Immunoglobulin A (IgA) nephropathy is the most common glomerulonephritis in many countries. Most patients progress to kidney failure for which kidney transplantation is the optimal therapy. Unfortunately, IgA nephropathy commonly recurs post transplant and shortens allograft survival. Multiple recipient and donor characteristics have been associated with the risk of recurrence, although these have varied between different cohorts. The clinical expression of post-transplant IgA nephropathy is modified by immunosuppression. Biomarkers have been identified and studied in native-kidney IgA nephropathy but need validation in transplantation. Treatment of recurrent IgA nephropathy hinges on supportive measures derived largely from evidence in native-kidney IgA nephropathy. The improved understanding of the autoimmune mechanisms of disease in native-kidney IgA nephropathy has led to promising new targets for treatment, which may in turn be deployed in post-transplant IgA nephropathy.