Recurrent Diseases After Kidney Transplantation
Recurrent disease after kidney transplantation
remains an important cause of proteinuria, graft dysfunction, and allograft
loss. This review summarizes the epidemiology, pathogenesis, clinical
presentation, diagnosis, risk factors, and treatment of the most relevant
recurrent diseases, including membranous nephropathy, primary focal segmental
glomerulosclerosis, IgA nephropathy, lupus nephritis, C3 glomerulopathy, and
amyloidosis. Recurrence is driven by persistent recipient-specific mechanisms
such as autoantibodies, circulating permeability factors, galactose-deficient
IgA1 immune complexes, complement dysregulation, or ongoing systemic
inflammatory or clonal plasma cell disorders. Clinical manifestations range
from isolated proteinuria and microscopic hematuria to nephrotic syndrome and
progressive graft dysfunction, although recurrence may also be subclinical. Kidney allograft biopsy remains the diagnostic
cornerstone and is essential for distinguishing recurrence from rejection,
calcineurin inhibitor toxicity, and chronic allograft injury. Serologic and
biomarker-based tools, including anti-PLA2R, anti-nephrin, complement markers,
and disease-specific hematologic parameters, may support risk stratification
and follow-up but do not replace histologic confirmation. Pretransplant disease
quiescence, assessment of antibody burden, and identification of genetic or monoclonal
causes are critical for recurrence prevention. Management is disease-specific and combines
optimized supportive care with tailored immunosuppression or targeted therapy.
Rituximab, plasmapheresis, corticosteroids, calcineurin inhibitors,
complement-directed agents, and clone- or inflammation-targeted regimens may be
used depending on the underlying disorder. Early recognition, close
post-transplant surveillance, and multidisciplinary management are essential to
preserve graft function and improve long-term outcomes
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