Cytomegalovirus infection is a frequent complication after transplantation. This infection occurs due to transmission from the transplanted organ, due to reactivation of latent infection, or after a primary infection in seronegative patients and can be defined as follows: latent infection, active infection, viral syndrome or invasive disease. This condition occurs mainly between 30 and 90 days after transplantation. In hematopoietic stem cell transplantation in particular, infection usually occurs within the first 30 days after transplantation and in the presence of graft-versus-host disease. The major risk factors are when the recipient is cytomegalovirus seronegative and the donor is seropositive as well as when lymphocyte-depleting antibodies are used. There are two methods for the diagnosis of cytomegalovirus infection: the pp65 antigenemia assay and polymerase chain reaction. Serology has no value for the diagnosis of active disease, whereas histology of the affected tissue and bronchoalveolar lavage analysis are useful in the diagnosis of invasive disease. Cytomegalovirus disease can be prevented by prophylaxis (the administration of antiviral drugs to all or to a subgroup of patients who are at higher risk of viral replication) or by preemptive therapy (the early diagnosis of viral replication before development of the disease and prescription of antiviral treatment to prevent the appearance of clinical disease). The drug used is intravenous or oral ganciclovir; oral valganciclovir; or, less frequently, valacyclovir. Prophylaxis should continue for 90 to 180 days. Treatment is always indicated in cytomegalovirus disease, and the gold-standard drug is intravenous ganciclovir. Treatment should be given for 2 to 3 weeks and should be continued for an additional 7 days after the first negative result for viremia.

OBJECTIVES: To evaluate the prevalence of cholecystopathy in chronic renal patients awaiting kidney transplants. INTRODUCTION: The prevalence and management of cholelithiasis in renal transplant patients is not well established. METHODS: A total of 342 chronic renal failure patients on the waiting list for a kidney transplant were studied. Patients were evaluated for the presence of cholelithiasis and related symptoms, previous cholecystectomies and other abdominal surgeries, time on dialysis, and general data (gender, age, number of pregnancies, and body mass index). RESULTS: Cholelithiasis was found in 41 out of 342 patients (12%). Twelve of these patients, all symptomatic, had previously undergone cholecystectomies. Five out of 29 patients who had not undergone surgery were symptomatic. Overall, 17 patients (41.5%) were symptomatic. Their mean age was 54 (range 32-74) years old; 61% were female, and their mean body mass index was 25.4. Nineteen (76%) out of 25 women had previously been pregnant, with an average of 3.6 pregnancies per woman. CONCLUSIONS: The frequency of cholelithiasis was similar to that reported in the literature for the general population. However, the high frequency of symptomatic patients points toward an indication of routine pre-transplant cholecystectomy to avoid serious post-transplant complications.

A pneumonia por Pneumocystis carinii (PPC) em transplantados renais é, habitualmente, prevenida pelo uso profilático de trimetoprim-sulfametoxazol (TMS). Foi demonstrado que o micofenolato mofetil (MMF) exerce um poderoso efeito protetor sobre a PPC experimental em ratos. Este efeito também foi sugerido em humanos pela ausência de PPC em pacientes recebendo MMF. A partir de janeiro de 1998 passamos a usar o MMF em transplantados renais sem profilaxia por TMS. Nos pacientes recebendo azatioprina (AZA) a profilaxia com TMS continuou a ser empregada. A incidência de PPC foi analisada em ambos os grupos. Os dados foram coletados após um mínimo de seis meses de seguimento. Foram analisados 272 pacientes. Não ocorreu nenhum caso de PPC tanto nos pacientes recebendo MMF como naqueles recebendo AZA. O MMF pode ter exercido um efeito protetor contra a PPC, já que nenhum paciente sob MMF e sem receber profilaxia por TMS desenvolveu PPC. Estudos maiores e controlados se fazem necessários para confirmar estas informações.

Pneumocystis carinii pneumonia (PCP) is usually prevented in transplanted patients by prophylactic trimethoprim-sulfamethoxazol (TMS). Mycophenolate mofetil (MMF) has been shown to have a strong protective effect against PCP in rats. This effect is also suggested in humans by the absence of PCP in patients receiving MMF. After January 1998 MMF has been used with no TMS prophylaxis in renal transplanted patients. In azathioprine (AZA) treated patients TMS prophylaxis was maintained. The incidence of PCP was analyzed in both groups. Data were collected in order to have a minimum 6-month follow-up. Two hundred and seventy-two patients were eligible for analysis. No PCP occurred either in patients under MMF without TMS prophylaxis nor in patients under AZA. MMF may have an effective protective role against PCP as no patient under MMF, despite not receiving TMS coverage, developed PCP. A larger, controlled, trial is warranted to consolidate this information.

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.