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Plasma matrix metalloproteinase-9 and ACE-inhibitor-induced improvement of urinary albumin excretion in non-diabetic, microalbuminuric subjectsSt Antonius Hospital, Department of Cardiology, Koekoekslaan 1, 3435 CM, Nieuwegein, The Netherlands
University Medical Center Groningen, University of Groningen, Department of Cardiology, Hanzeplein 1, 9700 RB, Groningen, The Netherlands, University Medical Center Groningen, University of Groningen, Department of Experimental Cardiology, A. Deusinglaan 1, 9713 AV, Groningen, The Netherlands
St Antonius Hospital, Department of Clinical Chemistry, Koekoekslaan 1, 3435 CM, Nieuwegein, The Netherlands
St Antonius Hospital, Department of Clinical Chemistry, Koekoekslaan 1, 3435 CM, Nieuwegein, The Netherlands
St Antonius Hospital, Department of Cardiology, Koekoekslaan 1, 3435 CM, Nieuwegein, The Netherlands
University Medical Center Groningen, University of Groningen, Department of Internal Medicine, Hanzeplein 1, 9700 RB, Groningen, The Netherlands
University Medical Center Groningen, University of Groningen, Department of Experimental Cardiology, A. Deusinglaan 1, 9713 AV, Groningen, The Netherlands
University Medical Center Groningen, University of Groningen, Department of Cardiology, Hanzeplein 1, 9700 RB, Groningen, The Netherlands, a.a.voors{at}thorax.umcg.nl Introduction. Elevated plasma matrix metalloproteinase-9 (MMP-9) levels have been suggested to precede the development of microalbuminuria. As angiotensin-converting enzyme (ACE) inhibitors effectively reduce urinary albumin excretion (UAE), in the present study we have investigated the potential association of plasma MMP-9 levels with UAE and treatment effects of ACE-inhibition. Material and methods. In a placebo-controlled randomised trial we determined plasma MMP-9 levels at baseline and after three months of randomisation to either placebo (n=202) or fosinopril (20 mg/day, n=204) treatment. Results. Baseline plasma MMP-9 levels were not related to baseline UAE (r=-0.008, p=0.871).Three months of fosinopril treatment effectively reduced UAE compared to placebo treatment (-10.4±2.4 vs. 1.8±1.3 mg/24 hours, p<0.001, respectively). However, fosinopril treatment failed to significantly change plasma MMP-9 levels compared to placebo (-0.47±7.68 vs. 0.06±9.20, p=0.646, respectively) . In addition, the change in UAE was not related with change in MMP-9 levels. Conclusion. The effective reduction of UAE with fosinopril was not related to plasma MMP-9 levels.
Key Words: angiotensin-converting enzyme ACE-inhibitors fosinopril matrix metalloproteinase-9 urinary albumin excretion
Journal of Renin-Angiotensin-Aldosterone System, Vol. 8, No. 4,
177-180 (2007) |
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