Abstract
Mohamed & Raal highlight the importance of investigating hypophosphatemia biochemically to allow a diagnosis of the underlying aetiology. Both parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) facilitate phosphate excretion in the urine. The tubular maximum reabsorption of phosphate for glomerular filtration rate (TmP/GFR) is a measure of renal tubular capacity to reabsorb phosphate. TmP/GFR is therefore reduced in a calcipenic state (vitamin D and/or calcium deficiency) due to secondary hyperparathyroidism and in the phosphopenic state, either due to a primary renal tubular defect or excess circulating FGF23 (genetic defects in FGF23 degradation or increased FGF23 production such as tumor-induced osteomalacia [TIO]). PTH increases 1,25-(OH)2Vitamin D (calcitriol) production while FGF23 reduces it. In this case of severe symptomatic hypophosphatemia, the low TmP/GFR, inappropriately normal calcitriol in the context of hypophosphatemia, and elevated FGF23 confirmed FGF23-induced renal phosphate wasting. A nuclear medicine scan established the diagnosis of TIO and assisted in the localization of the lesion.
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