Arterial hypertension and transplantation are closely linked, and its association may promote impaired graft and overall survival. Since the introduction of calcineurin inhibitors, it is observed in 50–80% of transplanted patients. However, many pathophysiological mechanisms are involved in its genesis. In this review, we intend to provide an updated overview of these mechanisms, dealing with the causes common to all kinds of transplantation and emphasizing special cases with distinct features, and to give a perspective on the pharmacological approach, in order to help clinicians in the management of this frequent complication. 1. Introduction Arterial hypertension (AH) occurs frequently after transplantation, and the association of both has been a well documented fact since many years. It may begin early or late after the procedure, or even in an accelerated fashion from a preexistent hypertension, and may appear in all forms of transplant, that is, solid organ (renal, cardiac, pancreatic, hepatic, and pulmonary) as well as nonsolid (bone marrow) transplants. Once the mechanism/s leading to AH are unleashed, a very deleterious situation may arise, because it has been demonstrated that its presence is associated to impaired graft and overall survival [1]. The incidence of AH in transplant recipients has increased notoriously, above all since the introduction of calcineurin inhibitors (ciclosporine, tacrolimus). With the use of these two drugs AH is observed with varying degrees in 50–80% of the patients [2]. Moreover, there are many more pathophysiological mechanisms involved in the genesis of AH which are basically dependent on the transplanted organ. There are also at least two main issues to take into account in this group of patients: first, that calcineurin inhibitors and corticosteroids are used jointly, which in turn may increase the hypertensive response; and second, that the use of cyclosporine and tacrolimus leads invariably to nephrotoxicity, which along with renal insufficiency predispose to AH independent of the direct effect of calcineurin [3]. We will outline in this review the main causes of AH in the transplanted patients, with a special focus on the pathophysiological mechanisms and emphasizing the causes common to all kinds of transplantation. Renal transplantation will be dealt apart due to the fact that it possesses some distinct features regarding etiology [4, 5]. After this, we will focus on the characteristics of the most widely used drugs in order to clarify the pharmacological approach. 2. Methods The search in the literature
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