Heart transplant recipients are at risk for a number of post-transplantation complications such as graft dysfunction, rejection, and infection. The rates of many complications are decreasing over time, and prognosis is improving. However, these patients continue to experience significant morbidity and mortality. This review focuses on the optimal management of heart transplant recipients in the postoperative period, based on current knowledge. More information is needed about the best ways to predict, prevent, and treat primary graft dysfunction, right ventricular failure, and cellular and antibody-mediated rejection.
Introduction
Approximately 2400 transplants are performed in the United States annually , and more than 4000 are performed worldwide . The most frequent indications for heart transplantation in the United States are cardiomyopathy (59%) and coronary artery disease (35%) . Although the survival of heart transplant recipients is steadily improving, patients continue to experience significant post-transplantation morbidity and mortality . This review focuses on the postoperative management of patients undergoing orthotopic heart transplantation (OHT).
Immediate postoperative management in the intensive care unit
Procedure and associated incisions
Orthotopic heart transplantation (OHT) is performed through median sternotomy and with cardiopulmonary bypass. If profound hemodynamic instability or right ventricular (RV) dysfunction occurs, the sternum may be left open to prevent compression of the allograft, with plans for definitive closure at a later time. In addition to the median sternotomy incision, patients may also have incisions from removal of a cardiac implantable electronic device or ventricular assist device (VAD) driveline. All wounds should be carefully monitored for bleeding, infection, and dehiscence.
Monitors and access
The patient will arrive to the intensive care unit (ICU) with several invasive lines. The International Society for Heart and Lung Transplantation (ISHLT) recommends monitoring the following hemodynamic variables in the immediate postoperative period: peripheral oxygen saturation, electrocardiogram, invasive arterial blood pressure, central venous pressure (CVP), pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and mixed venous oxygen saturation . A bladder catheter will be in place for strict measurement of urine output.
Vasoactive medications
The aims for hemodynamic management in the post-transplantation period are to optimize preload, contractility, and afterload of both the right and left ventricles (LV). Vasodilatory shock is common in the post-cardiotomy period; infusions of vasopressors, such as norepinephrine, phenylephrine, and vasopressin, should be titrated to maintain adequate mean arterial pressure (MAP). Methylene blue may be considered for refractory vasoplegia. Inotropes are started post-bypass in the operating room (OR) for the treatment of graft dysfunction and cardiogenic shock. Commonly used inotropes include epinephrine, dopamine, milrinone, and dobutamine. Inhaled pulmonary vasodilators, if started in the OR, should be continued for several postoperative days .
Mechanical circulatory support
A small percentage of patients will arrive to the ICU with some form of mechanical circulatory support (MCS). Intra-aortic balloon pumps (IABPs) that were present prior to transplantation are not usually removed in the OR because of the increased risk of bleeding due to both heparin administered intraoperatively for cardiopulmonary bypass and postoperative coagulopathy. Once no longer needed, IABPs can be removed in the ICU after coagulopathy has been corrected. De novo MCS [IABP, VAD, or extracorporeal membrane oxygenation (ECMO)] may be placed intraoperatively if the patient cannot be weaned from cardiopulmonary bypass or if profound ventricular dysfunction and hemodynamic instability occur despite maximal pharmacological therapy.
Ventilator management
Patients should remain intubated and mechanically ventilated in the immediate postoperative period. Goals of ventilator management include avoidance of hypoxia, hypercarbia, and acidosis, which may lead to increased PAP and exacerbate RV dysfunction, and avoidance of high inspiratory pressures and auto-PEEP (positive end-expiratory pressure), which can impair venous return . Hemodynamically stable patients can be weaned from the ventilator and extubated in the first 1–2 postoperative days.
Intravascular volume management
Volume status in the immediate post-transplantation period depends on several factors. Preoperative volume status can range from gross volume overload in patients with acute decompensated heart failure to relative euvolemia in patients bridged to transplantation with a VAD. Intraoperatively, large fluid shifts occur due to ultrafiltration (UF) performed during cardiopulmonary bypass, bleeding, fluid administration, and transfusion. In the ICU, the volume status may continue to change with ongoing bleeding and transfusion. Volume status may be assessed using hemodynamic monitors (CVP, diastolic PAP) or echocardiography. Maintaining euvolemia and avoiding volume overload of the RV are paramount. Postoperative diuresis may be hindered by acute kidney injury; thus, UF or renal replacement therapy (RRT) should be instituted early if adequate volume removal cannot be achieved with pharmacotherapy .
