Published online Jan 18, 2022. doi: 10.5500/wjt.v12.i1.15
Peer-review started: July 26, 2021
First decision: October 27, 2021
Revised: December 8, 2021
Accepted: January 6, 2022
Article in press: January 6, 2021
Published online: January 18, 2022
Post-transplant nephrotic syndrome (PTNS) in a renal allograft carries a 48% to 77% risk of graft failure at 5 years if proteinuria persists. PTNS can be due to either recurrence of native renal disease or de novo glomerular disease. Its prognosis depends upon the underlying pathophysiology. We describe a case of post-transplant membranous nephropathy (MN) that developed 3 mo after kidney transplant. The patient was properly evaluated for pathophysiology, which helped in the management of the case.
This 22-year-old patient had chronic pyelonephritis. He received a living donor kidney, and human leukocyte antigen-DR (HLA-DR) mismatching was zero. PTNS was discovered at the follow-up visit 3 mo after the transplant. Graft histopathology was suggestive of MN. In the past antibody-mediated rejection (ABMR) might have been misinterpreted as de novo MN due to the lack of technologies available to make an accurate diagnosis. Some researchers have observed that HLA-DR is present on podocytes causing an anti-DR antibody deposition and development of de novo MN. They also reported poor prognosis in their series. Here, we excluded the secondary causes of MN. Immunohistochemistry was suggestive of IgG1 deposits that favoured the diagnosis of de novo MN. The patient responded well to an increase in the dose of tacrolimus and angiotensin converting enzyme inhibitor.
Exposure of hidden antigens on the podocytes in allografts may have led to subepithelial antibody deposition causing de novo MN.
Core Tip: This is a case presentation of a patient who developed post-transplant nephrotic syndrome 3 mo after transplantation and was diagnosed with de novo membranous nephropathy (MN). He had received a well-matched living donor kidney. According to the literature, the most common causes of de novo MN include secondary causes and antibody mediated injury, which we ruled out. This patient was treated with increased dosage of tacrolimus and an angiotensin converting enzyme inhibitor, which resulted in a good recovery. We favoured a new concept of pathogenesis of de novo MN, which requires the identification of the causative antigens.