A 45-year-old African woman had iron deficiency for 4 years caused by abundant menstruation. Her past medical history included tuberculosis in 1985 and lung lobectomy for aspergilloma five years earlier. She had 4 healthy children and did not smoke. Gastroscopy performed initially was normal. She complained of fatigue and headache. She took oral iron supplementation but developed side effects that led to treatment discontinuation. In 2011, she received two infusions of iron sucrose (total dose: 200 mg) without any impact on the phosphate level (2.7 mg/dL after the second infusion). In 2012, laboratory findings were hemoglobin level (Hb) of 9.9 gr/L, serum ferritin of 6 mug/L (normal range: 13-150), and serum iron saturation of 6.7% (normal range: 15-50). She received 3 additional infusions of iron sucrose (total dose: 300 mg) which slightly reduced the phosphate level (2.1 mg/dL) but without symptoms. In 2014, her Hb was at 9.8 gr/dL with serum iron saturation at 6% and serum ferritin at 13 mug/L, and the plasma phosphate level before injection of FCM was of 2.5 mg/dL with a FEPO4 of 11%. This moderate elevation in phosphate clearance was probably due to 25-hydroxyvitamin D (25(OH)D3) deficiency and secondary hyperparathyroidism (PTH: 147.2 ng/L, normal range: 15-65; 25(OH)D3: 9 ng/mL, normal range: >30). She then received two injections of FCM (Injectafer, Vifor Pharma) (one-week interval, total dose: 1000 mg). Ten days after the second infusion, she complained of intense fatigue. Blood analysis showed a phosphate level at 0.93 mg/dL with FEPO4 at 23% confirming the diagnosis of phosphate diabetes. She received oral phosphate supplementation which improved fatigue and at, one month, the phosphate level increased to 1.2 mg/dL with FEPO4 at 29%. Two months after the first administration, the phosphate level returned to normal value at 2.34 mg/dL with FEPO4 at 13%.  Table 1 summarizes the evolution of laboratory results before and after FCM administration and the evolution of fractional phosphate excretion over time is presented in Figure 1.