A patient with unexplained hyperphosphataemia

Abstract

Hyperphosphataemia is not a common biochemical alteration outside the context of renal failure. In fact, phosphate homeostasis is mainly regulated by kidney function and parathyroid hormone (PTH) activity [1–4]. In the presence of normal renal function and normal PTH activity, serum phosphate values are tightly regulated within a reference range of 0.8–1.5mmol/l (2.5–4.5mg/dl). As phosphates are filtered by the glomerular barrier and excreted into the urine with a renal clearance of 15–20ml/min, serum phosphate levels do increase early from the beginning of renal failure, reaching levels as high as 4–5mmol/l in the case of end-stage renal failure in patients with poor compliance to therapeutic schedules [1,2]. Furthermore, true hyperphosphataemia can also result from impaired PTH activity, as PTH is the main factor responsible for phosphate secretion by renal tubular cells, eventually leading to the typical picture of hyperphosphataemia and hypocalcaemia in the presence of hypoparathyroidism [3,4]. Lastly, true hyperphosphataemia could be caused by phosphate poisoning, mainly attributed to phosphate enemas in children, even in the absence of renal failure [5,6]. From a clinical point of view, severe hyperphosphataemia stimulates PTH secretion, induces and worsens extra-osseous tissue calcification and can cause acute paralysis, convulsions and cardiac arrest mainly due to complexes with free serum calcium, resulting in hypocalcaemia [7,8]. We report a case of a patient with normal renal function, IgG myeloma and persistent hyperphosphataemia, in whom further laboratory analyses allowed a diagnosis of ‘pseudo-hyperphosphataemia’ caused by interferences of his paraproteinaemia with analytical procedure for phosphate measurement.