PMC9932912_01
Timeline of events.
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F1
Figure 1 is a timeline of the patient's clinical course and treatments. Vascular B-ultrasound showed bilateral popliteal vein blood flow, and bilateral mural thrombosis was considered (Figures 1E,F).
Clinical features of the current patient. Among auxiliary examinations, color Doppler ultrasound showed hypoechoic masses in the wall of the inferior vena cava (A), and of the right renal vein (B), considering the possibility of thrombosis. Pulmonary artery CT angiography (CTA) showed embolisms of the distal main pulmonary artery, left pulmonary artery trunk and its intrapulmonary branches, and the right lower pulmonary artery (C), considering the possibility of ischemic infarction. The thrombi disappeared after effective treatment (D). Vascular B-ultrasound showed bilateral popliteal vein blood flow, and bilateral mural thrombosis was considered (E-F).
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Color doppler ultrasound showed hypoechoic masses in the wall of the inferior vena cava (Figure 2A), and of the right renal vein (Figure 2B), considering the possibility of thrombosis. Pulmonary artery CT angiography (CTA) showed embolisms of the distal main pulmonary artery, left pulmonary artery trunk and its intrapulmonary branches, and the right lower pulmonary artery (Figure 2C), as well as exudation and consolidation of bilateral lower lobes, considering the possibility of ischemic infarction. After discharge, the patient underwent regular follow-up checkups, the thrombi disappeared (Figure 2D).
The renal pathology of the current patient. Immunofluorescence showed that IgA, IgG, C3, IgM, Fibrin, C4, C1q, MABalpha-1, MABalpha-3, and MABalpha-5 were all positive (A-E). Under the light microscope, there were 11 glomeruli, 9/11 glomeruli had bulbous sclerosis, the other 2 glomeruli had increased lobulation, mesangial cells (2-4 area) hyperplasia and mesangial matrix, capillaries did not open well, and endothelial proliferation and glomerulus exudation with peribulbar fibrosis and inflammatory cell infiltration were observed. Segmental thickening of the glomerular basement membrane was found, and deposition of polyerythrophilin was observed subcutaneously in the mesangial area. Additionally, there were vacuolar degeneration of renal tubules, abundant protein tubules, and marked edema and fibrosis of renal interstitium with focal inflammatory cell infiltration (F-G). The mesangial cells in 2 glomeruli showed mild to moderate proliferation of matrix with abundant electron deposits. Capillary basement membrane thickness extensively thickened (800-3000 nm). There were large high-density electron deposits on the endothelial side, extensive fusion of microvilli, and partial renal tubular epithelial edema in the foot process (H-I).
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Renal pathology suggested lupus nephritis (LN) (type VI according to ISN/RPS Classification Standard) (Figures 3A-I).