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Lisinopril reduces albuminuria during exercise in low grade microalbuminuric Type 1 diabetic patients: a double blind randomized study
Author(s) -
Poulsen P. L.,
Ebbehøj E.,
Mogensen C. E.
Publication year - 2001
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1046/j.1365-2796.2001.00821.x
Subject(s) - lisinopril , microalbuminuria , medicine , placebo , albuminuria , ace inhibitor , type 2 diabetes , blood pressure , urology , diabetic nephropathy , randomized controlled trial , endocrinology , angiotensin converting enzyme , diabetes mellitus , pathology , alternative medicine
. Poulsen PL, Ebbehøj E, Mogensen CE (Medical Department M (Diabetes & Endocrinology) Aarhus Kommunehospital, Aarhus, Denmark). Lisinopril reduces albuminuria during exercise in low grade microalbuminuric Type 1 diabetic patients: a double blind randomized study. J Intern Med 2001; 249: 433–440. Background. Antihypertensive treatment is presently recommended in most type 1 diabetic patients with microalbuminuria. The long‐term effect of angiotensin converting enzymes (ACE) inhibitor (ACE‐i) treatment on exercise urinary albumin excretion (E‐UAE) and exercise blood pressure (E‐BP) in type 1 diabetic patients with low grade microalbuminuria is not well documented. In addition, the possible predictive effect of baseline E‐UAE on the progression of overnight UAE remains to be clarified. Design and Methods. In a randomized placebo controlled double blind study the effects of 2 years treatment with either lisinopril (20 mg o.d.) or placebo was evaluated in 21 normotensive type 1 diabetic patients with overnight UAE between 20 and 70 μg min –1 . Determinations of E‐UAE and E‐BP were performed after exercise on an ergometercycle with a load of 70% of estimated maximal VO 2 for 20 min. Patients in the placebo and lisinopril groups were similar with regard to age (35.8 ± 11.3 vs. 29.3 ± 8.6 years), duration of diabetes (19.4 ± 8.2 vs. 16.8 ± 5.3 years), and HbA 1c (9.0 ± 1.0 vs. 9.4 ± 1.7%). Results. At baseline, E‐UAE was similar in the two groups (placebo: 150.1 ×/÷ 3.7, lisinopril: 96.8 ×/÷ 1.8 μg min –1 (geometric mean ×/÷ tolerance factor)). After 2 years treatment E‐UAE had increased in the placebo group, whereas E‐UAE was reduced in the lisinopril treated patients (placebo: 213.6 ×/÷ 6.9, lisinopril: 48.3 ×/÷ 3.1 μg min –1 , P =0.04). The relative increase in E‐UAE (E‐UAE/Pre‐exercise UAE) was similar at baseline in both groups (3.7 ×/÷ 2.3 vs. 2.8 ×/÷ 2.0) but significantly higher in the placebo group after 2 years (4.4 ×/÷ 2.4 compared with 1.6 ×/÷ 1.7 in the lisinopril group, P < 0.01) These changes over two years in relative increase in E‐UAE were significantly different ( P =0.03). Exercise blood pressure was similar in both groups at baseline and over 2 years increased in the placebo group (from 166.5 ± 15.1–179.9 ± 35.6 mmHg), in contrast to the lisinopril group where E‐BP was slightly reduced (from 168.5 ± 20.6–165.1 ± 16.6 mmHg) but the difference in blood pressure over the 2 years did not reach statistical significance. Exercise urinary albumin excretion and E‐BP were closely associated (correlation for year 2: r =0.734, P < 0.001), and also changes over the 2 years in E‐UAE and E‐BP were positively correlated ( r =0.53, P =0.01). At year 2, overnight UAE, pre‐exercise UAE (pre‐E‐UAE), E‐UAE and E‐BP were all closely linked ( r ‐values between 0.6 and 0.9, P ‐values <0.01). In the prediction of changes in overnight UAE over 2 years, neither baseline E‐UAE nor baseline E‐BP conveyed explanatory information in comparison with baseline overnight UAE and HbA 1c . Conclusions. In type 1 diabetic patients with low‐grade microalbuminuria, 2 years of ACE‐i treatment with lisinopril significantly reduced E‐UAE. Strong correlations were found between E‐UAE and E‐BP and also changes over 2 years in these parameters were significantly associated.