Phosphorus takes part indirectly in the pathogenesis of hyperparatyroi
dism through its effect on blood levels of calcium and calcitriol. Rec
ent data suggest a direct participation of phosphorus on parathormone
production. To analyse the influence of phosphorus on PTH secretion, w
e studied, in 15 uremis patients, the behavior of phosphocalcic metabo
lism parameters in a conventional HD with a calcium concentration of 7
mg/dl (HD phosphorus free, HD-PF) and in a HD session using a dialysa
te with phosphorus and the same calcium concentration (HD-WP). In the
HD-PF, phosphorus serum levels decreased quickly during the two early
hours of the session with stable values at the end of the HD (T0: 6.31
+/- 0.36; T120: 3.3 +/- 0.17 mg/dl, p < 0.001; T180: 3.2 +/- 0.2 mg/d
l). In the HD-WP, the blood levels of phosphorus were over the upper n
ormal limits during HD (T0: 5.74 +/- 0.43; T60: 5.61 +/- 0.41; T120: 5
.23 +/- 0.3; T180: 4.98 +/- 0.2 mg/dl). The calcium balance was simila
r in both methods. The ionized calcium increased in a significant way
in the HD-PF (4.62 +/- 0.16 vs 3.66 +/- 0.16 mg/dl, p < 0.01). This in
crease was less notorius in the HD-WP being nevertheless significative
(4.25 +/- 0.21 vs 3.73 +/- 0.14 mg/dl, p < 0.05). Meanwhile the PTH d
ecreased in a significant way in the HD-PF (T0: 309 +/- 55; T180: 181
+/- 72 pg/ml, p < 0.01), it did not modify in the HD-WP (T0: 227 +/- 5
8; T180: 266 +/- 133 pg/ml). The PTH response to ionized calcium incre
ase suffered a deviation to the right in the HD-WP as compared with HD
-PF. Our results demostrate for the first time, that, in uremic patien
ts and in an acute way, the hyperphosphoremia attenuates the dialytic
increase of calcium and interferes in the PTH suppression induced by c
alcium, moduling it and/or having a direct effect on PTH secretion.