Introduction: Renal transplantation is a treatment to chronic glomerular disease. However, the clinical course of renal allograft varies. A minority of allograft glomeruli has demonstrated crescents, either with or without other renal pathology. Crescentic glomerulonephritis (CGN) is categorized by immunohistology into anti-GBM CGN, immune complex CGN, or pauci-immune CGN. Crescents also occur in categories of glomerular injury that are not included in the three major categories of crescentic glomerulonephritis. Characteristics of crescents or CGN have been well documented, but little are known of their etiology in allograft kidney. Herein, we investigated the etiologies of crescents in allograft kidney.
Materials and Methods: A retrospective analysis was performed in cases of kidney transplant biopsies diagnosed with either cellular, fibrocellular, or fibrous crescent between January 2010 and December 2019. After excluding time-zero biopsy, the total number of allograft biopsy was 1602. Thirty-nine renal allograft biopsies showing crescents were collected. The number of crescents more than 10% of the total glomeruli were selected and the total cases were 27. Clinical and histological data were reviewed via electronic medical record.
Results: All biopsies showed focal crescents (mean 18.39% glomeruli, range 10-43%). Twenty-one cases showed cellular/fibrocellular crescents and 6 cases had fibrous crescents only. One case was diagnosed as recurrent pauci-immune CGN with previous same diagnosis in the native kidney. Crescents in 20 cases were associated with immune-complex. Sixteen were diagnosed as IgA nephropathy, 3 were immune-complex mediated CGN, and 1 was membranous nephropathy. Native kidney biopsy was available in 9 out of 20 cases. Six cases were IgA nephropathy, 1 was membranoproliferative glomerulonephritis (MPGN), 1 was chronic glomerulonephritis, and the other was end-stage renal disease without a specific diagnosis. The remaining 6 cases were not in the major categories of CGN; 2 cases showed chronic calcineurin inhibitor toxicity, 2 cases showed chronic rejection, 1 case showed chronic calcineurin inhibitor toxicity and chronic antibody-mediated rejection, and 1 case showed mild tubulitis and mild arteriosclerosis. One case was available for the native kidney diagnosis which was focal segmental glomerulosclerosis (FSGS). Pre-transplantation anti-neutrophil cytoplasmic antibody results were available for 2 patients and were negative.
Discussion: CGN is rare in allograft kidney. In our center, most of the renal allograft CGN were immune-complex mediated and majority of them were IgA nephropathy. The most prevalent diagnosis of native kidney was also IgA nephropathy. The graft outcome in allograft CGN according to different etiologies are not well known and yet to be studied.
Conclusion: Glomerular crescents in allograft kidney has different etiologies. Most of them are associated with immune-complex and IgA nephropathy.