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Angiotensin converting enzyme inhibitors and magnesium conservation in patients with congestive cardiac failure

R N Stevenson1, C Keywood, A A Amadi

  • 1Cardiac Department, Whittington Hospital, London.

Insights

Angiotensin converting enzyme inhibitors significantly reduce magnesium loss in patients with congestive cardiac failure taking diuretics. This magnesium conserving action may be linked to their effect on glomerular filtration rate.

Area of Science:

  • Cardiology
  • Pharmacology
  • Nephrology

Background:

  • Diuretics are commonly prescribed for congestive cardiac failure (CCF).
  • Diuretic therapy can lead to increased magnesium excretion, potentially causing hypomagnesemia.
  • The impact of angiotensin converting enzyme (ACE) inhibitors on diuretic-induced magnesium loss in CCF is not well understood.

Purpose of the Study:

  • To determine if ACE inhibitors reduce magnesium excretion in patients with CCF who are receiving diuretic treatment.
  • To explore the relationship between ACE inhibitors, magnesium balance, and renal function in this patient population.

Main Methods:

  • A cohort analytic study was conducted at a London district general hospital.
  • Thirty-four patients with chronic CCF were divided into two groups: 19 on diuretics alone and 15 on diuretics plus an ACE inhibitor (enalapril or captopril).
  • Urine magnesium and creatinine clearance were measured over 24 hours after an intravenous magnesium sulphate loading dose.

Main Results:

  • Patients receiving ACE inhibitors (group 2) showed significantly lower 24-hour urine magnesium excretion compared to those on diuretics alone (group 1).
  • Creatinine clearance was also significantly lower in group 2 and correlated with magnesium excretion, a relationship not observed in group 1.
  • No significant difference in the fractional clearance of magnesium was found between the two groups.

Conclusions:

  • ACE inhibitors possess a significant magnesium-conserving effect in patients with CCF on diuretics.
  • This effect is potentially mediated through the influence of ACE inhibitors on glomerular filtration rate.
Abstract

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