Kidney Week

Abstract: SA-PO0570

Primary Hyperparathyroidism Masquerading as CKD-MBD with PTH-Induced Distal Renal Tubular Acidosis

Session Information

• Bones, Stones, and Mineral Metabolism: Research and Cases
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Bone and Mineral Metabolism

• 502 Bone and Mineral Metabolism: Clinical

Authors

• Kritmetapak, Kittrawee, Khon Kaen University Faculty of Medicine, Khon Kaen, Thailand

Kittrawee Kritmetapak, MD, MS, MSc

• Sirirattanakorn, Shunyapat, Khon Kaen University Faculty of Medicine, Khon Kaen, Thailand

Shunyapat Sirirattanakorn, MD

• Raruenrom, Yutapong, Khon Kaen University Faculty of Medicine, Khon Kaen, Thailand

Yutapong Raruenrom, MD

• Sothornwit, Jin, Khon Kaen University Faculty of Medicine, Khon Kaen, Thailand

Jin Sothornwit, MD

Introduction

Secondary hyperparathyroidism is common in CKD; however, biochemical abnormalities disproportionate to GFR should prompt evaluation for alternative etiologies. We report a case of primary hyperparathyroidism (PHPT) presenting with severe bone disease, distal renal tubular acidosis (dRTA), and anemia, mimicking CKD-MBD.

Case Description

A 58-year-old woman with non-diabetic CKD G4 (baseline SCr 2.2–2.3 mg/dL; eGFR 22–23 mL/min/1.73 m²) presented with 3 months of diffuse lower back pain. Laboratory evaluation showed severe normocytic normochromic anemia (Hb 8.7 g/dL) with normal iron studies, non-anion gap metabolic acidosis (Na 141, K 3.7, Cl 116, HCO₃ 13.2 mmol/L), and markedly elevated PTH (1,392–1,526 pg/mL), disproportionate to the degree of CKD G4. Further evaluation demonstrated persistent urine pH 6.5, positive urine anion gap (+38 mEq/L), low urine osmolal gap (35 mOsm/kg), and profoundly reduced 24-hour urine ammonium excretion (4.2 mmol/day), suggesting distal RTA. ANA and serum free light chain ratio were normal. Persistent hypophosphatemia (2.2–2.4 mg/dL) with hyperphosphaturia (~400 mg/day) suggested PHPT despite normal corrected calcium (8.8–9.7 mg/dL), low urine calcium excretion (33 mg/day), and absence of nephrocalcinosis, likely related to CKD and severe vitamin D deficiency (25[OH]D 4.6 ng/mL). Skeletal evaluation revealed severe high-turnover bone disease with osteoporosis (radius T-score −3.9), osteolytic middle phalangeal lesions (brown tumors), acro-osteolysis, and markedly elevated ALP (1,456 U/L). Parathyroid sestamibi scan identified a 2.9 × 1.9 cm right parathyroid adenoma, confirming PHPT. Severe anemia was likely multifactorial, including CKD-related erythropoietin deficiency and possible PTH-induced bone marrow fibrosis.

Discussion

This case highlights PHPT as a CKD-MBD mimic in advanced CKD. Disproportionate hyperparathyroidism with hyperchloremic acidosis and impaired ammonium excretion led to the diagnosis of PTH-induced distal RTA from parathyroid adenoma. Low albuminuria relative to total proteinuria (UACR 410 mg/g vs. UPCR 1,910 mg/g) suggested chronic tubulointerstitial disease, potentially worsened by chronic acidosis. Management included cinacalcet, ergocalciferol, sodium bicarbonate, and erythropoiesis-stimulating agents, with close monitoring for post-parathyroidectomy hungry bone syndrome given markedly elevated PTH, ALP, and extensive skeletal involvement.