Chapter 9 - Hypophosphatemia

Abstract

Phosphate is a key element for several physiological pathways, such as skeletal development, bone mineralization, membrane composition, nucleotide structure, maintenance of plasma pH, and cellular signaling. The kidneys have a key role in phosphate homeostasis with three hormones playing important roles in renal phosphate handling (i.e., parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and 1,25 dihydroxy-vitamin D). Hypophosphatemia is defined as a serum phosphate level of less than 2.5 mg/dL. Hypophosphatemia is an electrolyte disorder frequently faced in inpatient and outpatient practice. Associated symptoms are very variable but are often nonspecific. The consequence is that it might be overlooked. Yet, when severe, hypophosphatemia is associated with a significant morbidity–mortality and, therefore, needs to be identified and treated appropriately. Treatment goes from identifying the cause to substitution according to whether it is symptomatic or not and its severity. Mild to moderate hypophosphatemia needs substitution only when symptomatic, in which case it will be administered orally, while severe hypophosphatemia requires an intravenous substitution. Independently of the genetic diseases affecting the FGF23 pathway (such as hypophosphatemic rickets), hypophosphatemia is a frequent condition in daily practice, and untreated severe hypophosphatemia can induce hemolysis, rhabdomyolysis, respiratory failure, cardiac dysfunction, and neurological impairment, thus requiring a rapid correction to avoid severe complications.