Laboratory assessment
Labs should be checked frequently in the postoperative period. Arterial blood gases can be used to manage ventilator settings and direct resuscitation. Trends in hemoglobin, platelet count, fibrinogen, and coagulation factors can guide the transfusion of blood products. Hypokalemia, hypomagnesemia, and hypocalcemia are common and should be corrected. Renal function can be monitored by blood urea nitrogen and creatinine levels.
Hemodynamic instability
Hemodynamic instability in the postoperative period can be due to a variety of factors. Determining the etiology of the instability can be challenging; laboratory values, hemodynamic monitoring, and imaging (e.g., echocardiography) can aid diagnosis. The presentation and management of specific complications are discussed in the following sections.
Immediate postoperative management in the intensive care unit
Procedure and associated incisions
Orthotopic heart transplantation (OHT) is performed through median sternotomy and with cardiopulmonary bypass. If profound hemodynamic instability or right ventricular (RV) dysfunction occurs, the sternum may be left open to prevent compression of the allograft, with plans for definitive closure at a later time. In addition to the median sternotomy incision, patients may also have incisions from removal of a cardiac implantable electronic device or ventricular assist device (VAD) driveline. All wounds should be carefully monitored for bleeding, infection, and dehiscence.
Monitors and access
The patient will arrive to the intensive care unit (ICU) with several invasive lines. The International Society for Heart and Lung Transplantation (ISHLT) recommends monitoring the following hemodynamic variables in the immediate postoperative period: peripheral oxygen saturation, electrocardiogram, invasive arterial blood pressure, central venous pressure (CVP), pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and mixed venous oxygen saturation . A bladder catheter will be in place for strict measurement of urine output.
Vasoactive medications
The aims for hemodynamic management in the post-transplantation period are to optimize preload, contractility, and afterload of both the right and left ventricles (LV). Vasodilatory shock is common in the post-cardiotomy period; infusions of vasopressors, such as norepinephrine, phenylephrine, and vasopressin, should be titrated to maintain adequate mean arterial pressure (MAP). Methylene blue may be considered for refractory vasoplegia. Inotropes are started post-bypass in the operating room (OR) for the treatment of graft dysfunction and cardiogenic shock. Commonly used inotropes include epinephrine, dopamine, milrinone, and dobutamine. Inhaled pulmonary vasodilators, if started in the OR, should be continued for several postoperative days .
Mechanical circulatory support
A small percentage of patients will arrive to the ICU with some form of mechanical circulatory support (MCS). Intra-aortic balloon pumps (IABPs) that were present prior to transplantation are not usually removed in the OR because of the increased risk of bleeding due to both heparin administered intraoperatively for cardiopulmonary bypass and postoperative coagulopathy. Once no longer needed, IABPs can be removed in the ICU after coagulopathy has been corrected. De novo MCS [IABP, VAD, or extracorporeal membrane oxygenation (ECMO)] may be placed intraoperatively if the patient cannot be weaned from cardiopulmonary bypass or if profound ventricular dysfunction and hemodynamic instability occur despite maximal pharmacological therapy.
Ventilator management
Patients should remain intubated and mechanically ventilated in the immediate postoperative period. Goals of ventilator management include avoidance of hypoxia, hypercarbia, and acidosis, which may lead to increased PAP and exacerbate RV dysfunction, and avoidance of high inspiratory pressures and auto-PEEP (positive end-expiratory pressure), which can impair venous return . Hemodynamically stable patients can be weaned from the ventilator and extubated in the first 1–2 postoperative days.
Intravascular volume management
Volume status in the immediate post-transplantation period depends on several factors. Preoperative volume status can range from gross volume overload in patients with acute decompensated heart failure to relative euvolemia in patients bridged to transplantation with a VAD. Intraoperatively, large fluid shifts occur due to ultrafiltration (UF) performed during cardiopulmonary bypass, bleeding, fluid administration, and transfusion. In the ICU, the volume status may continue to change with ongoing bleeding and transfusion. Volume status may be assessed using hemodynamic monitors (CVP, diastolic PAP) or echocardiography. Maintaining euvolemia and avoiding volume overload of the RV are paramount. Postoperative diuresis may be hindered by acute kidney injury; thus, UF or renal replacement therapy (RRT) should be instituted early if adequate volume removal cannot be achieved with pharmacotherapy .
