The discovery of FGF23, the missing link in the long researched and finally found phosphate metabolism, marked a turning point in the understanding and physiopathology of specific hypophosphatemia. By inhibiting the renal reabsorption of phosphate and the production of calcitriol, FGF23 behaves like a hypophosphatemia hormone.

Hypersecretion of FGF23 can occur in the case of genetic abnormalities (X-linked hypophosphatemic vitamin-resistant rickets, recessive or dominant hypophosphatemic rickets, McCune-Albright syndrome ...) or acquired abnormalities (oncogenic osteomalacia). Oncogenic osteomalacia can be induced by hyperproduction of FGF23 by benign tumours of mesenchymal origin. But more recently, several cases of malignant tumours secreting FGF23 have also been described (prostate, colon, breast, ovarian and lung cancers, pulmonary carcinoma, etc.)

To date, even if the incidence of FGF23-secreting tumours seems rare, no precise bibliographical data is available in the scientific literature. Future studies will have to address this issue in order not to underestimate the frequency of this complication.

In this context, investigators would like to study the incidence of inappropriate FGF23 increase from a collection of biological samples carried out on 500 patients treated at the Clermont-Ferrand University Hospital for hypophosphatemia.

Inclusion Criteria:

• Major patient, male or female
• Taken care of at the Clermont-Ferrand University Hospital or the Jean Perrin Centre
• In a context of hypophosphatemia (< 0.80 mmol/L), without immediate anteriority and not occurring during hospitalisation
• In capacity to express informed consent to participate in research
• Affiliated to a social security system

Exclusion Criteria:

• Previously diagnosed hypophosphatemia
• Hypophosphatemia during hospitalisation
• Haemodialysis patient
• Refusal to participate

Major patient, male or female with hypophosphatemia (< 0.80 mmol/L), without immediate anteriority