Abstract: TH-PO0082
Multifactorial Hypercalcaemia Causing Kidney Injury
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical Research
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Author
- Ahmed, Candeel, Watford General Hospital, Watford, England, United Kingdom
Group or Team Name
- WGH
Background
Sarcoidosis a multisystem disorder is associated with renal injury by direct infiltration and as a result of hypercalcaemia. We present a case of persistent hypercalcaemia causing renal dysfunction in a patient with coexisting primary hyperparathyroidism and biopsy-proven sarcoidosis.
Methods
A 59M, with a back ground of CKD3 (baseline Cr ~130µmol/L) and low-risk prostate cancer under active surveillance presented to hospital following blood test organised in primary care to investigate persistent tiredness ,revealed severe hypercalcaemia (adjusted Ca 3.52 mmol/L), raised parathyroid hormone (PTH 17.9pmol/L), hypophosphataemia (0.70 mmol/L) and acute kidney injury (AKI).
A CT TAP demonstrated symmetrical mediastinal and hilar lymphadenopathy concerning for Lymphoproliferative or granulomatous disease process while ruling out Lytic lesions that would have been associated with metastatic prostrate disease. Imaging of parathyroids were undertaken to investigate the cause or raised PTH, revealing a right inferior parathyroid adenoma.
Results
Managed with aggressive hydration and Cinacalcet therapy while awaiting EBUS-guided lymph node biopsy that demonstrating non-caseating granulomatous inflammatory lesions consistent with sarcoidosis. Corticosteroid therapy commenced resulting in improved Ca levels and stable renal function.
Parathyroidectomy 6 months following initial presentation resulted in suppressed post-op PTH levels. Unfortunately, the hypercalcaemia persisted postoperatively.
Hydroxychloroquine was added to a slower corticosteroid wean which led to good biochemical control. 3 months following these changes the calcium levels had normalized to 2.35 mmol/L with significant improvement in renal function (creatinine 108 µmol/L). This allowed for the eventual withdrawal of immunosuppressive therapy, without recurrence of severe hypercalcaemia.
Conclusion
This case highlights the complexity of persistent hypercalcaemic renal injury in the presence of coexisting primary hyperparathyroidism and sarcoidosis. A prolonged weaning cause of steroids with the addition of Hydroxychloroquine allowed for sustained biochemical remission of sarcoidosis and renal stabilization.