Laboratory assessment
Labs should be checked frequently in the postoperative period. Arterial blood gases can be used to manage ventilator settings and direct resuscitation. Trends in hemoglobin, platelet count, fibrinogen, and coagulation factors can guide the transfusion of blood products. Hypokalemia, hypomagnesemia, and hypocalcemia are common and should be corrected. Renal function can be monitored by blood urea nitrogen and creatinine levels.
Hemodynamic instability
Hemodynamic instability in the postoperative period can be due to a variety of factors. Determining the etiology of the instability can be challenging; laboratory values, hemodynamic monitoring, and imaging (e.g., echocardiography) can aid diagnosis. The presentation and management of specific complications are discussed in the following sections.
Early post-transplant complications
Hyperacute rejection
Hyperacute rejection occurs upon the reperfusion of the allograft due to preformed antibodies against the donor. Because of significant allograft dysfunction, this complication requires rapid diagnosis and treatment. In the case of profound hemodynamic instability, cardiac function can be supported with inotropes and vasopressors; MCS, in the form of VAD or ECMO, should be initiated if needed. Immediate administration of high-dose immunosuppressive medications should occur, including IV corticosteroids, cytolytic induction therapy, an anti-metabolite, and a calcineurin inhibitor (CNI). Plasmapheresis can be performed through the bypass circuit and intravenous immunoglobulin (IVIG) can be administered to remove and inactivate antibodies, respectively. An endomyocardial biopsy (EMB) can be performed in the OR to confirm the diagnosis. Urgent re-transplantation may be considered, but mortality is high .
Bleeding
Hemodynamic instability in the immediate postoperative period is frequently related to hemorrhagic shock. Chest tube output should be closely monitored. Clinical signs include hypotension, low CVP, and low CO. On echocardiography, both ventricles may appear underfilled, with decreased chamber dimensions. Blood for transfusion should be leukodepleted for all transplant recipients and be cytomegalovirus (CMV)-negative for CMV-negative recipients. Protamine can be administered for elevated partial thromboplastin time, and infusions of protamine or antifibrinolytics (tranexamic acid or aminocaproic acid) may be continued into the postoperative period for massive hemorrhage.
Tamponade
The classic presentation of tamponade, with tachycardia and equalization of pressures, may be absent or masked in the heart transplant recipient. Hypotension, elevated CVP, and low CO may be due to coexisting complications, such as RV failure or primary graft dysfunction (PGD). Transesophageal echocardiography (TEE) is preferred to aid in the diagnosis, as imaging windows with transthoracic echocardiography are often inadequate. However, the classic echocardiographic findings of tamponade may not be present. TEE imaging may reveal a collection of blood and specific chamber compression rather than the typical pattern of systolic RA collapse followed by diastolic RV collapse that is seen with concentric pericardial effusion. Additionally, in a mechanically ventilated patient, variations in transvalvular velocities and septal shift during the respiratory cycle may not be evident . Tamponade may be even more difficult to diagnose in the setting of ECMO where the cardiac chambers have been decompressed by ECMO flow. The diagnosis of tamponade by TEE in a hemodynamically unstable patient should prompt emergent surgical exploration.
Primary graft dysfunction
Definition and grading
Another common cause of hemodynamic instability in the immediate postoperative period is PGD. PGD is defined as allograft dysfunction that occurs within the first 24 h following transplantation not attributable to other causes . PGD is categorized into PGD-LV (includes both biventricular failure and isolated LV failure) and PGD-RV (isolated RV failure) . Biventricular (28%–78%) and isolated RV failure (17%–61%) are the most common, while isolated LV failure occurs less frequently (5%–11%) . PGD-LV should be graded as mild, moderate, or severe depending on criteria including hemodynamic instability, inotrope use, and dependence on MCS. There is no severity grading for PGD-RV; criteria for the diagnosis include hemodynamic instability in the absence of elevated left-sided pressures with or without the need for an RVAD. For a summary of PGD classification by the ISHLT, please refer to Table 2 in Chapter 9 (Classification and Severity of Primary Graft Dysfunction) .
