RESUMO
Vaccination against the SARS-CoV-2 virus (COVID-19) has proven to be the most effective measure to prevent the spread and reduce infection severity. A case report of de novo membranous nephropathy (MN) following immunization with inactivated virus vaccine (CoronaVac®, Sinovac Biotech) is presented here. A 53-year-old man presented with a sudden onset of leg edema a week after receiving an inactivated virus vaccine and a relapse of nephrotic syndrome (NS) with acute kidney injury (AKI) after a booster dose. Screening for serum anti-phospholipase A2 receptor antibody and secondary causes of MN were negative. Kidney biopsy revealed an early MN pattern with focal spike formation, whilst numerous subepithelial electron-dense deposits and a few small deposits in the mesangial area were observed through electron microscopy. A short course of steroids and oral cyclophosphamide was prescribed, resulting in the complete remission of NS and AKI. MN following SARS-CoV-2 vaccination should call for medical importance. Awareness of the association between vaccination and MN should be kept in mind to avoid unnecessary treatment with long-term immunosuppressive agents.
RESUMO
Activated T cells infiltrate a renal allograft during rejection and can respond to TGF-ß within the tubules, causing local differentiation and expression of the αE(CD103)ß7 integrin. This study was performed to examine the expression of latent TGF-ß within renal allograft tissues and to define a mechanism by which T cells can activate and respond to this latent factor. Rejecting renal allograft biopsy tissues showed increased expression of the latent TGF-ß complex, which was localized around the tubules by a mechanism that might involve interaction with heparan sulfate in the basement membrane. A cultured renal TEC line also expressed the latent complex, but these cells did not respond to this form of TGF-ß by pSmad 3. However, coculture of these cells with activated T cells induced the expression of CD103, suggesting that T cells can activate and respond to the latent TGF-ß associated with TEC. Although activated T cells expressed little cell-surface TSP-1, this was increased by culture with fibronectin or fibronectin-expressing renal TEC. Blockade of TSP-1 using LSKL peptides reduced the potential of activated T cells to differentiate in response to latent TGF-ß. This study suggests that penetration of renal tubules by activated T cells leads to increased expression of T cell-surface TSP-1, allowing activation of latent TGF-ß sequestered on heparan sulfate within the microenvironment. This mechanism may be important for localized phenotypic maturation of T cells that have infiltrated the kidney during allograft rejection.