TERIPARATIDE USE IN THE TREATMENT OF SEVERE HYPOCALCEMIA AFTER KIDNEY TRANSPLANTATION: A CASE REPORT

Hypocalcemia is a known complication following kidney transplantation, particularly in patients with prior parathyroidectomy. The pathogenesis is complex, often involving impaired parathyroid hormone (PTH) production and vitamin D metabolism. Traditional management involves calcium and vitamin D supplementation, but recalcitrant cases may necessitate more aggressive interventions. Teriparatide, a recombinant PTH analogue, is a potent osteoanabolic agent that increases osteoblast activity and bone formation, influencing calcium and phosphate homeostasis. This case report explores the use of teriparatide as a treatment for severe, refractory hypocalcemia in a kidney transplant recipient following parathyroidectomy, aiming to demonstrate its effectiveness and safety in this challenging clinical context. The study highlights the need for alternative therapeutic strategies for managing severe hypocalcemia in this specific patient population and the potential benefits of teriparatide in improving patient outcomes. The context of this research is the limitations of traditional treatment approaches and the search for effective and safe alternatives in managing severe post-transplant hypocalcemia. The importance of this study lies in providing clinical evidence for the efficacy of teriparatide, a relatively new approach, in this setting.

While the literature extensively covers the management of hypocalcemia post-kidney transplantation, there is limited data specifically focusing on teriparatide’s role in this context. Most studies focus on calcium and vitamin D supplementation as first-line treatments. The existing literature does support the use of teriparatide for various bone disorders, highlighting its efficacy in promoting bone formation and its impact on calcium and phosphate metabolism. However, its application in the specific context of post-transplant hypocalcemia, especially following parathyroidectomy, remains under-investigated. This case report, therefore, adds valuable clinical data to the existing literature, potentially guiding future research and clinical practice in managing severe hypocalcemia in this specific patient population.

This is a case report describing the treatment of a single patient. A 30-year-old female with end-stage kidney disease secondary to chronic glomerulonephritis underwent deceased-donor kidney transplantation. She had undergone total parathyroidectomy nine years earlier for tertiary hyperparathyroidism. Post-transplant, she developed severe hypocalcemia despite increased doses of oral and intravenous calcium and vitamin D. On day 17 post-transplant, subcutaneous teriparatide (20 mcg twice daily) was initiated. Serum calcium, phosphate, and creatinine levels were monitored. The dose of teriparatide was adjusted based on the patient’s response and the development of hypercalcemia. The patient's clinical symptoms, medication changes, and laboratory results were meticulously recorded to form the basis of this report.

The patient experienced a rapid normalization of serum calcium levels within two days of teriparatide initiation. This allowed for the discontinuation of intravenous calcium and a significant reduction in oral calcium and vitamin D supplements. Teriparatide was successfully tapered off after two weeks due to the emergence of hypercalcemia. Subsequently, the patient’s calcium levels remained stable with low doses of oral calcium and vitamin D. Phosphate levels showed a declining trend, and serum creatinine remained stable throughout the observation period. No adverse events related to teriparatide were observed. This demonstrates the effectiveness of teriparatide in rapidly correcting severe hypocalcemia in a patient with a history of parathyroidectomy. The rapid response to teriparatide underscores its potential benefit in reducing the duration of intravenous calcium supplementation and the overall medication burden in such cases. The absence of adverse events highlights the safety of teriparatide in this clinical scenario.

This case report demonstrates the successful and rapid correction of severe, recalcitrant hypocalcemia post-kidney transplantation with teriparatide in a patient with a history of parathyroidectomy. The rapid response observed suggests that teriparatide may be a valuable therapeutic option in cases unresponsive to conventional calcium and vitamin D supplementation. The ability to quickly normalize calcium levels may reduce the duration of hospitalization and associated costs. The absence of adverse events supports teriparatide's safety profile in this context. Future studies, including randomized controlled trials, are necessary to further evaluate the efficacy and safety of teriparatide in a larger cohort of patients. These trials could compare teriparatide to standard treatments, assessing its impact on hospitalization length, quality of life, and overall treatment costs.

This case report highlights the potential of teriparatide as a safe and effective treatment for refractory hypocalcemia in kidney transplant recipients with prior parathyroidectomy. The rapid normalization of calcium levels and reduction in medication burden observed in this patient suggest that teriparatide could significantly improve patient outcomes. Larger prospective studies are warranted to confirm these findings and establish its role as a first-line or adjunct therapy.

This study is a single-case report, limiting its generalizability. The observed effects may not be representative of the broader population of kidney transplant recipients with hypocalcemia. Further research, including larger-scale clinical trials, is needed to validate these findings and assess the long-term effects of teriparatide in this specific clinical setting. The absence of a control group prevents robust conclusions regarding comparative efficacy.