Tubular basement membrane (TBM) deposits are very uncommon in non-lupus membranous nephropathy. We report 5 patients with membranous nephropathy and extensive TBM deposits following allogeneic hematopoietic cell transplant. Patients presented with nephrotic syndrome (3 also had acute kidney injury) late post-transplant in association with chronic graft-versus-host disease (cGVHD). Kidney biopsies revealed global subepithelial and extensive TBM immune complex deposits, accompanied by acute tubular injury (n = 4) and tubulointerstitial inflammation (n = 4). Proteomic analysis of glomeruli in 4 cases identified PLA₂R in 1, with no significant protein spectra for PLA₂R, THSD7A, EX1/2, NELL-1, PCDH7, NCAM1, or SEMA3B detected in the remaining 3. On follow-up (for a mean 42 months), 4 patients had complete and 1 partial remission following prednisone and/or rituximab therapy. We propose that membranous nephropathy with extensive TBM deposits is a distinctive clinicopathologic lesion associated with allogeneic hematopoietic cell transplant. Pathogenesis likely involves cGVHD-driven antibodies against glomerular and TBM components, the identity of which remains to be elucidated.

管状基底膜（TBM）沉积在非狼疮膜性肾病中非常罕见。我们报告了 5 例异基因造血细胞移植后出现膜性肾病和广泛 TBM 沉积的患者。患者在移植后晚期出现与慢性移植物抗宿主病（cGVHD）相关的肾病综合征（3 名患者还患有急性肾损伤）。肾脏活检显示整体上皮下和广泛的 TBM 免疫复合物沉积，伴有急性肾小管损伤 (n = 4) 和肾小管间质炎症 (n = 4)。4 例肾小球的蛋白质组学分析在 1 例中鉴定出 PLA ₂ R，在其余 3 例中未检测到 PLA ₂ R、THSD7A、EX1/2、NELL-1、PCDH7、NCAM1 或 SEMA3B 的显着蛋白质谱。 （平均 42 个月），4 名患者在泼尼松和/或利妥昔单抗治疗后获得完全缓解，1 名部分缓解。我们认为，伴有广泛 TBM 沉积的膜性肾病是一种与异基因造血细胞移植相关的独特临床病理病变。发病机制可能涉及 cGVHD 驱动的针对肾小球和 TBM 成分的抗体，其身份仍有待阐明。