RECURRENT SECONDARY HYPERPARATHYROIDISM DUE TO END STAGE RENAL DISEASE
Presentation Number: SAT-267
Date of Presentation: June 15th, 2013
Rachel Bier*1, Carla Maria Romero2 and Adrienne M. Fleckman3
1Beth Israel Med Ctr, New York, NY, 2Beth Israel Medical Center, New York, NY, 3Beth Israel Med Center, New York, NY
Rachel Bier MD1, Carla Romero MD1, Adrienne Fleckman MD1, Nikolas Harbord MD2, Jennifer L Marti MD3
1Division of Endocrinology and Metabolism, Department of Medicine, 2Division of Nephrology, Department of Medicine, 3Division of Endocrine Surgery, Department of Surgery;
Beth Israel Medical Center, New York, New York.
Objective: To discuss the management of renal secondary hyperparathyroidism (SHPT) due to recurrent disease in the forearm autograft and neck.
Case: A 34 yo man with end stage renal disease (ESRD) on hemodialysis failed medical therapy for SHPT with phosphate binders and vitamin D, and was intolerant to cinacalcet. Preoperative labs were Ca++ 10.4 mg/dL, PO4 4.4 mg/dL, and PTH 1299pg/mL. Total parathyroidectomy with autotransplantation in the forearm was performed, with a decrease in intraoperative PTH from 1400 to 41pg/mL. Over the next 3 years he developed recurrent disease with Ca++10.8 mg/dL, Ca++-Phos product 58-81, and PTH 3948pg/mL. The forearm graft increased in size to a 4 cm palpable soft mass. Sestamibi scan showed forearm and right (R) lower neck uptake. Residual disease in the R neck was also evident on ultrasound, likely due to inadvertent transection of the R lower gland at the initial operation. Casanova test (R arm occlusion) confirmed hypersecretion of the forearm graft (PTH fell from 4357 to 1129 pg/mL). A staged operation was planned. The forearm graft was excised en bloc, and a new autograft created. Intraoperative PTH decreased from 2500 to 259pg/mL. Cervical exploration is planned for a later date.
Discussion: In chronic kidney disease, decreased phosphate clearance, decreased activity of 1-α hydroxylase, and hypocalcemia are inciting factors for SHPT. Recurrent HPT after parathyroidectomy can be treated medically with phosphate binders, vitamin D and calcimimetics. If medical management fails, indications for surgery include persistent hypercalcemia with PTH > 800, elevated Ca++ -PO4 product, bone loss, bone pain, vascular calcification, calciphylaxis and uremic pruritus. Our patient developed recurrent disease in both the forearm graft and neck. Surgery was indicated for hypercalcemia with PTH > 800pg/mL, and an elevated Ca++-PO4product.
Conclusion: This case holds many lessons for endocrinologists. A minority of patients with renal SHPT will fail medical therapy and require subtotal parathyroidectomy. Patients are at high risk for recurrence unless the underlying pathology is corrected (i.e. renal transplant). All sites of recurrent disease should be identified before re-operation. Post-operatively, care must be taken to avoid severe hypocalcemia due to hungry bone syndrome. Endocrinologists, nephrologists and endocrine surgeons can work together to offer a multidisciplinary approach in the management of these high risk patients.
Nothing to Disclose: RB, CMR, AMF