More than one-third of patients on waiting lists for kidney transplant are sensitized. Most have previously formed donor-specific and non-donorspecific serum antibodies and/or positive crossmatch by complement-dependent cytotoxity and/or flow cytometry. Two categories of alloantibodies include antibodies against major histocompatibility complex human leukocyte antigen class 1 and class 2 and antibodies against minor histocompatibility complex. A current positive crossmatch is an absolute contraindication for transplant. Positive historical panel reactive antibody and/or donor-specific antibodies (human leukocyte antigen and minor histocompatibility complex), even in the absence of a historical positive crossmatch, are associated with an increased risk for allosensitization, antibodymediated rejection, and accelerated graft failure. Desensitization protocols are numerous, complex, and expensive. It is recommended to perform a systematic determination of historical and current panel reactive antibody, donor-specific antibodies (human leukocyte antigen and minor histocompatibility complex), and crossmatch by the most sensitive assays. The risk of sensitization may be estimated from the combined results of the crossmatch with the donor and those of the recipient's panel reactive antibody and donor-specific antibodies at baseline. The adoption of a scoring system for risk stratification may facilitate the task of organ allocation for sensitized patients. Recipients with an estimated sensitization risk ≥ high may be referred preferably to the national waiting priority list and informed about the financial and the medical risks that may incur with future transplant. Sensitized patients at high risk for antibody-mediated rejection may benefit from a structured monitoring process involving systematic and regular immunologic, histologic, and functional assessments of the graft after transplant. We recommend the adoption and regular updating of these approaches to ensure safe and appropriate therapeutic standards in these sensitized patients, in accordance with best clinical practice.
We report a case of early recurrent membranous glomerulonephritis after kidney transplant from a deceased donor. The patient received induction therapy and was discharged with a serum creatinine level of 0.78 mg/dL on triple maintenance immunosuppressive therapy, which included tacrolimus, mycophenolate mofetil, and prednisone. At 7 months after transplant, a graft biopsy for new-onset isolated proteinuria (2.7 g/day) revealed stage 2 recurrent membranous glomerulonephritis. In the face of persistent proteinuria despite combined conservative rituximab therapy over several months and the total eradication of CD20-positive cells, bortezomib was introduced. This resulted in a substantial decline in proteinuria within 2 months and its subsequent disappearance several months later. This was paralleled by a considerable drop in plasma CD34-positive and CD138-positive cell counts. These preliminary observations indicate that recurrent posttransplant membranous glomerulonephritis is associated in part with a B-cell-mediated immunologic process that may involve both CD20-positive and plasma cells. Rituximab-resistant or partially responsive recurrent posttransplant membranous glomerulonephritis may benefit from a proteasome inhibitor-based therapy.
All three had had many years of homosexual activity and many different sexual partners a year, and therefore their primary infections had probably occurred many years earlier. Our finding of excretion of the virus in these men might indicate that some homosexual men continue to excrete cytomegalovirus in seminal fluid over many years or, alternatively, that there had been recent reinfection, perhaps with a different strain of cytomegalovirus. More probably, however, latent cytomegalovirus re-emerges in men with immunosuppression.Recently there have been many reports of homosexual men developing illnesses, including Kaposi's sarcoma, that are related to immune suppression. Clinical and epidemiological aspects of these illnesses were recently summarised.'2 Evidence of abnormal ratios of T cell helpers to suppressors in apparently healthy homosexual men has also been documented," and the low ratios reported are similar to those that we found in the older homosexual men who were excreting cytomegalovirus in their seminal fluid. Excretion of cytomegalovirus in the seminal fluid of these more experienced homosexual men and of a homosexual patient with Kaposi's sarcoma is therefore probably the result of immune dysfunction. Serological examination suggested schistosomiasis, but there were no parasites in the urine and the rectal mucosa looked normal on endoscopy. Nevertheless, rectal biopsy showed schistosomal proctitis and many ova of S mekongi. Two courses of praziquantel cleared the ova from his rectal mucosa.
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