End-stage renal disease (ESRD) patients on regular haemodialysis (HD) are at high risk to develop several neurological complications affecting both the central and peripheral nervous systems. 1 Moreover, neurological complications may be silent and not detected clinically but accidentally identified by magnetic resonance imaging (MRI) as silent brain infarction (SBI). Several studies documented a decrease in estimated glomerular filtration rate (eGFR), associated with a higher prevalence of SBI. [2][3][4] Many factors are implicated in the development of neurological deficits in ESRD patients on HD, including uremic toxins, immunologic disturbances, and acid base disequilibrium, 5 cerebral hypoperfusion, increase cytokine release, 6 cerebral atrophy secondary to frequent hypotension attacks during dialysis session, 7,8 vitamin D deficiency and anaemia, 9 small and large blood vessel disease, increasing susceptibility to cerebrovascular diseases 6 and secondary hyperparathyroidism (SHPT). KDOQI guidelines 2003 underline that the target range of intact parathyroid hormone (PTH) concentrations in Stage 5 chronic kidney disease (CKD) or HD patients are 150-300 pg/mL, 10 the newer KDIGO guidelines 2017 recommend maintaining PTH levels two-to ninefold the upper normal limit, corresponding to a range of 130-600 pg/mL 11,12