Fahr’s Syndrome Secondary to Hypoparathyroidism in Patients Undergoing Chronic Hemodialysis

Abstract

Fahr’s syndrome is a rare neurological disorder characterized by bilateral and symmetrical calcifications of the basal ganglia, thalamus, and cerebellum, with heterogeneous clinical presentations ranging from asymptomatic cases to severe neuropsychiatric impairment. While idiopathic or hereditary forms are well documented, secondary etiologies have gained increasing attention, particularly hypoparathyroidism. In the context of chronic hemodialysis, Fahr’s syndrome represents a diagnostic challenge, as neurological symptoms such as seizures, tremors, parkinsonism, and cognitive decline are often attributed to uremia or cerebrovascular complications. Hypoparathyroidism contributes to persistent hypocalcemia and hyperphosphatemia, favoring ectopic calcium deposition within the brain parenchyma.

This integrative review aimed to analyze studies published between 2021 and 2024 addressing Fahr’s syndrome secondary to hypoparathyroidism in patients undergoing chronic hemodialysis. Case reports, narrative reviews, and clinical studies were evaluated. The findings show that most cases occur in individuals with long-term mineral and bone disorders, with computed tomography (CT) of the brain being the most accurate diagnostic tool. Laboratory markers consistently demonstrate low calcium and parathyroid hormone (PTH) levels with elevated phosphate. Therapeutic strategies focus on strict correction of mineral metabolism, calcium and active vitamin D supplementation, and dialysis regimen adjustments. Nevertheless, neurological sequelae often persist, particularly when diagnosis is delayed. Recognition of Fahr’s syndrome as a possible complication in chronic hemodialysis is therefore crucial to avoid irreversible disability and improve patient outcomes.