Tuberculose (TB) foi diagnosticada em 25 de 466 pacientes submetidos a transplante renal. A TB surgiu entre 1 mês e 9 anos pós-transplante. O pulmão foi acometido em 76% dos casos, isoladamente (56%), ou associado a outras localizações (20%). Os outros órgãos envolvidos foram: pele, articulações, testículos, trato urinário, sistema nervoso central e linfonodos. O diagnóstico foi confirmado por biópsia em 64% dos casos, pela identificação do bacilo em 24% e apenas à necrópsia em 12%. Três formas histológicas foram identificadas: exudativa (nos casos de aparecimento precoce e de maior gravidade) granulomatosa (naqueles benignos e de aparecimento tardio) e mista (naqueles intermediários). As doses de azatioprina foram constantes ao longo do período pós-transplante, tanto no grupo tuberculoso como no controle, bem como nos pacientes tuberculosos que faleceram e que se curaram. O número de crises de rejeição tratadas foi maior no grupo TB do que no grupo controle. As doses de prednisona e o número de crises de rejeição foram maiores nos pacientes tuberculosos que faleceram do que naqueles que sobreviveram. Quinze pacientes se curaram e 10 faleceram, oito de causas relacionadas à TB, Seis destes óbitos ocorreram nos 6 primeiros meses pós-transplante. Em um paciente a TB foi transmitida pelo enxerto.

Tuberculosis (TB) was diagnosed in 25 of 466 patients who underwent renal transplant over a period of 15 years. TB developed from 1 month to 9 years post-transplant. In 56% of the cases the onset was within the first post-transplant year. TB affected several isolated or combined organs. Pulmonary involvement was present in 76% of cases, either as isolated pleuro-pulmonary (56%) or associated with other sites (20%). The non-pulmonary sites were: skin, joints, tests, urinary tract, central nervous system and lymphonodules. The diagnosis was confirmed by biopsy in 64% of the cases, by identification of tubercle bacilli in 24% and only at necropsy in 12% Biopsy specimens could be classified in three histological forms: exudative, that occurred in early onset and more severe cases granulomatous in late onset and benign cases; and mixed in intermediate cases. Azathioprine dosages were similar along post-transplant time periods in TB patients and in the control groups; and in TB patients who were cured and who died. The number of steroid treated rejection crises was greater in TB than in the control group. Prednisone doses were higher and the number of rejection crises was greater in TB patients who died than in those who were cured. Fifteen patients were cured and ten died, two of them of causes unrelated to TB. Six of the eight TB-related deaths occurred in the first 6 post-transplant months. The outcome was poor in patients in whom TB arose early in post-transplant period and where the exudative or mixed forms were present; whereas the prognosis was good in patients with late onset and granulomatous form of TB. In one patient TB was transmitted by the allograft.

Os Autores registram caso de histoplasmose generalizada em paciente transplantado com rim de doador não aparentado. Além da infecção fúngica diagnosticada sorologicamente e pela histopatologia, a autópsia revelou cirrose hepática macro e micronodular, de provável etiologia viral (vírus B), hepatocarcinoma, depleção linfóide do baço e glomerulopatia de transplante. Revendo a literatura sobre o assunto, chegam à conclusão de que, provavelmente, com a imunodepressão medicamentosa, as lesões pulmonares por reinfecção endógena foram as primeiras a aparecer sob a forma de uma histoplasmose pulmonar crônica.

The Authors report a case of disseminated histoplasmosis in a patient during the course of non related kidney transplant. Besides the fungal infection detected by serology and histopathology, autopsy showed macro and micro-nodular hepatic cirrhosis, probably of viral etiology (B virus), hepatocarcinoma, lymphoid depletion of the spleen and transplant glomerulonephritis. After concerning literature review the Authors conclude that probably due to immunosuppressive therapy, the pulmonary lesions by endogenous reinfection were the first to appear under the form of a chronic pulmonary histoplasmosis.