CYCLOSPORINE-INDUCED HYPERTENSION AFTER TRANSPLANTATION

Objective: To describe the features and mechanisms of posttransplantat ion hypertension and suggest appropriate management of the disorder. D esign: We review our own experience and reports from the literature on hypertension in cyclosporine A (CSA)-treated transplant recipients. R esults: Soon after immunosuppression with CSA and corticosteroids, hyp ertension develops in most patients who undergo transplantation. The b lood pressure increases, which are usually moderate, occur universally because of increased peripheral vascular resistance. Disturbances in circadian patterns of blood pressure lead to loss of the normal noctur nal decline, a feature that magnifies hypertensive target effects. Cha nges in blood pressure sometimes are severe and associated with rapidl y developing target injury, including intracranial hemorrhage, left ve ntricular hypertrophy, and microangiopathic hemolysis. The complex mec hanisms that underlie this disorder include alterations in vascular re activity that cause widespread vasoconstriction. Vascular effects in t he kidney lead to reduced glomerular filtration and impaired sodium ex cretion. Many of these changes affect local regulation of vascular ton e, including stimulation of endothelin and suppression of vasodilating prostaglandins. Effective therapy includes use of vasodilating agents , often calcium channel blocking drugs. Caution must be exercised to a void interfering with the disposition of CSA or aggravating adverse ef fects relative to kidney and electrolyte homeostasis. Conclusion: Reco gnition and treatment of CSA-induced hypertension and vascular injury are important elements in managing the transplant recipient.