Candida species are part of the kidney transplant recipient’s endogenous flora, and risk factors for the development of systemic disease by this organism include immunosuppression, diabetes, broad-spectrum antibiotics, total parenteral nutrition, active cytomegalovirus (CMV) infection, and indwelling intravenous or bladder catheterization (5,8,31). The renal transplant recipient is particularly prone to developing urinary tract infections with Candida species, a pathogen that is associated with between 18% and 88.5% of fungal infections in kidney transplant patients (1,3). Candida albicans is the species most frequently associated with disease, but other nonalbicans candidal species (including C. krusei, C. glabrata, C. parapsilosis, and C. tropicalis) have been increasingly recognized as pathogens in immunocompromised hosts, including transplant recipients, in recent years (3,4). Although the kidney allograft itself can be a source of infection with Candida (4), candidal urinary tract infection is generally an early, nosocomial infection associated with the use of indwelling bladder catheters which can become manifest within the first 2 months posttransplant (6). Ascending infection with Candida species has been associated with ureteral obstruction from the formation of fungus balls (6,32), and renal parenchymal disease can threaten allograft survival (3,4). Central intravenous catheters and esophagitis serve as the other two main sources for infection by Candida species (33) which can occur at any time post-transplantation but is encountered most frequently during the first 6 months (1,6). Invasive infections with Candida species, which lead to candidemia and sometimes endocarditis, are associated with 23% to 71% mortality in the renal transplant recipient (3). Invasive Candidal infections were the second most common infectious cause of death in one autopsy series of kidney transplant patients spanning 20 years (34).

Aspergillus species are the most common mycelial fungi to cause disease in the kidney transplant patient, generally acquired from the environment by inhalation of spores and often beginning as a nosocomial pneumonia within the first 2 to 3 months after transplantation (3,4,6). Less frequently, Aspergillus infection may occur via the paranasal sinuses, a cutaneous lesion, or gastrointestinal source (4). The primary risk factors for Aspergillus infection in this group of patients include graft failure and increased immunosuppression (14,35), with both functioning macrophages and neutrophils known to be particularly important for warding off infection (4). In addition, high creatinine, neutropenia, and active
CMV infection can predispose renal transplant recipients to Aspergillus infection (4).