Incidence
The reported incidence of PGD ranges widely from 2% to 36% of transplants . Prior to the ISHLT consensus report, there was no standard definition for PGD; thus, accurate incidence and prevalence data are lacking. The reported incidence of PGD may increase in the future as many patients who now meet criteria for mild PGD under the ISHLT guidelines would have previously gone undiagnosed.
Mortality
Patients suffering from PGD experience profound morbidity and mortality, which increases with worsening PGD severity . In fact, PGD is a leading cause of death in the early postoperative period . Reported 30-day mortality ranges widely from 17% to 80% , which again may be due to variations in definition. Early mortality has improved over time as the use of MCS for PGD has increased . Re-transplantation rates range from 6% to 15% . Despite high early mortality, survival of patients who recover from PGD is comparable to that of OHT recipients with no history of PGD .
Risk factors
Many risk factors for developing PGD have been identified and can be classified into donor-related (age, cause of death, duration of resuscitation, multi-organ donation, and comorbidities such as diabetes and hypertension), recipient-related (age, prior cardiac surgery, preexisting renal or liver dysfunction, and preoperative inotrope requirement, MCS, or mechanical ventilation), or procedure-related (donor-recipient size mismatching, ischemic time, and transplant center volume) . A risk score has been developed to assist in identifying patients at risk for PGD. The RADIAL score assigns 1 point for each of the following six criteria: right atrial pressure ≥10 mmHg, recipient age ≥60 years, diabetes, inotrope dependence, donor age ≥30 years, and ischemic time ≥240 min. Increasing RADIAL scores have been associated with increased mortality .
Management
The ISHLT suggests a stepwise approach to managing PGD. Identification and treatment of any causes of secondary graft failure are essential. Once PGD is diagnosed, pharmacotherapy should be optimized with inotropes, vasopressors, and inhaled pulmonary vasodilators. If hemodynamic instability persists, early initiation of MCS is recommended, first with an IABP, followed by temporary VAD or ECMO as needed . If there is no evidence of graft recovery and MCS is unable to be weaned after several days, re-transplantation may be considered .
Right ventricular failure
When RV failure (RVF) occurs within 24 h of transplantation, without a known cause, it is classified as PGD-RV. However, RVF in the post-transplantation period can often be attributed to known conditions, such as pulmonary hypertension, ischemia, and arrhythmias; these conditions are considered causes of secondary graft dysfunction.
Risk factors
RV malperfusion can result from air emboli to the right coronary artery, inadequate protection on bypass, and hypotension. The donor RV may experience additional transplant-specific stressors, such as cold ischemic time, reperfusion injury, mechanical obstruction at the level of the pulmonary artery anastomosis, and donor-recipient size mismatch. Many recipients have pre-existing pulmonary hypertension; the implanted donor RV, previously naïve to elevated PAP, must now eject against increased afterload. Pulmonary hypertension may be exacerbated by hypercarbia, hypoxia, acidosis, and protamine reactions. As discussed previously, large intraoperative volume shifts occur. The thin-walled RV is very sensitive to acute changes in pressure and volume, leading to RV dilation, decreased contractility, and tricuspid regurgitation (TR). Postoperatively, RV injury may persist with refractory hypotension due to vasodilatory shock, recurrent acid-base derangements, and ongoing blood loss with subsequent transfusion .
Diagnosis
RVF should be suspected in a hemodynamically unstable patient with elevated CVP, decreased CO, and normal PCWP. Echocardiography is often the best diagnostic tool. In addition to qualitative assessment of RV wall motion by TEE, the RV can be quantitatively evaluated by a number of parameters. Dilation of the tricuspid annulus is often present, and the resulting TR can be visualized using color flow Doppler . RV pressure and volume overload may result in a leftward shift of the interventricular septum and a “D-shaped” LV. The LV may also appear underfilled because of ventricular interdependence .
Prophylaxis and treatment
Prophylaxis against RVF is empirically initiated in the OR and continued for several days post-transplantation, regardless of the presence of actual RV dysfunction.
Both hypo- and hypervolemia of the RV must be avoided, with judicious fluid and blood administration, aggressive diuresis, and early UF/RRT, as described above. Large inspiratory pressures or auto-PEEP during mechanical ventilation can reduce venous return and result in relative hypovolemia; ventilator settings should be adjusted to achieve adequate ventilation and oxygenation using the lowest pressures .
