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Lowering of Microalbuminuria in Diabetic Patients by a Sympathicoplegic Agent: Novel Approach to Prevent Progression of Diabetic Nephropathy?

KRZYSZTOF STROJEK^*, WLADYSLAW GRZESZCZAK^*, JUTA GÓRSKA^*, MONIKA I. LESCHINGER and EBERHARD RITZ

^* Department of Internal Diseases and Diabetology, Silesian Medical Academy, Zabrze, Poland
Lilly Deutschland GmbH, Bad Homburg, Germany.
Department of Internal Medicine, Ruperto Carola University, Heidelberg, Germany.

Correspondence to Professor Dr. Eberhard Ritz, Department of Internal Medicine, University of Heidelberg, Bergheimer Strasse 56a, D-69115 Heidelberg, Germany. Phone: 6221-91120; Fax: 6221-162476; E-mail: prof.e.ritz{at}t-online.de

Abstract

Abstract. There is convincing evidence for a specific BP-independent effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on albuminuria in glomerular disease. Because progression of glomerular disease is not consistently halted by these agents, there is a need to explore potential renoprotective effects of other drugs. Recent animal work documented that nonhypotensive doses of moxonidine, a sympathicoplegic agent, reduce albuminuria and development of glomerulosclerosis in a BP-independent manner. A randomized, crossover design was used to assess the human relevance of the experimental data in 15 normotensive, nonsmoking type 1 diabetic mellitus patients with good glycemic control (age, 37.3 ± 6.6 yr; 9 men/6 women; duration of diabetes, 23.6 ± 5.1 yr) with baseline urinary albumin excretion rates (AER) >20 µg/min in the run-in phase. AER was assessed in overnight timed urine collections. The patients were assigned to a 3-wk placebo and a 3-wk moxonidine (0.2 mg twice a day) period, respectively, in random order. This dose causes modest BP lowering in hypertensive individuals but does not affect BP in normotensive individuals. There was no significant effect on ambulatory BP (mean arterial pressure, 91.8 ± 7.1 mmHg in the third week of placebo and 91.1 ± 8.7 mmHg on moxonidine). There was a significant (P < 0.006) difference of the treatment effects between placebo and moxonidine, respectively, on AER; median AER at the end of the placebo period was 39.8 µg/min (range, 15.9 to 117 µg/min) versus 29.0 (range, 9.03 to 85.8 µg/min) at the end of the moxonidine period. The data document an antialbuminuric effect of nonhypotensive doses of moxonidine. Diminished sympathetic traffic to the kidney is the most plausible explanation for the finding.

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