PMC8821965_01
Light and electron microscopy analysis. (A-C) Light microscopy using hematoxylin-eosin staining showing diffuse endocapillary proliferation composed of heteromorphic lymphocytes and a small number of neutrophils (A, B) and multifocal interstitial infiltration of lymphocytes and monocytes with focal tubular necrosis (C) [magnification, x100 (A); magnification, x400 (B, C)]. (D) Electron microscopy showing endocapillary proliferation of heteromorphic lymphocytes (red arrows) and low-density electron-dense deposition in the mesangial area (blue arrows) with the extensive fusion of podocyte foot processes.
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Most heteromorphic lymphocytes and a small number of neutrophils were observed in the intra-glomerular capillaries ( Figure 1 ). In addition, lymphocyte and monocyte ( Figure 1C  and  Figure 2 ) interstitial infiltration was revealed in histology, proving that tubulointerstitial injury might also be involved in the pathogenesis of the kidney injury.
Immunohistochemistry analysis. (A) Immunochemistry analysis showing CD20-/CD3+/CD8+/GranzymeB+ phenotype of the infiltrating endocapillary glomerular cells (magnification, x200). (B) Immunochemistry analysis on tubulointerstitial compartment showing CD20+/CD3+/CD8+ cells infiltrating the interstitium (magnification, x200).
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T cell immunophenotype ( Figure 2 ). The above-mentioned findings of renal pathology suggested endocapillary proliferative glomerulonephritis associated with T-LGLL. In addition, lymphocyte and monocyte ( Figure 1C  and  Figure 2 ) interstitial infiltration was revealed in histology, proving that tubulointerstitial injury might also be involved in the pathogenesis of the kidney injury.
Changes of serum creatinine and blood urea nitrogen during the disease course.
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Supportive therapy was initiated after the patient was admitted to our hospital, including hemodialysis and transfusion of platelet and plasma, while the levels of SCr and BUN continued to increase as shown in  Figure 3 .