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Pathophysiology and treatment of posttransplant hypertension
1Department of Internal Medicine, University of Cincinnati College of Medicine, OH 45267-0557.
Insights
Post-renal transplant hypertension is common, often caused by chronic rejection or cyclosporine. Cyclosporine-induced hypertension involves renal vasoconstriction and sodium retention, suggesting calcium channel blockers as a potential therapy.
Area of Science:
- Nephrology
- Transplant Medicine
- Cardiovascular Research
Background:
- Post-renal transplant hypertension is a frequent complication following kidney transplantation.
- Chronic rejection and cyclosporine are the leading causes of this condition.
- Historically, renin-dependent hypertension predominated, but cyclosporine use has shifted the major mechanism to salt-dependency.
Purpose of the Study:
- To review the common causes and pathophysiological mechanisms of post-renal transplant hypertension.
- To discuss the role of cyclosporine in inducing hypertension and its potential therapeutic targets.
- To highlight surgically remediable causes in severe cases of post-transplant hypertension.
Main Methods:
- Review of current literature on post-renal transplant hypertension.
- Analysis of pathophysiological mechanisms, including renin-dependency and salt-dependency.
- Evaluation of cyclosporine's hypertensive effects and potential therapeutic strategies.
Main Results:
- Cyclosporine is a significant cause of hypertension in transplant recipients, acting via renal vasoconstriction and sodium retention.
- The primary site of cyclosporine-induced vasoconstriction is the afferent arteriole.
- Increased sensitivity to various vasoconstrictors is observed in cyclosporine-induced hypertension.
- Surgically correctable causes like allograft artery stenosis or native kidney renin release should be considered in severe cases.
Conclusions:
- Post-renal transplant hypertension is often multifactorial, necessitating combination antihypertensive therapy.
- Calcium channel blockers may be optimal for cyclosporine-induced hypertension due to the apparent site of action.
- Understanding the shift from renin-dependent to salt-dependent hypertension is crucial for effective management.
Abstract:
Post-renal transplant hypertension remains a common problem. The most frequent causes now are chronic rejection and cyclosporine-induced hypertension. Before the development of cyclosporine, renin-dependent hypertension was the dominant pathophysiological mechanism but now, with the widespread use of cyclosporine, a salt-dependent mechanism is the major one. In severe "inappropriate" hypertension, potentially surgically remediable causes such as renal artery stenosis of the allograft artery or renin release from the native kidneys should be considered. Cyclosporine causes hypertension in normal subjects and in all solid organ transplants. The most likely mechanism is renal vasoconstriction with subtle retention of sodium chloride together with systemic vasoconstriction. The vasoconstriction, as yet, is not associated with any specific vasoconstricting agent nor does there appear to be a specific antagonist. Indeed, increased sensitivity to many different vasoconstrictors has been demonstrated. The major site of vasoconstriction appears to be in the afferent arteriole, and optimum antihypertensive therapy is probably provided by calcium channel blockers if the hypertension is due to cyclosporine. Because post-renal transplant hypertension is often multifactorial in origin, however, it is not surprising that the use of combined antihypertensives is often necessary.
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