Primary membranous nephropathy (MN) is a frequent cause of NS in adults. In native kidneys the disease may progress to ESRD in the long term, in some 40-50% of untreated patients. The identification of the pathogenic role of anti-podocyte autoantibodies and the development of new therapeutic options has achieved an amelioration in the prognosis of this disease. MN may also develop in renal allograft as a recurrent or a de novo disease. Since the de novo MN may have some different pathogenetic and morphologic features compared to recurrent MN, in the present paper we will deal only with the recurrent disease. The true incidence of the recurrent form is difficult to assess. This is mainly due to the variable graft biopsy policies in kidney transplantation, among the different transplant centers. Anti-phospholipase A2 receptor (PLA2R) autoantibodies are detected in 70-80% of patients. The knowledge of anti-PLA2R status before transplant is useful in predicting the risk of recurrence. In addition, the serial survey of the anti-PLA2R titers is important to assess the rate of disease progression and the response to treatment. Currently, there are no established guidelines for prevention and treatment of recurrent MN. Symptomatic therapy may help to reduce the signs and symptoms related to the nephrotic syndrome. Anecdotal cases of response to cyclical therapy with steroids and cyclophosphamide have been published. Promising results have been reported with rituximab in both prophylaxis and treatment of recurrence. However, these results are based on observational data, and prospective controlled trials are still missing.

Membranous Nephropathy (MN) Recurrence after Renal Transplantation / P. Passerini, S. Malvica, F. Tripodi, R. Cerutti, P. Messa. - In: FRONTIERS IN IMMUNOLOGY. - ISSN 1664-3224. - 10(2019 Jun 12). [10.3389/fimmu.2019.01326]

Membranous Nephropathy (MN) Recurrence after Renal Transplantation

S. Malvica
Secondo
;
F. Tripodi;P. Messa
Ultimo
2019

Abstract

Primary membranous nephropathy (MN) is a frequent cause of NS in adults. In native kidneys the disease may progress to ESRD in the long term, in some 40-50% of untreated patients. The identification of the pathogenic role of anti-podocyte autoantibodies and the development of new therapeutic options has achieved an amelioration in the prognosis of this disease. MN may also develop in renal allograft as a recurrent or a de novo disease. Since the de novo MN may have some different pathogenetic and morphologic features compared to recurrent MN, in the present paper we will deal only with the recurrent disease. The true incidence of the recurrent form is difficult to assess. This is mainly due to the variable graft biopsy policies in kidney transplantation, among the different transplant centers. Anti-phospholipase A2 receptor (PLA2R) autoantibodies are detected in 70-80% of patients. The knowledge of anti-PLA2R status before transplant is useful in predicting the risk of recurrence. In addition, the serial survey of the anti-PLA2R titers is important to assess the rate of disease progression and the response to treatment. Currently, there are no established guidelines for prevention and treatment of recurrent MN. Symptomatic therapy may help to reduce the signs and symptoms related to the nephrotic syndrome. Anecdotal cases of response to cyclical therapy with steroids and cyclophosphamide have been published. Promising results have been reported with rituximab in both prophylaxis and treatment of recurrence. However, these results are based on observational data, and prospective controlled trials are still missing.
anti-PLA2R antibodies; kidney transplant; membranous nephropathy; prognosis; proteinuria; recurrent membranous nephropathy; rituximab
Settore MED/14 - Nefrologia
12-giu-2019
Article (author)
File in questo prodotto:
File Dimensione Formato  
Passerini P MN Front Immunol 2019.pdf

accesso aperto

Tipologia: Publisher's version/PDF
Dimensione 697.69 kB
Formato Adobe PDF
697.69 kB Adobe PDF Visualizza/Apri
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/652383
Citazioni
  • ???jsp.display-item.citation.pmc??? 7
  • Scopus 10
  • ???jsp.display-item.citation.isi??? 9
social impact