SAT-815 - A Stone-Cold Diagnosis: Primary Hyperparathyroidism Revealed by Staghorn Calculus and Renal Atrophy

Introduction

Primary hyperparathyroidism (PHPT) is a common endocrine disorder, with nephrolithiasis being a known complication. However, advanced renal disease (e.g., staghorn calculi, renal atrophy, bilateral hydronephrosis) can represent severe late-stage manifestation. We present a rare case of profound multi-systemic renal damage from undiagnosed PHPT, highlighting the consequences of delayed diagnosis and value of early recognition and management.

Case Description

A 50-year-old female with previously normal kidney function and recurrent nephrolithiasis, including an 8-year prior percutaneous nephrolithotomy, presented after a fall with dysuria and severe PTH-dependent hypercalcemia (corrected calcium: 13.1 mg/dL, PTH 247 pg/mL). Hypercalcemia was refractory to intravenous fluids and bisphosphonates. Her renal function was compromised (eGFR 49 mL/min/1.73m2) on admission. Imaging showed a large right staghorn calculus with associated renal atrophy and a left mid-ureteral 1 cm stone causing bilateral hydronephrosis. She also had severe vitamin D deficiency (15.1 ng/mL). A 4D CT neck showed a left inferior parathyroid adenoma (2.2 cm). Her hospital course was complicated by a multi-drug-resistant Pseudomonas aeruginosa urinary tract infection requiring prolonged antibiotics. Due to refractory hypercalcemia, she underwent urgent parathyroidectomy, left lithotripsy and stent placement. Stone analysis confirmed 70% calcium oxalate and 30% calcium phosphate composition. Her renal function improved post-surgery (eGFR 68%). Postoperatively, she developed hypocalcemia with paresthesia, consistent with hungry bone syndrome, and required oral calcium, calcitriol, and high-dose vitamin D. Despite severe lab abnormalities and extensive renal disease, she reported few classic hypercalcemic symptoms prior to presentation, suggesting physiological adaptation to chronic hypercalcemia.



Discussion

This case illustrates severe renal complications from prolonged, undiagnosed PHPT: nephrolithiasis, obstructive uropathy, renal atrophy, and damage. The presence of staghorn calculi with bilateral hydronephrosis underscores the need to consider PHPT in complex nephrolithiasis. Substantial end-organ damage may occur despite minimal symptoms, highlighting routine evaluation over symptom-based detection. The patient’s post-parathyroidectomy hypocalcemia illustrates importance of close post-operative monitoring for hungry bone syndrome requiring aggressive calcium, phosphorus, magnesium, and vitamin D replacement. Concurrent vitamin D deficiency likely worsened her pre-existing bone disease. Management required a multidisciplinary approach, reflective of PHPT's systemic impact and complexity of manifestations. Early recognition and definitive treatment are essential to prevent irreversible renal and skeletal complications.

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