Aim-To investigate the eVect of diVerent interventions on the inclusion of data items in the histopathology reports of resected colorectal carcinomas. Study population-272 routine histopathology reports on colorectal carcinomas from the department of histopathology, Royal Hallamshire Hospital, SheYeld. Methods-The presence or absence of 10 specific data items was recorded for each report. The reports were divided into five audit periods. In the initial period reports were generated using free text with no agreed guidelines. In period 2, text guidelines had been issued; in period 3, flow diagram guidelines had been issued; and in periods 4 and 5, template proformas were attached to each specimen request form. Results-All interventions produced some increase in inclusion rate for some features, but only with the introduction of template proformas did these rates approach 100% for all data items. Inclusion rates were 100% for all items in all cases reported using a proforma. In the final audit period 96% of specimens were reported using proformas. Conclusions-Template proformas produce a high rate of inclusion of data items in reports of colorectal carcinoma resection specimens. (J Clin Pathol 1998;51:481-482)
Transplant glomerulopathy (TG) is a lesion with specific morphology and strong evidence of an immune mechanism. The incidence of TG is approximately 20% by 5 years after transplantation. TG is characterized by proteinuria, hypertension and declining graft function. Appearances on light microscopy include thickened capillary walls and double contours, with reduplication or lamination of the glomerular basement membrane on electron microscopy. TG is associated with acute rejection, the antibody status before transplantation and de novo HLA antibodies. HLA class II and/or donor-specific antibodies incur additional risks. Desensitization protocols do not always prevent the development of TG in highly sensitized individuals. Associations between TG, past or current C4d and the presence of alloantibodies are recognised, however, C4d in the peri-tubular capillaries or glomeruli is not a prerequisite at the time of diagnosis. Clinical observation and animal models suggest that TG arises as a consequence of chronic endothelial cell (EC) injury by the humoral arm of the immune system. In some cases, this follows a period of EC accommodation after an episode of acute injury. Proposed treatments include augmentation of background immunosuppression, and trials of monoclonal therapies targeted at CD20-positive B cells are underway.
Proteinuria is associated with DSA detection and is likely to be an important factor that determines rapid GFR decline and earlier graft failure in patients developing de novo HLA antibodies.
Recent evidence suggests that alloantibody may play an aetiological role in the pathogenesis of membranous glomerulopathy in native kidneys. There is an increased awareness of the significance of alloantibody on renal transplant outcome, particularly with the development of more sensitive assays. We describe a kidney transplant patient who developed de novo membranous glomerulopathy (DNMG) with heavy proteinuria in the context of a donor-specific alloantibody (DSA) directed against HLA DQ7. Proteinuria resolved and kidney function stabilized following treatment with mycophenolate mofetil and an angiotensin receptor blocker. The titre of the DSA fell in parallel with resolution of the proteinuria. This is the first reported case of DNMG after kidney transplantation clearly associated with a DSA. We hypothesize that de novo membranous glomerulopathy may be an atypical manifestation of acute antibody-mediated damage. Cases of DNMG should be screened for alloantibody and the presence of alloantibody may influence the choice of therapy.
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