• The most common findings are fever and tachypnea.

• Chest examination may reveal crackles and rhonchi. Radiographic Tests

• Chest radiographs may be normal in up to 25% of patients.

• The most common radiographic abnormalities are diffuse, bilateral, interstitial, or alveolar infiltrates.

Fungal Infections

Fungal infections are an important cause of morbidity and mortality in solid organ transplant recipients. Immunologic (i.e., immunosuppressants, CMV infection), anatomic (i.e., tissue ischemia and damage), and surgical (i.e., duration of surgery, transfusion requirements) factors contribute to the risk for invasive fungal infections. Mucocutaneous candidiasis (i.e., oral thrush, esophagitis) is associated with corticosteroid and ALA use. Oral nystatin or clotrimazole troches are effective prophylactic options for the prevention of thrush. However, clotrimazole inhibits the CYP3A system in the gut and can alter immunosuppressive levels.9 The use of systemic fungal prophylaxis, such as oral fluconazole, is controversial due to the potential for DDIs and the risk of developing resistance. The American Society of Transplantation and the American Society of Transplant Surgeons have recommended antifungal prophylaxis in liver, lung, and intestine transplantation.58 The choice of agents depends on the fungal risk in that particular population. For example, liver and intestine transplant recipients are at high risk for candidiasis; therefore, the use of medications that cover Candida spp. is crucial, such as the triazole antifungals (i.e., fluconazole, itraconazole) or the echinocandins (i.e., caspofungin, micafungin). Lung transplant recipients are at high risk for aspergillosis; therefore, it is imperative to use antifungal prophylaxis that covers Aspergillus spp., such as the echinocandins or polyenes (i.e., amphotericin B, lipid-based amphotericin B products).58


© Cardiovascular disease has been identified as one of the leading causes of death in organ transplant recipients.59 Post-transplant hypertension is associated with an increase in cardiac morbidity and patient mortality in all transplant patients and is also an independent risk factor for chronic allograft dysfunction and loss.60 Based on all of the available post-transplant morbidity and mortality data, it is imperative that post-transplant hypertension be identified and managed appropriately.

There are several underlying mechanisms responsible for post-transplant hypertension. Some causes of hypertension in transplant recipients may include renal dysfunction, increased sensitivity to endothelin-1 and angiotensin, increased density of glucocorticoid receptors in the vascular smooth muscle, and decreased production of vasodilatory prostaglandins.61 However, one of the most easily recognized causes of post-transplant hypertension is the use of corticosteroids and the calcineurin inhibit-

/'o ¿r i ors. ' Corticosteroids usually cause sodium and water retention, thus increasing blood pressure, whereas calcineurin inhibitors are associated with a number of effects that may result in hypertension, including reduced glomerular filtration rate (GFR) and renal blood flow (RBF), increased systemic and intrarenal vascular resistance, sodium retention, reduced concentrations of systemic vasodilators (i.e., prostacyclin, nitric oxide), and increased concentrations of vasoconstrictive thromboxanes.64 When compared with cyclosporine in clinical trials, tacrolimus displayed significantly less severe hypertension, and patients taking tacrolimus required significantly fewer antihypertensive medications at both 24 and 60 months post-transplant.65-67

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