Neurological complications after
kidney transplantation may appear early in the postoperative period and are
frequently related to immunosuppressive treatment, metabolic vulnerability,
infection, vascular instability, or drug interactions. Among immunosuppression-related
disorders, calcineurin inhibitor (CNI) neurotoxicity is the most clinically
relevant entity. Tacrolimus and cyclosporine may cause a broad neurological
spectrum ranging from tremor, headache, insomnia, paresthesia, and mild
cognitive symptoms to encephalopathy, seizures, posterior reversible
encephalopathy syndrome (PRES), and, rarely, coma or focal neurological
deficits. The presentation may be subtle because fever, leukocytosis, and
inflammatory responses can be blunted in immunosuppressed recipients. Early
recognition is essential because neurological toxicity may be reversible when
precipitating factors are corrected and immunosuppressive therapy is
appropriately adjusted. Mechanistic target of rapamycin (mTOR) inhibitors and
corticosteroids may also contribute to neurological and psychiatric symptoms,
either directly or through metabolic, vascular, and pharmacokinetic mechanisms.
Acute delirium and metabolic encephalopathy require a structured differential
diagnosis including hypoxia, dysglycemia, electrolyte disturbances, renal or
hepatic dysfunction, infection, hypertensive emergency, and medication
toxicity. Seizures and status epilepticus in kidney transplant recipients
demand rapid standard treatment while considering renal function, dialysis,
interactions with immunosuppressants, and avoidance of enzyme-inducing
antiseizure medications whenever possible. This chapter summarizes the clinical
spectrum, diagnostic approach, and practical management of
immunosuppression-related early neurological complications after kidney
transplantation, with emphasis on calcineurin inhibitor toxicity, delirium,
metabolic encephalopathy, seizures, and status epilepticus.
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