Commentary on Severe Hypophosphatemia: The Hidden Truth.

Abstract

Abnormal phosphate results are common in daily practice, but often neglected by laboratorians and clinicians. This case of severe hypophosphatemia highlights the critical implications that a delayed diagnostic workup of the underlying cause can have. Early diagnosis and treatment could have prevented years of continuous bone loss and immobility. Therefore, severe hypophosphatemia should always trigger additional investigations to find the underlying cause. Determination of the tubular maximum reabsorption of phosphate for glomerular filtration rate was pivotal for establishing renal phosphate wasting and for guiding further diagnostic measures. This rarely used parameter can easily be determined in most laboratories, but pathologists are often unaware of its diagnostic value. Consequently, many laboratories limit themselves to the measurement of timed urinary phosphate excretion, despite the fact that a wide reference interval limits its diagnostic utility. In adult patients with renal phosphate wasting, measurement of fibroblast growth factor-23 (FGF-23) helps to further narrow the spectrum of potential causes. Elevated FGF-23 concentrations are typical in tumor-induced osteomalacia, but normal values can occur when the underlying tumor secretes other phosphatonins or in the presence of interfering heterophile antibodies or human antimouse antibodies that disturb the assay (1).