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BRIEF COMMUNICATION

Effects of Sodium Intake on Albumin Excretion in Patients with Diabetic Nephropathy Treated with Long-Acting Calcium Antagonists

right arrow George L. Bakris, MD, and Amy Smith, RN

1 August 1996 | Volume 125 Issue 3 | Pages 201-204

Objective: To determine whether sodium intake alters albumin excretion in patients with nephropathy from non-insulin-dependent diabetes mellitus who were treated with two different long-acting calcium antagonists.

Design: Prospective, crossover, open-label trial.

Setting: Rush-Presbyterian-St. Luke's Medical Center.

Patients: 9 men and 6 women (mean age ±SD, 56 ± 8 years) with non-insulin-dependent diabetes mellitus, hypertension, renal insufficiency, and macroalbuminuria.

Intervention: Diltiazem (mean dose, 392 ± 27 mg/d) or nifedipine (mean dose, 83 ± 9 mg/d) was used to decrease blood pressure to less than 140/90 mm Hg. All patients also received furosemide concomitantly for blood pressure control.

Results: Blood pressure reduction with once-daily diltiazem decreased urine albumin excretion (2967 ± 784 mg/d at baseline compared with 1294 ± 679 mg/d after diltiazem therapy; P < 0.05) at 4 weeks while patients received a diet consisting of 50 mEq of sodium per day. Albumin excretion did not decrease when sodium intake was increased to 250 mEq/d, and blood pressure was reduced to levels similar to those seen with the low-sodium diet. Similar blood pressure reduction with once-daily nifedipine did not significantly alter albumin excretion regardless of sodium intake.

Conclusion: Sodium intake affects the albumin-decreasing effects of certain calcium antagonists. Recent studies suggest that antihypertensive medications that reduce albumin excretion and arterial pressure correlate with reduced renal mortality compared with medications that do not have albumin-decreasing effects. Thus, a low-sodium diet should be prescribed to maximize the albumin-decreasing effects of certain calcium antagonists.

Author and Article Information
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From Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois.
Acknowledgments: The authors thank Dr. Sue Leurgans for technical help with statistical analyses.
Grant Support: By an unrestricted investigator-initiated grant from Hoechst Marion Roussell.
Requests for Reprints: George Bakris, MD, Rush-Presbyterian-St. Luke's Medical Center, Rush Hypertension Center, Suite 117, 1725 West Harrison Street, Chicago, IL 60612.
Current Author Addresses: Dr. Bakris and Ms. Smith: Rush-Presbyterian-St. Luke's Medical Center, Rush Hypertension Center, Suite 117, 1725 West Harrison Street, Chicago, IL 60612.




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