CHANGES IN BLOOD-PRESSURE AND RENAL-FUNCTION FOLLOWING SUBTOTAL PARATHYROIDECTOMY IN RENAL-TRANSPLANT PATIENTS PRESENTING WITH PERSISTENT HYPERCALCEMIC HYPERPARATHYROIDISM

Citation
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
Citations number
47
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
03010430
Volume
47
Issue
4
Year of publication
1997
Pages
248 - 255
Database
ISI
SICI code
0301-0430(1997)47:4<248:CIBARF>2.0.ZU;2-H
Abstract
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.