Baker IDI Heart and Diabetes Research Institute (M.E.C.), Melbourne, Australia; Department of Medical Endocrinology (H.-H.P.), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; Faculty of Health Sciences (H.-H.P.), Aarhus University, Aarhus, Denmark; Julius Center for Health Science and Primary Care (D.E.G.), University Medical Center Utrecht, Utrecht, The Netherlands; Sshahinfar Consulting (S.S.), Children Hospital of Philadelphia, Philadelphia, PA – sequence: 2 givenname: Stefan surname: Ottenbros middlename: A. fullname: Ottenbros, Stefan A. – sequence: 3 givenname: Goos surname: Laverman middlename: D. fullname: Laverman, Goos D. – sequence: 4 givenname: Barry surname: Brenner middlename: M. fullname: Brenner, Barry M. – sequence: 5 givenname: Mark surname: Cooper middlename: E. fullname: Cooper, Mark E. – sequence: 6 givenname: Hans-Henrik surname: Parving fullname: Parving, Hans-Henrik – sequence: 7 givenname: Diederick surname: Grobbee middlename: E. fullname: Grobbee, Diederick E. – sequence: 8 givenname: Shahnaz surname: Shahinfar fullname: Shahinfar, Shahnaz – sequence: 9 givenname: Dick surname: de Zeeuw fullname: de Zeeuw, Dick – sequence: 10 givenname: Hiddo surname: Lambers Heerspink middlename: J. fullname: Lambers Heerspink, Hiddo J. |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24258659$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21632472$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1111/j.1523-1755.2004.00653.x 10.1681/ASN.2006050445 10.1046/j.1523-1755.1999.00739.x 10.1097/HJH.0b013e328337da1d 10.1016/j.amjmed.2010.03.027 10.1053/j.ajkd.2010.01.019 10.1056/NEJMra0800885 10.1186/1471-2458-4-9 10.1053/j.ajkd.2010.01.024 10.1007/BF00266358 10.1111/j.1523-1755.2005.00074.x 10.1007/s11255-007-9253-3 10.2174/138161205774913309 10.1681/ASN.2005050572 10.1007/s00125-010-1951-1 10.2337/db09-0014 10.3317/jraas.2000.062 10.1097/HJH.0b013e3282f240bf 10.1097/00004872-200018080-00021 10.1038/ajh.2008.245 10.7326/0003-4819-130-6-199903160-00002 10.2215/CJN.01580210 10.1016/S0021-9150(00)00474-3 10.1124/jpet.106.112755 10.1016/S0272-6386(99)70093-4 10.1111/j.1523-1755.2004.00484.x 10.1053/j.ajkd.2005.10.006 |
| ContentType | Journal Article |
| Copyright | 2011 American Heart Association, Inc. 2015 INIST-CNRS |
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| Keywords | Endocrinopathy Type 2 diabetes Imidazole derivatives Tetrazole derivatives Prognosis Peptide hormone Non peptide compound Cardiovascular disease angiotensin receptor blocker Octapeptide Losartan type 2 diabetes mellitus serum uric acid Angiotensin II Kidney disease Hypertension Urinary system disease Metabolic diseases Uric acid Nephropathy Treatment Biphenyl derivatives Antihypertensive agent Sartan derivatives Angiotensin antagonist diabetic nephropathy |
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| PublicationTitle | Hypertension (Dallas, Tex. 1979) |
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| SubjectTerms | Angiotensin II Type 1 Receptor Blockers - administration & dosage Antihypertensive agents Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cardiovascular system Creatinine - blood Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - physiopathology Diabetic Nephropathies - etiology Diabetic Nephropathies - physiopathology Diabetic Nephropathies - prevention & control Dose-Response Relationship, Drug Double-Blind Method Female Follow-Up Studies Glomerular Filtration Rate - drug effects Humans Hypertension - blood Hypertension - complications Hypertension - drug therapy Losartan - administration & dosage Male Medical sciences Middle Aged Pharmacology. Drug treatments Risk Factors Time Factors Treatment Outcome Uric Acid - blood |
| Title | Effect of a Reduction in Uric Acid on Renal Outcomes During Losartan Treatment: A Post Hoc Analysis of the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial |
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