#2183 Tubuloreticular inclusions in native kidney biopsies and recurrence after transplantation

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Abstract Background and Aims Tubuloreticular inclusions (TRIs) are 20–28nm subcellular structures composed of phospholipid and glycoprotein that arise from the endoplasmic reticulum in endothelial and lymphoreticular cells. Enhanced type 1 Interferon expression can induce TRIs in endothelial cells both in vitro and in vivo. Interferons are produced in the setting of viral infection and autoimmune disease. Hence, TRIs are commonly seen in glomerular endothelial cells in patients with systemic lupus erythematosus (SLE) or viral infection when visualized using electron microscopy (EM). Method This study describes the clinicopathological findings in patients with TRIs on native kidney biopsies between 2005–2022 at a single centre. We further investigate the longitudinal persistence in the native and post-transplant setting, and association with outcomes. Results 593 patients had at least one native kidney biopsy showing TRIs. These patients had 1054 native kidney biopsies (mean 1.78; range 1–8) with 755 biopsies TRI+. The median age at index biopsy was 40 (3–92) years. 406 (68.5%) patients were female. After a median follow of 7 years, 236/593 (40%) patients had at least 2 native biopsies with EM, of whom 117/236 (49.5%) had persistent TRIs. 29 patients had previous biopsies with no TRIs. Table 1 shows the index biopsy diagnosis; 348 (58.7%) patients had SLE. 60 patients had positive virology (HIV: n = 19; hepatitis B: n = 35; hepatitis C: n = 8; hepatitis A: n = 9; hantavirus: n = 1); 21 patients had SLE and positive virology. 17.9% (n = 106) progressed to end-stage renal failure and 10.8% (n = 64) died. 54 (9.1%) patients underwent a renal transplant, of whom 26/54 had a transplant biopsy with EM, 11/26 (42%) patients had transplant biopsies that showed TRIs. Table 1 shows diagnosis of TRI+ transplant biopsies. 6/11 patients with transplant TRIs returned to dialysis. 13/54 (24%) patients returned to dialysis, 5/13 of these went on to receive a second kidney transplant. 6/54 (11.1%) of transplant recipients died. Conclusion 35% of patients in our cohort did not have SLE or positive viral serology; the aetiology and significance of TRIs in this group of patients is unknown. TRIs can be recurring or transient findings and may persist in the transplant setting. 55% of transplant allografts with recurrent TRIs failed, the underlying mechanisms for this require further research.

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