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In this issue of Nephrology, Dialysis, Transplantation, Mirza et al. [1] present a very interesting but also puzzling case of membranous nephropathy (MN) transplanted in a patient with a history of long-term diabetes mellitus and severe atherosclerosis. Simultaneous heart and kidney transplantation were carried out at a time when the recipient’s estimated glomerular filtration rate was 28 mL/min and proteinuria 1+. His native kidney histology was unknown and although the aetiology of his nephropathy was multifactorial, it can be safely ascertained that the grafted kidney benefitted, in a broad sense, from a ‘non-immunologic’ environment. This case thus provides a unique opportunity to observe the outcome of immune deposits after cessation of the immunological aggression. The donor was a young woman who had died from a hypertensive subarachnoid haemorrhage. Prior to her death, she was not proteinuric. A pre-transplant biopsy of the donor’s kidney led to the discovery of lesions of Stages II, III and IV MN, a puzzling finding in the absence of proteinuria. The authors hypothesize that the preservation of the glomerular filtration barrier to proteins might be explained by the mild podocyte injury that was observed on the four serial biopsies that were performed up to Day 812. Each yielded a substantial number of glomeruli and showed by light microscopy, electron microscopy and immunofluorescence, a striking improvement of the initially severe membranous lesions. As in the donor, and despite persistence of Stages II and III glomerular basement membrane (GBM) lesions and immunoglobulin and complement staining, proteinuria was never significant and the kidney recipient maintained good function. This case is exceptional, although not the first one describing progressive wash-out of membranous immune deposits in kidneys transplanted into a non-immunologic environment. Parker et al. [2] reported the case of a patient with end-stage renal disease (ESRD) secondary to Type II diabetes mellitus who received a cadaveric renal transplant from a 37-year-old woman who died of cerebral infarction. A biopsy of the donor’s kidney performed at the time of transplantation showed MN by electron microscopy. There was immediate graft function and the recipient continued to have good kidney function 3 years post-transplantation. Nakazawa et al. [3] presented the case of a 41-year-old man grafted with a cadaver kidney. An allograft biopsy obtained during the operation showed spike formation on periodic acid-silver methenamine staining and deposition of IgG along the glomerular capillary loop on immunoperoxidase staining. Immunofluorescence staining for IgG persisted in the specimens obtained on Day 11 and after 4 weeks, but markedly decreased in the specimen obtained 7 weeks after transplantation. Electron-dense deposits also decreased in amount, but irregular thickening of the glomerular basement membrane with spikes, electron-lucent lesions and small amounts of electron-dense deposits remained 20 months after the transplantation. Akioka et al. [4] transplanted a kidney from a father, diagnosed with MN and mild proteinuria, to his son. At 39 months after transplantation, allograft biopsy showed a wash-out of electron-dense deposits and electron-lucent lesions. These reports are interesting but were not analyzed as meticulously as Mirza et al. did in their case. Their recipient’s kidney was studied by a pre-transplant histology followed by four biopsies up to 27 months post-transplantation. Along with light and electron microscopy, they used a wide panel of antibodies for immunofluorescence including staining for type-M phospholipase A2 receptor (PLA2R) that was negative. This is suggestive of a secondary aetiology of membranous glomerulonephritis (GN) but does not exclude a PLA2R-unrelated primary form [5]. PLA2R is a major target antigen in autoimmune idiopathic membranous GN. PLA2R is revealed in normal human glomeruli, and in idiopathic MN, PLA2R and IgG4 are shown to co-localize within subepithelial deposits. Early recurrence of MN in kidneys transplanted to recipients with circulating anti-PLA2R antibodies lends credit to a pathogenic role of these antibodies [6–8]. Their decrease IN F O C U S

Allotransplantation using a diseased kidney: when a swallow makes a summer