Hyperphosphoremia is said to cause secondary hyperparathyroidism by depress
ing ionized calcium plasma levels and by affecting serum calcitriol levels.
Recent studies suggest a direct stimulatory role of phosphorus in PTH prod
uction. The aim of this study was to analyse the influence of acute hyperph
osphoremia on PTH production. The study was performed on 6 stable patients
on regular dialysis therapy. We compared the biochemical data and phospho-c
alcium metabolism parameters obtained from a conventional five hours hemodi
alysis session (C-HD) with those obtained during a hemodialysis in which, a
fter 120 minutes, a dialysate with phosphate (6 mg/dl) was used (P-HD).
The calcium balance was similar in both HD. We observed a similar behavior
of the phospho-calcium metabolism parameters in both procedures until the 1
20 minutes (T120). From then, in the P-HD it was observed a significant inc
rease of phosphorus serum levels (T120: 3.2 +/- 0.18 mg/dl; T180: 5.44 +/-
0.38 mg/dl (p < 0.05). It was also observed a decrease in Ca2+ (T120: 4.1 /- 0.06; T180: 3.8 +/- 0.07 mg/dl). After the introduction of the phosphate
dialysate, the PTH levels increased significantly (T120: 212 +/- 88; T180:
274 +/- 107 pg/ml; (p < 0.051. The PTH behavior in P-HD was similar to tha
t observed in HD patients when a slight decrease of serum Ca++ was induced
by changing calcium concentration of dialysate.
Our results demostrate that in uremic patients the intradialytic acute hype
rphosphoremia increases PTH production by depressing ionized calcium plasma
levels.