CASE 23 (January 2008)
A 42-year-old woman with unknown cause end-stage renal disease underwent kidney allograft transplantation from cadaveric donor six years ago. She was in hemodialysis during five months previous to transplantation. There were three HLA mismatches, one of these DR. The patient did not present cytotoxic antibodies on immunologic pre-transplantation tests. Other personal antecedents: arterial systemic hypertension, there is not history of diabetes, autoimmune diseases or other diseases. There is not familiar history of renal or autoimmune diseases.
Renal function was well, although there was an episode of acute rejection in the second post-transplantation month, treated with steroid boluses, but it was not histologically confirmed. Renal function was normal until 5th post-transplantation year when serum creatinine increase was detected, the serum levels continued increasing, and the increase was slow but progressive. Due to social and economical difficulties her immunosuppressor treatment was irregular (cyclosporine, mycophenolate mofetil, and prednisone). The patient developed end-stage-renal disease and she starts hemodialysis at six post-transplantation years.
The immunosuppression was stopped and days after she develops pain in the allograft area. Main renal artery thrombosis was diagnosed by Doppler. Graft nephrectomy was carried out 25 days after the immunosuppression was stopped.
The patient does not present systemic alterations, blood pressure has been controlled, there are not skin lesions, there are not lung abnormalities on examination, there are not clinical signs suggesting vasculitis.
See the images.
Figure 1. Macroscopic image of allograft nephrectomy. See the obstruction of the main renal artery, magnified on the right.
Figure 2. Extensive chronic changes in cortex and medulla (ci3 and ct3 on Banff graduation scheme). Left and right: H&E, X200.
Figure 3. In several areas with non-athophic tubules there is acute rejection, with severe tubulitis (t3) and plasma cell infiltrates (right). Left and right: H&E, X400.
Figure 4. There are many arteries with evidence of chronic rejection, and changes suggesting a T-cell mediated process. In the left image we can see a segment of the main renal artery with intimal inflammatory cells, foam cells, and disruptions of the elastica (does not seen in the image). In the right image we can see a cortical radial artery with chronic rejection changes. Left: H&E, X200, right: H&E, X400.
Figure 5. In several glomeruli (approximately 10% of viable glomeruli) there are crescents, some cinrcumferential and others circumscribed. H&E, left X100, right X400.
Figure 6. Other glomeruli with circumscribed crescents. Left and right: H&E, X400.
With methenamine-silver stain double contours are observed in capillary loops (cg1), but there are not other changes suggesting antibody-mediated rejection.
Immunostaining for C4d: Negative in peritubular capillaries
Immunofluorescence for IgA, IgG, C3, and C1q were negative; there are some focal and segmental glomerular unspecific IgM deposits.
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