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Tacrolimus Cerebellar Toxicity — ESENeph MCQ

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HardTransplantationTacrolimus Cerebellar ToxicityESENeph

A kidney transplant recipient on Tacrolimus develops posterior fossa syndrome with cerebellar ataxia and dysarthria. MRI shows posterior fossa white matter changes. Tacrolimus trough is 18 ng/mL. What CNI-related neurological complication beyond PRES should be considered?

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Correct answer: DTacrolimus-induced cerebellar toxicity (calcineurin inhibitor-associated posterior fossa syndrome) – characterised by cerebellar dysfunction with posterior fossa MRI changes

Beyond PRES, calcineurin inhibitors can cause posterior fossa syndrome with cerebellar toxicity (ataxia, dysarthria, tremor, nystagmus) and posterior fossa white matter changes on MRI. This is distinct from PRES (which predominantly affects the occipital/parietal lobes). The supratherapeutic Tacrolimus level (18 ng/mL) strongly supports drug toxicity. Management involves Tacrolimus dose reduction or withholding, close neurological monitoring, and consideration of switching to a CNI-free regimen (Belatacept). Most cases are reversible with prompt drug level correction.

Reference: KDIGO 2009 – Transplant; Wong et al 2008 – CNI Cerebellar Toxicity