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  • Glomerular diseases that cause end-stage kidney failure in native kidneys can also recur in kidney allografts following transplantation.

  • Several of these recurrent glomerular diseases can lead to significant allograft failure and loss.

  • In this chapter, we review several primary and secondary recurrent glomerular diseases seen after kidney transplantation


Focal Segmental Glomerulosclerosis (FSGS)

Recurrence rate: 20–40%.

Risk factors: Childhood onset and rapid progression of primary FSGS in native kidney, white race, older age, lower body mass index and history of recurrent FSGS in previous allograft.

Clinical features: Varying degree of proteinuria can be seen within 1–2 weeks after transplantation, especially in children. Acute-onset nephrotic range proteinuria is also a common clinical feature. Patients may present with nephrotic syndrome, microscopic hematuria, and acute allograft failure.

Treatment: Plasmapheresis (based on the assumption that a circulating factor exists), rituximab, cyclophosphamide, high-dose corticosteroids, cyclosporine, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor blockers.

Allograft prognosis: Graft loss varies in different studies from 13% to 63% at 5–10 years.

Membranous Nephropathy (MN)

Recurrence rate: 10–42%.

Risk factors: High antiphospholipase A2 receptor (PLA2R) antibody titers at time of kidney transplantation.

Clinical features: Varying degree of proteinuria, more commonly seen a year to 15 months following kidney transplantation. Decline in allograft function occurs with progressive disease.

Treatment: For patients with proteinuria < 1 g/day and normal or stable kidney function, treat with ACE inhibitor or angiotensin II receptor blocker. Blood pressure should also be optimally controlled. For patients with proteinuria > 2 g/day and/or declining kidney function, additional treatment with immunosuppressive agents (rituximab, cyclophosphamide) should be considered.

Allograft prognosis: Graft loss varies in different studies from 12.5% to 41% at 5–10 years.

Membranoproliferative Glomerulonephritis (MPGN)

Recurrence rate:

Immune complex-mediated MPGN

  • Polyclonal immune complex-mediated MPGN: 30–35%

  • Monoclonal immune complex-mediated MPGN: 66%

C3 glomerulopathy (complement-mediated MPGN)

  • Dense deposit disease (DDD): 80–90%

  • C3 glomerulonephritis (C3GN): 70%

Risk factors: Higher risk of recurrence in recipients of living related donor kidneys, persistent or recurrent low complement levels following kidney transplantation, history of recurrent MPGN in previous allograft.

Clinical features: Proteinuria, hematuria, hypertension, declining kidney function. Hypocomplementemia is commonly observed.

Treatment: The treatment depends on the severity and type of MPGN. For secondary MPGN, treat the underlying cause. For mild disease (proteinuria <1.5 g/day, stable kidney function), treat with ACE inhibitors or angiotensin II receptor blockers. For moderate disease (proteinuria >1.5 g/day to <3.5 g/day, declining kidney function), increase dose of transplant immunosuppressive therapy (in addition to ACE ...

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