Related Experiment Videos
Cyclosporine-induced hypertension after transplantation
S C Textor1, V J Canzanello, S J Taler
1Division of Hypertension, Mayo Clinic Rochester, MN 55905.
Insights
Posttransplantation hypertension, often caused by cyclosporine A (CSA), increases vascular resistance and impairs kidney function. Management focuses on vasodilators while monitoring CSA levels and electrolyte balance.
Area of Science:
- Nephrology
- Immunology
- Cardiology
Background:
- Posttransplantation hypertension is a common complication in organ transplant recipients.
- Cyclosporine A (CSA) is a frequently used immunosuppressant that can induce hypertension.
Purpose of the Study:
- To elucidate the features and underlying mechanisms of posttransplantation hypertension.
- To provide guidance on the appropriate management of this disorder.
Main Methods:
- Review of the authors' clinical experience with CSA-treated transplant recipients.
- Comprehensive literature review on hypertension in this patient population.
Main Results:
- Hypertension universally develops post-immunosuppression with CSA and corticosteroids, primarily due to increased peripheral vascular resistance.
- Disturbances in circadian blood pressure patterns, including loss of nocturnal decline, exacerbate hypertensive effects.
- Severe cases can lead to target organ injury (e.g., intracranial hemorrhage, left ventricular hypertrophy, microangiopathic hemolysis) driven by vasoconstriction, altered renal vascular function, and imbalances in vasoactive mediators like endothelin and prostaglandins.
Conclusions:
- Recognizing and effectively treating CSA-induced hypertension and associated vascular injury are critical for optimal management of transplant recipients.
- Therapeutic strategies should include vasodilating agents, such as calcium channel blockers, with careful consideration of potential interactions with CSA metabolism and renal/electrolyte homeostasis.
Objective:
To describe the features and mechanisms of posttransplantation hypertension and suggest appropriate management of the disorder.
Design:
We review our own experience and reports from the literature on hypertension in cyclosporine A (CSA)-treated transplant recipients.
Results:
Soon after immunosuppression with CSA and corticosteroids, hypertension develops in most patients who undergo transplantation. The blood 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 nocturnal decline, a feature that magnifies hypertensive target effects. Changes in blood pressure sometimes are severe and associated with rapidly developing target injury, including intracranial hemorrhage, left ventricular hypertrophy, and microangiopathic hemolysis. The complex mechanisms that underlie this disorder include alterations in vascular reactivity that cause widespread vasoconstriction. Vascular effects in the kidney lead to reduced glomerular filtration and impaired sodium excretion. Many of these changes affect local regulation of vascular tone, 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 avoid interfering with the disposition of CSA or aggravating adverse effects relative to kidney and electrolyte homeostasis.
Conclusion:
Recognition and treatment of CSA-induced hypertension and vascular injury are important elements in managing the transplant recipient.