PTH, FGF-23 and early CKD.

Patients with early CKD (GFR > 30 ml/min per 1.73 m2) do not usually have changes in the serum calcium and phosphate concentration. PTH may be minimally increased and more recent publications have shown that the phosphaturic hormone, FGF-23, is clearly increased. Thus in early CKD, serum levels of phosphate and calcium are maintained within normal levels because hormonal changes compensate for the decrease in GFR. The aim of the study by Isakova et al. [1] was to analyze postprandial changes in serum calcium and phosphate which may serve as an intermittent stimulus for PTH and FGF-23 production. The study included 21 healthy volunteers and 13 CKD patients with a mean GFR of 41 ± 8 ml/min per m2 and normal serum levels of calcium, phosphate and PTH. In the fasting state, CKD patients had significantly higher levels of FGF23, a higher fractional excretion of phosphate (FEPO4) and a lower fractional excretion of calcium (FECa). After standardized meals, urinary phosphate excretion increased only in healthy volunteers despite unchanged FGF-23 levels and minimal changes in serum phosphate values. Although the postprandial urinary excretion of calcium increased in both groups, a significant reduction in serum calcium with a concomitant, but delayed increase in PTH was observed only in CKD patients. Thus, in this study, FGF-23 did not change in response to a meal (phosphate load). The authors also concluded that a postprandial decrease in serum calcium with enhanced calcium excretion may represent an early mechanism in the development of hyperparathyroidism.