Abstract
Hypophosphatemia is a rare ion disorder in children, but it carries the risk of serious clinical sequelae in tissues and organs with high energy requirements, such as bone tissue. This article discusses the metabolism of phosphate in the body, the clinical manifestations of hypophosphatemia, and the diagnostic tests necessary in patients with this disorder. Extra-renal causes are analyzed, and renal forms of hypophosphatemia are discussed in detail. Renal hypophosphatemia, depending on the mechanism, is divided into PTH-dependent (e.g., primary hyperparathyroidism), FGF23-dependent (e.g., X-linked hypophosphatemia), and intrinsic renal hypophosphatemia (e.g., Fanconi syndrome). The treatment of hypophosphatemia involves compensating for phosphate deficiency, often simultaneously with the supply of an active form of vitamin D. Always seek causal treatment, such as parathyroidectomy in primary hyperparathyroidism. In the FGF-23-dependent forms of X-linked hypophosphatemia and tumor-induced osteomalacia, burosumab has proven to be an effective and safe drug. Conclusions: a child with hypophosphatemia requires a multidisciplinary approach and determination of the mechanism of phosphate deficiency in the body.