Inotropic support is provided with infusions of epinephrine, dopamine, milrinone, and/or dobutamine. Vasopressors can be titrated to achieve adequate MAP. Hypocalcemia should be corrected as it is associated with decreased contractility.
Inhaled pulmonary vasodilators are used to reduce RV afterload. Inhaled nitric oxide (iNO) is an oxygen-free radical that promotes the relaxation of vascular smooth muscle, resulting in vasodilation. iNO may lead to methemoglobinemia . Veletri ® [epoprostenol or prostacyclin (PGI 2 )] and Ventavis ® (iloprost, a synthetic analog of PGI 2 ) cause direct vasodilation of pulmonary vascular beds. Both may cause inhibition of platelet aggregation with increased risk of bleeding. Of note, Veletri ® is contraindicated in patients with severe LV dysfunction as it increases mortality . All three agents are effective at reducing PAP and augmenting CO . Inhaled pulmonary vasodilators are preferred over intravenous medications because they have minimal effects on systemic blood pressure . Finally, dynamic elevations in PAP must be avoided by ensuring adequate oxygenation and ventilation and normal acid–base status.
If RVF develops or worsens despite maximal medical management, MCS should be provided with an IABP , temporary RVAD, or ECMO .
Arrhythmias
Conduction abnormalities in the heart transplant recipient are multifactorial and can be related to transplant physiology, surgical technique, and transplant-related complications, such as rejection and cardiac allograft vasculopathy (CAV).
Mechanism
The denervated transplanted heart does not exhibit normal autonomic behavior or response to medications. The loss of parasympathetic input from the vagus nerve results in a higher resting heart rate for transplant recipients, typically 90–100 beats per minute. Patients are also unlikely to experience angina in response to ischemia because of the loss of efferent signaling. Cardiac re-innervation may be possible several years after transplant, but reports are variable .
Some conduction abnormalities are related to the transplantation surgical technique. In the biatrial technique, a portion of the recipient’s right atrium (RA) is anastamosed to the donor RA; this is associated with risk of injury to the sinoatrial node. The biatrial technique is associated with increased risk for atrial arrhythmias . These patients also experience higher rates of bradyarrhythmias requiring permanent pacemaker implantation and slightly worse mortality than patients who undergo bicaval transplantation. The use of the bicaval technique, in which the donor venae cavae are anastomosed to the recipient venae cavae, is increasing .
Atrial arrhythmias
Atrial arrhythmias, including atrial fibrillation (AF), atrial flutter (AFL), and supraventricular tachycardias, are the most common type of post-transplant arrhythmia . Despite their frequency, atrial arrhythmias occur in OHT recipients at a much lower rate than in other post-cardiac surgery patients . The majority of AF episodes occurred within 2 weeks of transplantation, whereas AFL most commonly presents after the first 2 weeks . A significant proportion of AF and AFL is associated with acute rejection and/or CAV , so new or sustained AF/AFL should prompt appropriate workup .
Ventricular arrhythmias
Documented ventricular arrhythmias are not common but are associated with increased mortality . Ventricular tachycardia (VT) years after transplantation may be indicative of severe CAV . The ISHLT recommends coronary angiography and EMB for any patient with sustained VT . ICD implantation should also be considered .
Immunosuppression
Immunosuppressive therapy is key for graft survival after OHT. Rejection can occur at any time over the life of the allograft, from hyperacute rejection immediately upon allograft reperfusion to acute rejection throughout the post-OHT period and, finally, to chronic rejection in the form of CAV. Acute rejection can result from either cellular (T-cell mediated) or antibody-mediated mechanisms . The majority of immunosuppressive medications currently in use are designed to combat T-cell function and proliferation. All types of rejection are associated with significant morbidity and mortality; thus, aggressive measures must be taken to prevent and treat rejection. Unfortunately, immunosuppressive therapy comes with its own complications, most notably the increased risk of infection and malignancy and toxic drug side effects . Immunosuppression can be divided into three distinct phases: induction therapy, maintenance therapy, and treatment of rejection.
Induction
Induction therapy is administered in the early stages after OHT and may reduce both the incidence of acute rejection and the progression of CAV . However, induction therapy remains controversial as an overall survival benefit has not been demonstrated . The ISHLT does not recommend the routine use of induction agents, although they can be considered in patients with renal insufficiency to delay the start of nephrotoxic CNIs . Patients at the highest risk for rejection ( i . e ., sensitized patients, patients undergoing re-transplantation, and multiparous women) may also benefit from induction therapy with improved survival . Approximately half of all patients undergoing transplantation currently receive induction therapy as part of their immunosuppressive regimen .
