CHANGES IN BLOOD-PRESSURE AND RENAL-FUNCTION FOLLOWING SUBTOTAL PARATHYROIDECTOMY IN RENAL-TRANSPLANT PATIENTS PRESENTING WITH PERSISTENT HYPERCALCEMIC HYPERPARATHYROIDISM
L. Rostaing et al., CHANGES IN BLOOD-PRESSURE AND RENAL-FUNCTION FOLLOWING SUBTOTAL PARATHYROIDECTOMY IN RENAL-TRANSPLANT PATIENTS PRESENTING WITH PERSISTENT HYPERCALCEMIC HYPERPARATHYROIDISM, Clinical nephrology, 47(4), 1997, pp. 248-255
The aims of this retrospective study were to assess renal function and
blood pressure after subtotal parathyroidectomy (PTx) performed in re
nal transplant (RT) patients presenting with persistent hypercalcemic
hyperparathyroidism. We identified 34 patients (group A) from our reco
rds who had undergone PTx between 1981 and 1994. Group A included 18 w
omen and 16 men with a mean age of 45 +/- 12 years and a mean time on
dialysis therapy of 102 +/- 59 months. Thirty of the patients received
cyclosporine A (CsA) with or without steroids and/or azathioprine (AZ
A) and the remaining 4 patients received conventional therapy i.e. AZA
and steroids. Twenty-three patients were treated for hypertension and
11 were normotensive. PTx was performed in 21 patients within the fir
st year following renal transplantation and in 13 patients after this
period, The study was divided into 3 periods: period 1 - pre-PTx; peri
od 2 - the month following PTx; period 3 - six months after PTx. Param
eters were assessed for every patient in each of these periods, Result
s of group A were compared to those observed in 34 matched (control) R
T patients (group B) who did not experience secondary hyperparathyroid
ism. PTx was associated with a Significant decrease in parathyroid hor
mone (PTH) levels (45 +/- 8 pg/ml vs 338 +/- 54 pg/ml; p = 0.0002) and
in calcemia (2.32 +/- 0.18 mmol/l vs 2.75 +/- 0.15 mmol/l; p = 0.0003
) during period 3. However, we observed a significant increase in seru
m creatinine (124 +/- 30 mu mol/l vs 110 +/- 25 mu mol/l, p = 0.0016)
in this group during period 3. Nevertheless, an increase in serum crea
tinine greater than 30% from baseline which still persisted six months
after PTx was only observed in 8 patients (23.5%). There were more hy
pertensive patients in this latter subgroup (7 out of 8 i.e. 87.5%) th
an in the rest of the group (16 out of 26 i. e. 64.5%). Renal function
impairment in group A was not related to pre-PTx: SBP, DBP, MBP, calc
emia, creatinine, CsA whole blood trough Levels or PTH levels. Convers
ely, we did not observe significant changes in serum creatinine in the
control group during the same periods. During period 2 there was a si
gnificant decrease in SBP (134 +/- 16 vs 140 +/- 16 mmHg; p = 0.046),
DBP (81 +/- 9 vs 85 +/- 9 mmHg; p = 0.03) and MBP (99.5 +/- 10.5 vs 10
3.5 +/- 11 mmHg: p = 0.03) of group A. These differences persisted in
period 3. with the exception of SBP, although they were no longer stat
istically significant, Following PTx we were able to discontinue (n =
4) or decrease (n = 4) antihypertensive drugs. In the control group ba
seline SBP, DBP and MBP were lower than in the PTx group, although the
difference was statistically significant only for SBP (132.5 +/- 17 v
s 140.5 +/- 16 mmHg: p = 0.05). During the study periods there was no
significant changes in SBP, DBP or MBP in the control group. This stud
y shows that RT patients with hypercalcemic hyperparathyroidism are of
ten hypertensive (68%). Subtotal PTx is associated with a significant
but transient decrease in SBP, DBP and MBP. Surprisingly we observe a
significant and persistent increase in serum creatinine levels in 8 pa
tients (23.5%), particularly in those presenting with hypertension bef
ore PTx. These results could reflect a dual effect of parathyroid horm
one i.e. a balance between a vasodilating and hypertensive effect.