Phosphorus (P) is an essential micronutrient found in virtually all structural molecules.1 Overall, 85% of P in the body is found in the bone, 14% in the intracellular space and 1% in the extracellular fluid.2 Correct homeostasis of P is essential for synthesising adenosine triphosphate, nucleic acids or second messengers, among others, as well as for the formation of the phospholipids that make up cell membranes.1

The normal concentration of plasmatic P varies between 2.5 and 4.5 mg/dl2 and is determined by the complex interaction of different organs, mainly the intestine, parathyroid glands, bone and kidney. This interaction is controlled by various endocrine mediators, some classic ones such as parathyroid hormone (PTH) and vitamin D, and others that have gained prominence more recently, such as fibroblast growth factor 23 (FGF-23). Renal reabsorption of P in the proximal tubule through sodium-phosphate (Na-Pi) co-transporters1 is ultimately considered the main determinant of phosphataemia.

Anorexia nervosa (AN) is an eating disorder (ED) characterised by an oral intake less than the requirements despite low weight, with an intense fear of weight gain and an alteration in the perception of the body image.3 AN also brings numerous medical complications derived from undernutrition itself and from compensatory behaviours,4 as well as an increased risk of mortality.5

Complications of AN have been described involving multiple body systems in the body such as the digestive, cardiovascular, neurological, endocrinological, bone and metabolic systems.4 Electrolyte disturbances are among the most frequent complications of AN and usually derive from repeated vomiting, compulsive water intake, laxative or diuretic abuse, or the refeeding syndrome (RS). AN is a recognised risk factor for the development of RS, a potentially serious complication that can occur in the first few days after aggressive nutritional repletion in undernourished patients and/or after prolonged fasting.6 Hypophosphataemia is one of the most common anomalies in this syndrome and a key fact for diagnosis.6, 7 Outside the context of RS, no frequent abnormalities in P homeostasis have been reported in subjects with AN. However, in our clinical practice, we have observed hyperphosphataemia in the late stages of renutrition in severely undernourished patients with AN, a finding that has been poorly described in this group so far and for which we have not found any of the recognised causes of hyperphosphataemia In our study, we describe the incidencia,magnitud and temporal pattern of this finding. We also explore the association with other variables to help predict its appearance and/or propose aetiological hypotheses.