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Recurrence of idiopathic immune complex-mediated membranoproliferative glomerulonephritis (MPGN) after transplantation

Anuja Java, MD
Daniel C Brennan, MD, FACP
Section Editor
Barbara Murphy, MB, BAO, BCh, FRCPI
Deputy Editor
Albert Q Lam, MD


Membranoproliferative glomerulonephritis (MPGN, also called mesangiocapillary or lobular glomerulonephritis) is a disease defined by a pattern of glomerular injury observed by light microscopy on renal biopsy. An MPGN pattern of injury may result from multiple causes including infection, autoimmune diseases, monoclonal gammopathies, and complement dysregulation. In addition, an MPGN pattern of injury may occur in the absence of an obvious cause. This is referred to as idiopathic MPGN.

Patients with MPGN may progress to end-stage renal disease (ESRD) and require renal replacement therapy, including dialysis and/or transplantation. Among patients who undergo transplantation, idiopathic MPGN and MPGN resulting from complement dysregulation commonly recur. Patients with MPGN that is secondary to infection, autoimmune disorders, and monoclonal gammopathies are generally not eligible for transplantation, unless the underlying cause is addressed.

This topic reviews recurrent idiopathic MPGN in the transplanted kidney. The recurrence in the transplanted kidney of MPGN resulting from complement dysregulation is discussed elsewhere. (See "Recurrence of C3 glomerulopathies after transplantation".)

The presentation, classification, causes, and treatment of MPGN in the native kidney are discussed elsewhere. (See "Clinical presentation, classification, and causes of membranoproliferative glomerulonephritis" and "Evaluation and treatment of membranoproliferative glomerulonephritis" and "C3 glomerulopathies: Dense deposit disease and C3 glomerulonephritis".)


MPGN is classified into subtypes, including immune complex-mediated MPGN and C3 glomerulopathy. Immune complex-mediated MPGN is characterized by both immunoglobulin and complement protein deposition in the kidney, as identified by immunofluorescence microscopy. C3 glomerulopathy is characterized by complement deposition in the absence of immunoglobulin deposition.

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Literature review current through: Nov 2017. | This topic last updated: Dec 09, 2016.
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