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Sequential effects of cyclosporine therapy on blood pressure, renal function and neurohormones

N D Sturrock1, C C Lang, P H Baylis

  • 1Department of Pharmacology and Clinical Pharmacology, Ninewells Hospital and Medical School, Dundee, Scotland.

Kidney International
|April 1, 1994
PubMed

Insights

Cyclosporine rapidly increases blood pressure and reduces urine output within four days. Early effects suggest hypertension is not sodium-dependent, with altered water handling and potential distal nephron effects.

Area of Science:

  • Nephrology
  • Pharmacology
  • Physiology

Background:

  • Cyclosporine is a vital immunosuppressant with known nephrotoxicity and hypertensive side effects.
  • Understanding early cyclosporine effects is crucial for mitigating adverse renal outcomes.

Purpose of the Study:

  • To investigate the sequential physiological effects of cyclosporine initiation over the first four days.
  • To elucidate the primary and secondary mechanisms in cyclosporine-induced nephrotoxicity and hypertension.

Main Methods:

  • Sequential monitoring of systemic blood pressure, urine volume, plasma renin activity, and renal sodium excretion.
  • Assessment of glomerular filtration rate and effective renal plasma flow.
  • Evaluation of cyclosporine's antidiuretic effects with and without vasopressin infusion.

Main Results:

  • Acute increase in systemic blood pressure and decreased urine volume by day 1.
  • Suppression of plasma renin activity by day 2.
  • Natriuresis observed by day 4, with augmented antidiuretic effects and unchanged renal hemodynamics.
  • Hypertension was not sodium-dependent; antidiuresis suggested a distal nephron effect.

Conclusions:

  • Early cyclosporine administration triggers hypertension independent of sodium balance.
  • Altered renal water handling, potentially at the distal nephron, contributes to cyclosporine's effects.
  • These findings inform strategies to manage cyclosporine-associated nephrotoxicity and hypertension.

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