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
RECURRENT PRIMARY GLOMERULAR DISEASES
Focal Segmental Glomerulosclerosis (FSGS)
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)
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)
Immune complex-mediated MPGN
C3 glomerulopathy (complement-mediated MPGN)
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 ...