Background: Acute allograft glomerulopathy (AAG) is an unusual glomerular lesion of allografts with endocapillary hypercellularity, markedly enlarged endothelial cells occluding the capillary lumen, and absence of immune complex deposits. AAG is not currently a rejection lesion recognized by the Banff schema.

Design: We searched a database for biopsies that showed AAG. Light microscopy slides and C4d staining status were reviewed, as were follow-up biopsies. Treatment and clinical follow up data were obtained.

Results: We identified 17 patients with AAG in renal allograft biopsies from Jan 2009-Aug 2015, accounting for <1% of biopsies showing rejection during this time period. The mean patient age was 56 years (range 22-76); ~64% of transplants were from living donors. The median time post-transplant was 2.0 months (range 0.1 to 70). The indication for biopsy in 13 was increased serum creatinine (SCr), mean 3.1 mg/dl (range 1.5-9.4); 2 were protocol biopsies.

All biopsies showed glomerulitis by definition. In addition, the glomeruli showed focal segmental to global marked endothelial enlargement with occlusion of the capillary lumens and infiltrating mononuclear cells and rare neutrophils. Two biopsies showed segmental GBM duplication focally. 13/17 (76%) showed arteritis (Banff v lesions), including 4 with v2 or v3 lesions. 9/17 (53%) showed mild or no interstitial inflammation and 10/17 (59%) showed mild or no tubulitis. 15/17 (88%) were C4d negative; one showed focal C4d PTC staining, and 3 showed moderate peritubular capillaritis. 4/17 (24%) showed focal thrombi in vessels or mesangiolysis. Immunofluorescence was negative for immune complex glomerulonephritis.

8/14 (57%) of patients with data available had a history of donor-specific antibody. 11 patients were on routine triple immunosuppression. Treatment information was available in 12 patients; all but one were treated with immunosuppression (anti-thymocyte globulin in 5 and steroid bolus in 7). Up to 12 months after the biopsy showing AAG, the SCr decreased in 9/15 (60%) patients with data available, mean 1.6 mg/dl (range 0.9-3.3). One graft was lost one month following biopsy. Of 8 follow up biopsies, 6 (75%) showed continued AAG lesions.

Conclusion: AAG is a rare but distinct histopathologic lesion that is highly correlated with vascular rejection and rarely accompanied by histologic lesions associated with alloantibody. AAG should be considered a manifestation of cellular rejection of the glomerulus, possibly by a mechanism similar to endarteritis.

CITATION INFORMATION: AL-Badri O, Alexander M, Cosio F, Cornell L. Acute Allograft Glomerulopathy: A Distinct Form of Cellular Rejection. Am J Transplant. 2016;16 (suppl 3).

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