A 70-year-old white male with a history of benign prostatic hyperplasia, recurrent atrial fibrillation and right hemithyroidectomy for nodular hyperplasia, as well as unstudied chronic renal failure (baseline creatinine 1.5 mg/dl).
He came to the emergency department with three months of clinical manifestations of gait instability and generalised weakness (he had previously been admitted to another centre for these symptoms). On physical examination, the patient was dehydrated, confused, bradypsychic and with distal tremor.
The analytical data are summarised in (table 1), highlighting significant deterioration of renal function, severe hypercalcaemia and marked elevation of PTH (twenty times the laboratory reference value). Serum therapy, perfusion of furosemide and intravenous corticosteroids, bisphosphonates and calcitonin were started. Due to the severity of the neurological symptoms, urgent renal replacement therapy by haemodialysis with low calcium concentration in the dialysate was simultaneously indicated. There was a transitory clinical improvement, but due to persistent renal failure and rebound of hypercalcaemia (increase in calcaemia > 2 mg/dl 24 hours post-hemodialysis), daily sessions were required.
As part of the aetiological study, myeloproliferative processes and other neoplasms (no monoclonal component in the proteinogram, negative Bence-Jones proteinuria), infectious pathology (negative serologies) and autoimmune diseases were ruled out. Urinary ultrasound showed kidneys of normal size and adequate cortico-medullary differentiation. Thoracic-abdominal CT scan showed a retroesophageal mass measuring 5.6 × 3.2 × 6.8 cm, suspicious for parathyroid tumour, and the image was confirmed by parathyroid scintigraphy, as well as bilateral hypodense adrenal nodules: right 27 × 18 mm and left 15 × 11 mm.
With these findings, the patient consulted Endocrinology, which ruled out pheochromocytoma (negative urine catecholamines and metanephrines). In a joint session with General Surgery it was decided to perform surgery, resecting an 8 cm parathyroid tumour. Anatomical pathology reports parathyroid adenoma without capsular or vascular invasion.
In the immediate postoperative period, "hungry bone syndrome" occurred and the patient required intravenous and oral calcium supplementation due to severe hypocalcaemia, and daily haemodialysis sessions for nine days after surgery.
Nine months later, the patient is asymptomatic, with calcaemia in range without the need for supplementation, and with partial recovery of renal function (creatinine 2.7 mg/dl). It is noteworthy that renal function remains impaired one year after surgery, despite normalisation of calcaemia.
