Recurrent Diseases After Kidney Transplantation
Özet
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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