Dr Angela Au1, Dr Sanjeev Baweja1, Dr Victoria Sasongko1
1Department of Renal Medicine, Lismore Base Hospital , Lismore, Australia
Biography:
Angela Au is a second year Renal Advanced Trainee currently working at Royal Prince Alfred Hospital network in Sydney, NSW. She graduated from University of Newcastle in 2019 and is currently studying a Masters of Medicine at the University of Sydney.
Background:
Hypophosphatemia is a recognised complication of intravenous iron formulations, particularly ferric carboxymaltose and may be exacerbated by concurrent antiresorptive agents like denosumab. While often well tolerated, excessive phosphate supplementation can cause calcium phosphate crystal deposition and acute phosphate nephropathy.
Case Report:
A 70-year-old woman was referred with asymptomatic hypophosphataemia, four weeks after receiving intravenous ferric carboxymaltose and three days following subcutaneous denosumab. Laboratory investigations revealed a corrected calcium of 1.88 mmol/L, phosphate 0.30 mmol/L, parathyroid hormone (PTH) 40 pmol/L, and creatinine of 68 µmol/L (eGFR 79 mL/min).
She was treated with 20 mmol of intravenous potassium dihydrogen phosphate and 2.2 mmol of intravenous calcium gluconate, then discharged on oral calcium and phosphate supplements. She was re-referred following persistently low phosphate (0.45 mmol/L) and was administered an additional 10 mmol of intravenous phosphate. She was subsequently discharged on 3000 mg of oral Phosphate Sandoz daily.
One week later, she re-presented with acute kidney injury (serum creatinine 199 µmol/L) and elevated phosphate (1.78 mmol/L). Urinalysis showed no haematuria, proteinuria, or casts. CT KUB excluded urinary tract obstruction. A diagnosis of acute phosphate nephropathy from phosphate overload was made. Oral phosphate was discontinued, and the patient was treated with 2 litres of intravenous fluids.
Her creatinine improved to 191 µmol/L after 5 days, 110 µmol/L at 2 weeks, and 91 µmol/L at 6 months, hence a renal biopsy was not performed.
Conclusion:
This case highlights the risk of acute phosphate nephropathy following aggressive phosphate replacement. Caution is advised with high-dose phosphate supplementation, particularly in asymptomatic patients—even those with normal renal function. Ferric carboxymaltose and denosumab require careful monitoring due to their synergistic effects on phosphate metabolism.