Donor-specific antibodies against HLA, MICA, and GSTT1 in patients with allograft rejection and C4d deposition in renal biopsies.

Background: Production of antibodies against donor-specific antigens is one of the central mechanisms of allograft rejection. This antibody-mediated rejection (AMR) is evidenced by the presence of circulating donor-specific antibodies and deposition of complement component C4d on renal endothelium. Although anti-human leukocyte antigen (HLA) antibodies account for a high proportion of AMR, in many cases anti-HLA antibodies cannot be demonstrated.

Anti-glutathione S-transferase T1 antibody-mediated rejection in C4d-positive renal allograft recipients.

Background: Chronic humoral rejection is a progressive form of graft injury, with defined diagnostic criteria, the crucial one being the evidence of circulating anti-donor antibodies. These antibodies are mainly directed against human leucocyte antigens (HLA), but other targets have also been described. We previously reported that antibodies against the Glutathione S-transferase T1 (GSTT1) enzyme appear in recipients without the GSTT1 gene who receive a graft from a GSTT1-positive donor.

[Nephrotic syndrome in scleroderma].

The renal affectation is infrequent in scleroderma, unlike other collagen diseases. The appearance of nephrotic syndrome has been related to the drug use, specially the D-penicilamine, or rarely as a manifestation of secondary amilodosis, quite infrequent in scleroderma. We report a case of nephrotic syndrome in a patient with systemic scleroderma, produced by a membranous glomerulonephritis, exceptionally described in literature.

Disseminate and fatal cytomegalovirus disease with thymitis in a naive HIV-patient after early initiation of HAART: immune restoration disease?

We describe a naive HIV-infected patient who developed a Pneumocystis carinii pneumonia and disseminate and fatal cytomegalovirus disease within 3 months after initiation of HAART, suggesting due to coincidence in time, an immune restoration disease. We propose an alternative hypothesis.

Bone involvement and abcess formation by neutrophil-rich CD30+ anaplastic large-cell lymphoma mimicking skeletal infection in an AIDS patient.

Neutrophil-rich CD30+ anaplastic large-cell lymphoma (ALCL) is a rare pathological entity without distinct clinical behavior. Twelve cases of neutrophil-rich CD30+ anaplastic large-cell lymphoma (ALCL) have been reported, three of them were HIV-infected patients. All these reports stressed the presence of neutrophil infiltration as a new morphologic feature of CD30+ ALCL.