Neurological Complications After Pediatric Liver and Kidney Transplantation: A Comprehensive Review of Acute Symptomatic Seizures

Acute symptomatic seizures (ASS) represent one of the most frequent and clinically significant neurological complications following pediatric liver and kidney transplantation. Despite their clinical relevance, available evidence remains fragmented; pediatric-specific data are limited, and no standardized diagnostic or management framework has been established. To summarize current evidence regarding the epidemiology, etiological mechanisms, diagnostic evaluation, risk factors, and management strategies of acute symptomatic seizures after pediatric liver and kidney transplantation, and to propose a practical clinical diagnostic and management algorithm. A structured narrative review with elements of a semi-systematic approach was conducted using PubMed/MEDLINE, Scopus, and Web of Science databases. Studies published between 2000 and 2025 addressing neurological complications after pediatric liver and kidney transplantation were reviewed. Particular emphasis was placed on metabolic disturbances, calcineurin inhibitor neurotoxicity, posterior reversible encephalopathy syndrome (PRES), structural central nervous system lesions, infectious complications, hypertensive encephalopathy, dialysis disequilibrium syndrome, and uremic encephalopathy. Pediatric-specific evidence was prioritized whenever available, while adult-derived data were included for contextual interpretation when pediatric evidence was limited. The reported incidence of acute symptomatic seizures ranges from 2.8% to 42% after liver transplantation and up to 30% after kidney transplantation. In liver transplant recipients, the most common etiologies include calcineurin inhibitor neurotoxicity, metabolic disturbances, PRES, sepsis-associated encephalopathy, central nervous system infections, and cerebrovascular events. In kidney transplant recipients, seizures are more frequently associated with electrolyte imbalance, hypertensive encephalopathy, dialysis disequilibrium syndrome, uremic encephalopathy, and PRES. Early postoperative hyponatremia, renal dysfunction, severe metabolic abnormalities, elevated tacrolimus concentrations, malnutrition, and severe systemic infection represent major risk factors for seizure development. Diagnostic evaluation relies on biochemical assessment, immunosuppressant level monitoring, neuroimaging, and electroencephalography, particularly in patients with persistent encephalopathy or suspected non-convulsive status epilepticus. Based on the synthesized evidence, a practical diagnostic and management algorithm was proposed integrating early stabilization, etiological stratification, neurodiagnostic assessment, and targeted therapy. Acute symptomatic seizures after pediatric liver and kidney transplantation arise from heterogeneous and frequently overlapping mechanisms. Early identification of reversible triggers and individualized management are essential to reduce neurological morbidity and improve outcomes. The proposed diagnostic and management framework may support earlier recognition, structured evaluation, and targeted treatment of acute symptomatic seizures in pediatric transplant recipients.

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