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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Castleman disease (CD) is a benign lymphoproliferative disorder characterized by generalized lymphadenopathy and polyclonal hypergammaglobulinemia, and kidney involvement has been reported in approximately 21–54% of cases. Although various pathological findings, such as AA amyloidosis and thrombotic microangiopathy (TMA), have been described as CD-associated kidney lesions, a detailed description of kidney histopathology limited to CD alone has not yet been established, mainly because previous studies often included cases of TAFRO syndrome, a distinct clinical entity.
We retrospectively compared kidney histopathological findings between 12 patients with CD and 23 patients with TAFRO syndrome who underwent kidney biopsy at our institution.
Among the 12 CD cases, the diagnoses were as follows: AA amyloidosis (n = 2), IgA nephropathy (n = 2; both showing positive mesangial deposition of IgA and C3 on immunofluorescence and electron-dense deposits in the paramesangial area by electron microscopy, although mild in degree), membranous nephropathy (n = 2), nephrosclerosis (n = 1), secondary focal segmental glomerulosclerosis (FSGS) (n = 1), minor glomerular abnormalities (MGA) (n = 3), and crescentic membranoproliferative glomerulonephritis (MPGN) (n = 1).
In all nine cases except those with MGA—thus, in all CD cases with kidney lesions—focal plasma cell infiltration into the tubulointerstitium was observed. However, tubulitis was absent or only minimal. Interstitial fibrosis and tubular atrophy (IFTA) were disproportionately advanced relative to the degree of glomerular sclerosis. No endothelial injury was noted in any of the CD cases.
In contrast, among the 23 TAFRO syndrome cases, 21 exhibited TMA, one of which was accompanied by acute tubular necrosis (ATN). The remaining two cases were diagnosed with ATN (n = 1) and membranous nephropathy (n = 1), respectively.
Although TMA has long been considered a common kidney pathological finding in Castleman disease, our analysis suggests that most of these cases may, in fact, have been attributable to TAFRO syndrome. Unlike TAFRO syndrome, in which TMA is observed in nearly all cases, CD showed no evidence of endothelial injury. Instead, CD was characterized by heterogeneous glomerular pathologies accompanied by focal plasma cell infiltration in the tubulointerstitium without tubulitis, which may contribute to gradual kidney function decline. This study provides the first detailed characterization of kidney histopathology specific to CD and highlights both its distinct and overlapping histopathological features.
