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Hypertension commonly occurs post-renal transplantation. As many as 70% of renal allograft recipients receiving CsA have hypertension severe enough to require medical therapy. Hypertension in this setting is usually multifactorial in nature. Pre-existing disease, renal insufficiency, and immunosuppressant medication (CsA and Prednisone) all may contribute to the hypertension in patients post renal transplantation. While no randomized, controlled study has been performed, it would be reasonable to assume that hypertension in this setting incurs the same risk of end organ damage as it does in the population at large.

It appears that among the medications given posttransplantation, CsA appears to have the most negative effect on blood pressure control. It is interesting to note that while Tacrolimus shares the same immunosuppressant mechanism of action as CsA it does not seem to produce as much hypertension. CsA probably produces elevated pressure by both volume dependent and volume independent mechanisms of action. CsA will induce a predictable increase in tubular sodium resorption and thus increases plasma volume. In addition, CsA can produce vasoconstriction in several vascular beds, particularly in the afferent arteriole of the glomerulus. CsA-induced vasoconstriction appears to be related to an increase in endothelin levels, a decrease in nitric oxide, and an imbalance of vasodilating and vasocon-strictive prostanoids. Calcium channel blockers of all three classes appear to be the best agents in obviating the renal vasoconstriction induced by CsA.

Many patients with pre-existing hypertension often will have a worsening of their hypertension posttransplant and require more intensive medical therapy.

Stenosis of the transplanted renal artery can be the etiology of a resistant posttransplant hypertension. Patients with RAS of the transplanted artery will often have a deterioration of their renal function as blood pressure is controlled. In these patients, an interventional procedure (e.g., stenting, angioplasty or bypass) often is helpful in both controlling blood pressure and preserving renal function.

Treatment of posttransplant hypertension should broadly have the same goal as treatment in the nonrenal transplant recipient, that of prevention of end organ damage to the heart, kidney, and prevention of cerebral vascular events. In this regard, basic principles of hypertension control should be followed in this setting, e.g., p-blockers for patients with coronary artery disease. Table 18.1 outlines various antihypertensive medications and lists possible positive and negative effects of these agents.

There appears to be no consensus on the routine use of any particularly antihy-pertensive regimen in the posttransplant period. However, certain theoretic and practical issues should be kept in mind. In general, calcium channel blockers have been shown to ameliorate CsA-induced renal vasoconstriction. In addition to this possible advantage, there are certain caveats to their use. Both Verapamil and Diltiazem can significantly increase CsA and tacrolimus levels, probably by both inhibiting cytochrome P450 IIIA activity as well as interstitial p glycoprotein

Table 18.1. Various antihypertensive medications




Specific ß1 blockers, e.g., Atenelol, Metoprolol function.

Agents of choice in patients with CAD and good LV

J cardiac output. May J renal blood flow.

Alpha 1 blockers, e.g., Terazosin

May help in patients with BPH. May ] RBF.

Orthostatic hypotension.

Alpha 1 blocker, + nonspecific ß-blocker, e.g., Labetelol

May be effective for patients who need both vasodilatation and heart rate control.

Bronchospasm. Avoid with PVD. Possible f of CVA. Induce hyperkalemia. J CO.

Calcium Channel Blockers: a. dihydropyridines, e.g., Nifedipine

Best agents to prevent CsA-induced vasoconstriction.

Edema (nonsodium retentive). Reflex tachycardia. Avoid with active CAD.

b. Diltiazem

Can prevent CsA-induced vasoconstriction.

f CsA, Tacrolimus levels.

c. Verapamil

Can prevent CsA-induced vasoconstriction.

f CsA, Tacrolimus levels. Constipation. Bradycardia. J CO.

ACE inhibitors, e.g., enalapril, angiotensin II blockers, e.g., losartan

May be best agents for patient with J LV function or LV dilatation. May be best agents to decrease proteinuria experimentally may decrease CsA medicated renal fibrosis.

Hyperkalemia. Deterioration in renal function (particularly in patients with RAS).

Alpha 2 agonists, e.g., Clonidine

Effective in many people. Decreases central sympathetic discharge.

Drowsiness, dry mouth.

Direct vasodilators, e.g., Hydralazine, Minoxidil

Hydralazine often used with patients intolerant to ACEI or AII blocker with CHF. Minoxidil effective in refractory patients.

Reflex tachycardia. Na+ retention.

Diuretics, e.g., Furosemide

Often necessary in volume extended patients.

Electrolyte disorder. Experimentally may exacerbate CsA-induced fibrosis.

activity. In general, the dyhydropyridines exhibit much less pharmacokinetic interaction with either of these agents. The dihydropyridine calcium channel blockers may exacerbate CsA-induced gingival hyperplasia as well. Nonspecific p-blockers may exacerbate CsA-induced hyperkalemia. ACE inhibitors can pre cipitate a decrease in GFR in the setting of CsA or tacrolimus afferent arteriola vasoconstriction. Volume depletion induced by diuretics may activate the Renin-AII system and at least in experimental models may worsen CsA-induced chronic toxicity. Again, the goal is to individualize therapy for the particular patient, bearing in mind both long-term benefits and keeping in mind the specific issues involved with patients on current immunosuppression therapy.

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