Medications
There are two classes of induction medications: T-cell depleting agents and interleukin-2-alpha receptor antagonists (IL-2 RA). Anti-thymocyte globulin (ATG) is a polyclonal antibody that results in T-cell death through CD3-mediated cytolysis. Alemtuzumab is a humanized rat monoclonal antibody that causes both T- and B-cell death through a CD52-mediated pathway. Basiliximab is a chimeric (mouse/human) monoclonal antibody IL-2 RA, which reduces T-cell proliferation . ATG can result in cytokine release syndrome, serum sickness, and cytopenias . In addition, infection occurs more frequently with ATG than with basiliximab or with no induction . Basiliximab is generally well tolerated .
Efficacy
The efficacy of induction therapy is unclear as the data are mixed. Several meta-analyses could not demonstrate a clear benefit of one agent over another or over no induction agent at all . There may be a survival benefit only for patients at very high risk of death from rejection . A recent large-volume analysis of the ISHLT registry demonstrated a 5- and 10-year survival benefit with ATG over basiliximab , but other studies have failed to show any difference .
Maintenance
Maintenance immunosuppression is intended to prevent acute rejection. The four classes of drugs used for maintenance include CNIs, anti-metabolites, corticosteroids, and proliferation signal inhibitors (PSIs). More than 80% of patients are on a regimen that includes tacrolimus (a CNI), mycophenolate mofetil (MMF) (an anti-metabolite), and prednisone, as this combination is the most effective in preventing rejection . The general approach to immunosuppression involves an aggressive strategy early after transplant, with a gradual decrease in intensity over time .
Calcineurin inhibitors
CNIs lead to inhibition of interleukin-2 transcription, which ultimately interferes with T-cell proliferation . Tacrolimus and cyclosporine are the two CNIs currently in use, although tacrolimus has effectively replaced cyclosporine as the preferred agent. Tacrolimus is associated with a lower incidence of rejection than cyclosporine, although survival rates are similar . The side effects of tacrolimus are better tolerated than those of cyclosporine; tacrolimus results in lower rates of hypertension and hyperlipidemia but increases the risk of diabetes mellitus . Rates of nephrotoxicity, neurotoxicity, infection, and malignancy are comparable between the two drugs .
The ISHLT recommends a CNI as a fundamental component to the immunosuppressive regimen. Tacrolimus should be started immediately after OHT, unless initiation has been purposely delayed because of chronic renal insufficiency, in which case induction immunosuppression should be considered. Tacrolimus serum levels should be monitored frequently to guide dosing. If a patient experiences intolerable side effects, lowering the CNI dose, switching to a different CNI, or adding a PSI may be helpful .
Anti-metabolites
Anti-metabolites are used in conjunction with CNIs for maintenance immunosuppression. Azathioprine and MMF, the two agents currently in use, work by interfering with de novo purine synthesis and DNA replication, leading to the inhibition of T- and B-cell proliferation. MMF has become the preferred agent as it is associated with less rejection and improved survival than azathioprine .
Corticosteroids
Corticosteroids are the third component of the so-called triple therapy of maintenance immunosuppression. Corticosteroids work through multiple mechanisms of action to generate a profound anti-inflammatory and anti-immune response. The side effect profile is extensive and includes hypertension, poor wound healing, and diabetes mellitus, among others . Corticosteroids are administered in very high doses, starting intraoperatively, to blunt the recipient’s immune response; an aggressive taper is started immediately thereafter. To reduce the risk of side effects, attempts should be made to wean steroids completely off when the risk of rejection is low .
Proliferation signal inhibitors
PSIs are a fourth class of medications that are sometimes included in the maintenance regimen. The mechanism of action of sirolimus and everolimus involves interfering with cell signaling to result in decreased proliferation of T- and B-lymphocytes . PSIs are currently not recommended as initial maintenance therapy in OHT recipients because of higher rates of rejection and other side effects in the first 6 months . In patients with significant renal dysfunction, switching from nephrotoxic CNI to PSI, or simply reducing dose of CNI after starting PSI, can lead to improvements in kidney function . However, these benefits may not be sustained on long-term follow-up .
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