RESUMO
The aims of this retrospective study were to assess renal function and blood pressure after subtotal parathyroidectomy (PTx) performed in renal transplant (RT) patients presenting with persistent hypercalcemic hyperparathyroidism. We identified 34 patients (group A) from our records who had undergone PTx between 1981 and 1994. Group A included 18 women 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 (AZA) 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 first year following renal transplantation and in 13 patients after this period. The study was divided into 3 periods: period 1-pre-PTx; period 2-the month following PTx; period 3-six months after PTx. Parameters were assessed for every patient in each of these periods. Results of group A were compared to those observed in 34 matched (control) RT patients (group B) who did not experience secondary hyperparathyroidism. PTx was associated with a significant decrease in parathyroid hormone (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 serum creatinine (124 +/- 30 mumol/l vs 110 +/- 25 mumol/l, p = 0.0016) in this group during period 3. Nevertheless, an increase in serum creatinine greater than 30% from baseline which still persisted six months after PTx was only observed in 8 patients (23.5%). There were more hypertensive patients in this latter subgroup (7 out of 8 i.e. 87.5%) than 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, calcemia, creatinine, CsA whole blood trough levels or PTH levels. Conversely, we did not observe significant changes in serum creatinine in the control group during the same periods. During period 2 there was a significant 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 103.5 +/- 11 mmHg; p = 0.03) of group A. These differences persisted in period 3, with the exception of SBP, although they were no longer statistically significant. Following PTx we were able to discontinue (n = 4) or decrease (n = 4) antihypertensive drugs. In the control group baseline SBP, DBP and MBP were lower than in the PTx group, although the difference was statistically significant only for SBP (132.5 +/- 17 vs 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 study shows that RT patients with hypercalcemic hyperparathyroidism are often 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 patients (23.5%), particularly in those presenting with hypertension before PTx. These results could reflect a dual effect of parathyroid hormone i.e. a balance between a vasodilating and hypertensive effect.
