Case report: Early and persistent post-transplant proteinuria due to multiple concomitant etiologies

Abstract

Post-transplant proteinuria is an early warning sign of allograft injury and is often caused by multiple concurrent mechanisms, originating either from the transplanted kidney or from the native kidneys. We report the case of a 26-year-old male who developed low-grade proteinuria immediately after kidney transplantation, which rapidly progressed to overt nephrotic syndrome within the first three months. The initial allograft biopsy revealed features of membranoproliferative glomerulonephritis (MPGN) with diffuse C4d deposition in the glomerular capillaries, suggesting chronic active antibody-mediated rejection. The patient was treated with high-dose corticosteroids and rituximab, resulting in partial improvement of proteinuria; however, recurrence occurred, accompanied by deterioration of graft function. A second allograft biopsy demonstrated combined lesions of chronic antibody-mediated rejection, acute calcineurin inhibitor (CNI) nephrotoxicity, and chronic glomerular injury, which guided treatment modification, leading to better control of proteinuria and improvement of graft function. This case highlights the importance of early recognition of post-transplant proteinuria and emphasizes a multifactorial diagnostic and therapeutic approach to optimize management and preserve long-term graft function.