Posttransplantation hypertension related to calcineurin inhibitors

Stephen C. Textor, Sandra J. Taler, Vincent J. Canzanello, Lora Schwartz, Jo Ellen Augustine

Research output: Contribution to journalArticle

104 Scopus citations

Abstract

Calcineurin inhibitors are a mainstay of transplant immunosuppression and commonly induce hypertension. They are highly lipid soluble and penetrate vascular smooth muscle cell membranes readily. Changes in vascular tone are universally observed during administration of these agents, particularly within the kidney, leading to diminished glomerular filtration and enhanced sodium retention. Disturbances of endothelial function are prevalent in many tissues, including stimulation of endothelin and impaired nitric oxide synthesis. Multiple additional pathways produce increased vasoconstriction, leading to an increase in arterial pressure. Clinical manifestations include disturbances in circadian blood pressure patterns, left ventricular hypertrophy, and acceleration of atherosclerotic and renal injury. Rapid increases in pressure occasionally produce accelerated hypertension and microangiopathic tissue damage. Principles of therapy require recognition of hazards of changing arterial pressures during calcineurin use and preferential use of vasodilating drugs, particularly dihydropyridine calcium channel blocking agents. Attention must be paid to interactions between antihypertensive agents and calcineurin inhibitor blood levels.

Original languageEnglish (US)
Pages (from-to)521-530
Number of pages10
JournalLiver Transplantation
Volume6
Issue number5
DOIs
StatePublished - Jan 1 2000

ASJC Scopus subject areas

  • Surgery
  • Hepatology
  • Transplantation

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