Approach to the hypophosphatemic patient

Abstract

Hypophosphatemia is commonly missed due to nonspecific signs and symptoms, but it causes considerable morbidity and in some cases contributes to mortality. Three primary mechanisms of hypophosphatemia exist: increased renal excretion, decreased intestinal absorption, and shifts from the extracellular to intracellular compartments. Renal hypophosphatemia can be further divided into fibroblast growth factor 23-mediated or non-fibroblast growth factor 23-mediated causes. Proper diagnosis requires a thorough medication history, family history, physical examination, and assessment of renal tubular phosphate handling to identify the cause. During the past decade, our understanding of phosphate metabolism has grown greatly through the study of rare disorders of phosphate homeostasis. Treatment of hypophosphatemia depends on the underlying disorder and requires close biochemical monitoring. This article illustrates an approach to the hypophosphatemic patient and discusses normal phosphate metabolism.

Fig. 1.

Nomogram for determining TmP/GFR. The tubular reabsorption of phosphate (TRP) is calculated using the formula: 1 − [(urine phosphate * serum creatinine)/(serum phosphate * urine creatinine)]. Left axis, PO₄ indicates phosphate in mg/dl to the outside of the axis and mmol/l to the inside of the axis. Right axis, TmPO₄/GFR is the renal threshold phosphate concentration in mg/dl to the outside of the axis and in mmol/l to the inside of the axis. CPO₄ is the clearance of phosphate. Ccreat is the clearance of creatinine. [Reprinted from R. J. Walton and O. L. Bijvoet: Nomogram for derivation of renal threshold phosphate concentration. Lancet 306:309–310, 1975 (47), with permission. © Elsevier.]