Аннотация
Abstract Relevance Long-standing postoperative hypoparathyroidism is a rare endocrine disorder with significant clinical interest due to its chronic course and systemic complications. Prolonged use of active vitamin D metabolites carries a high risk of renal and extraskeletal complications. Renal complications, including nephrocalcinosis and nephrolithiasis, occur in 20%-40% of patients. This case demonstrates the severe consequences of conventional therapy and highlights the need for reconsideration of treatment strategies. Aim To analyze the clinical course of long-standing postoperative hypoparathyroidism with systemic complications, evaluate limitations and risks of standard therapy using active vitamin D metabolites, and emphasize the need for transition to parathyroid hormone therapy to prevent progression and preserve organ function. Case description Hypoparathyroidism affects approximately 20-40 per 100 000 population, mainly postoperative. In Kazakhstan, reliable epidemiological data are limited due to restricted access to specialized care, insufficient laboratory diagnostics, and absence of national registries. Standard therapy with active vitamin D metabolites does not replicate parathyroid hormone effects and causes chronic hypercalciuria and elevated calcium–phosphate product, mechanisms underlying renal and extraskeletal complications. The patient has a 20-year history of endocrine disease. At 23, she underwent total thyroidectomy for diffuse toxic goiter, complicated by persistent hypoparathyroidism and hypothyroidism, requiring lifelong hormone replacement. Pregnancy at 32 occurred with chronic hypocalcemia, requiring careful monitoring and therapy adjustment. From age 34, she received alfacalcidol 3-5 μg/day, maintaining normocalcemia. At 46, nephrocalcinosis and a left renal calculus were detected; at 48, nephrolithiasis exacerbation led to acute kidney injury (eGFR 24 mL/min). Surgery was performed, and alfacalcidol reduced to 2 μg/day. At 49, partial renal recovery (eGFR 58 mL/min) was observed, but recurrent hypocalcemia required an increase to 3 μg/day. At 50, a right renal calculus was identified. At 52, brain MRI revealed basal ganglia calcifications. Conclusions Even with normocalcemia, conventional therapy with active vitamin D metabolites does not prevent severe systemic complications. Progressive nephrocalcinosis, recurrent nephrolithiasis, renal function decline, and cerebral calcifications highlight the limited efficacy of this approach. Transition to recombinant parathyroid hormone therapy is pathogenetically justified, clinically appropriate, and may help prevent further progression of systemic complications while preserving organ function.