Drug reactions, variable tissue reactions to rejection, and a host of other findings may be observed in the lungs of lung transplant recipients. Alveolar proteinosis has developed in up to 5% of new lung transplant recipients in the past 3 years, possibly as a result of macrophage dysfunction caused by immunosuppressants. Impaired macrophage lipoprotein processing due to newer immuosuppressive therapies and acute lung injury are believed to be the potential cause of alveolar proteinosis in these patients. Histology on biopsy shows alveolar spaces expanded by granular eosinophilic material, and material with similar features can be found on bronchoalveolar lavage (see Chapter 76).

Possible causes of intra-alveolar hemorrhage in lung transplant recipients include perioperative bleeding, bleeding diathesis due to sepsis or pancytopenia secondary to immunosuppressive therapy, severe rejection, and infection. Alveolar hemosiderin is a frequent finding in transplant lung biopsy characterized by numerous hemosiderin-laden macrophages within intra-alveolar spaces and may be the result of surgical procedure. It has been related to the number and grade of episodes of acute rejection in a given patient and bleeding. Prussian blue stain can be used to highlight the hemosiderin. Deposits of hemosiderin around blood vessels are thought to be evidence of previous involvement of those vessels by previous episodes of acute rejection. Tiny focal parenchymal calcifications are thought in some cases to represent foci of previous infection including cytomegalovirus. Foci of previous infection may also have hemosiderin deposits.