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[A complex case of renal phosphate wasting…].

Sébastien Daude¹, Thomas Quinaux², Benjamin Collet-Fenêtrier³

¹Service d'hépato-gastro-entérologie, CHRU de Nancy, 1, rue du Morvan, 54500 Vandœuvre-lès-Nancy, France.

Nephrologie & Therapeutique

|May 17, 2021

Summary

A patient experienced severe hypophosphatemia after ferric-carboxymaltose infusion, indicating renal phosphate wasting. Genetic testing for familial phosphate wasting syndrome was inconclusive despite kidney stones in the family.

Keywords:

Carboxymaltose ferrique Diabète phosphaté FGF-23 Ferric carboxymaltose Hypercalciuria Hypercalciurie Hypophosphatemia Hypophosphatémie Kidney stone Lithiase rénale Renal phosphate carriers Renal phosphate wasting Transporteurs rénaux de phosphates

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Area of Science:

Nephrology
Endocrinology
Gastroenterology

Background:

Ferric-carboxymaltose is used to treat iron deficiency anemia.
Hypophosphatemia is a potential side effect of ferric-carboxymaltose, characterized by low phosphate levels.
Renal phosphate wasting and elevated Fibroblast Growth Factor 23 (FGF-23) are key indicators of phosphate imbalance.

Observation:

A 34-year-old man presented with hemorrhagic rectocolitis and severe hypophosphatemia following ferric-carboxymaltose infusion.
The patient exhibited a very low renal maximal reabsorption rate of phosphate and high plasma FGF-23 levels.
The patient and his father reported a history of kidney stones (weddellite and carbapatite) and hypercalciuria.

Findings:

The clinical presentation suggested a diagnosis of renal phosphate wasting syndrome.
Despite the suspicion of a familial phosphate renal wasting syndrome, no mutations in renal phosphate carriers were identified.
The patient's hypophosphatemia was linked to impaired renal phosphate reabsorption, potentially exacerbated by the ferric-carboxymaltose infusion.

Implications:

This case highlights a potential adverse effect of ferric-carboxymaltose, leading to significant hypophosphatemia and renal phosphate wasting.
The investigation into familial kidney stones and hypercalciuria suggests a possible underlying genetic predisposition or a complex interplay of factors.
Further research is needed to elucidate the genetic basis of familial phosphate wasting syndromes and their association with kidney stone formation.