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NDT Advance Access originally published online on March 19, 2007
Nephrology Dialysis Transplantation 2007 22(6):1730-1737; doi:10.1093/ndt/gfm044
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Parathyroidectomy after successful kidney transplantation: a single centre study

Pieter Evenepoel1, Kathleen Claes1, Dirk R. Kuypers1, Frans Debruyne2 and Yves Vanrenterghem1

1Department of medicine, Division of Nephrology and 2Department of Ear–Nose–Throat and Head and Neck Surgery, University Hospital Leuven, B-3000 Leuven, Belgium

Correspondence and offprint requests to: P. Evenepoel, MD, PhD, Dienst nefrologie, Universitair Ziekenhuis Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium. Email: Pieter.Evenepoel{at}uz.kuleuven.ac.be



   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
Background. Successful kidney transplantation is believed to cure secondary hyperparathyroidism, but persistent disease has emerged in a significant number of allograft recipients. A parathyroidectomy is ultimately required in some of these patients. To gain insight into the incidence, risk factors and consequences of parathyroidectomy in patients with a functioning renal graft, we performed a retrospective case-controlled study.

Methods. Charts of 1743 recipients of a kidney allograft, transplanted between 1989 and 2004, were reviewed. Patients with a functioning graft subjected to parathyroidectomy were identified. Their charts were checked for various demographic, clinical and biochemical variables. The data were compared with those obtained from patients transplanted in the same period, but not subjected to parathyroidectomy (controls).

Results. Persistent hyperparathyroidism in patients with a functioning graft requiring parathyroidectomy developed in 90 patients, corresponding to an overall parathyroidectomy rate of 8.89 per 1000 person-years at risk. Female gender (OR 1.79, P < 0.05) and higher pre-transplant serum concentrations of PTH (OR per 1 ng/l increase, 1.003, P < 0.0001) and calcium (OR per 1 mg/dl increase, 2.58, P < 0.0001) were identified as independent predictors of post-transplant parathyroidectomy. A significant increase of the serum creatinine was observed after parathyroidectomy (1.91 ± 0.72 vs 1.76 ± 0.63 mg/dl, P < 0.01). Graft survival, however, was similar in cases and controls.

Conclusion. Persistent hyperparathyroidism requiring parathyroidectomy after successful renal transplantation is a common clinical problem. Female patients with a high pre-transplant serum level of PTH and calcium are especially at risk. Although graft function deteriorates shortly after parathyroidectomy, graft survival, overall, is not different from controls.

Keywords: hyperparathyroidism; parathyroidectomy; transplantation



   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Acknowledgements
 References
 
Secondary hyperparathyroidism (HPT) is an almost universal complication in patients with chronic renal failure. Although present knowledge is incomplete, several mechanisms have been identified by which HPT is initiated and maintained in renal failure [1]. Abnormal calcium–phosphorus and vitamin D metabolism play a key role in the development of secondary HPT in chronic renal failure [2]. As a consequence of the latter, morphological changes occur progressively in the parathyroid glands. The nature of these changes is not well established yet. Histopathological studies indicate that parathyroid cells initially increase diffusely with a normal lobular structure (diffuse hyperplasia). In a later stage, the hyperplasia becomes nodular and multiclonal and the glandular enlargement asymmetric (nodular hyperplasia) [3]. This morphological transformation goes along with a decreased expression of the calcium and vitamin D receptor on the surface of the parathyroid cells [3].

Successful renal transplantation at least partly corrects these endocrine and metabolic imbalances and the main abnormalities responsible for secondary HPT in the first months. Nevertheless, the early favourable events are not always followed by the rapid normalization of parathyroid hormone (PTH) secretion. Elevated PTH levels were observed in up to 25% of patients 1 year after transplantation despite adequate renal function [4]. A subgroup of these patients are referred for parathyroidectomy (PTX), mainly because of associated hypercalcaemia.

The present article provides an in-depth analysis of patients who required a PTX for treatment of persistent HPT after successful renal transplantation and aims to elucidate the incidence, risk factors and the long-term impact of this procedure on renal transplant function and parameters of mineral metabolism. Analysing a similar patient cohort (i.e. recipients of a renal transplant at the University Hospital Leuven) we previously described the natural history of secondary HPT after successful renal transplantation [4] as well as the short-term impact of a PTX on blood pressure, lipids and renal function [5]. The present study extends the data from these two observational studies.



   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Acknowledgements
 References
 
Subjects
Computer records from all the patients who received a kidney transplant at the University of Leuven between 1 January 1989 and 1 January 2004 (n = 1743) were reviewed retrospectively. All patients were followed until the first occurrence of death, renal transplant failure (defined as need for renal replacement therapy or preemptive re-transplantation), or 1 January 2004 (end of study). Patients with a history of post-transplant PTX were identified (cases). Information obtained from their medical charts included demographic data, laboratory data, mode and duration of dialysis and previous PTX. In patients with a history of post-transplant PTX, data concerning the operative technique and the histology of parathyroid glands were extracted from surgical and pathology reports. Results of ultrasonography of the parathyroid glands, whenever available, were noted as well.

In order to identify risk factors for post-transplant PTX, present at the time of transplantation, pre-transplant clinical and biochemical parameters were compared with that of transplant recipients with no history of PTX (controls A). To compare graft survival and patient survival between cases and controls, non-parathyroidectomized (non-PTX) renal transplant recipients matched for date of transplantation and having a post-transplant follow-up exceeding the time interval between transplantation and PTX of the corresponding case were selected (1:2). These patients are referred to as controls B. Finally, to evaluate the outcome of the surgical procedure, laboratory and clinical data as well as therapy were monitored. For descriptive purposes, data were grouped and averaged by time of analysis (relative to the time of the PTX, referred to as day 0): day 31–day 0, day 1–30, day 31–90, day 91–180, day 181–365, day 366–729, day 730–1460, day 1460 and later. To evaluate the long-term impact of a PTX on graft function, the slope of the reciprocal serum creatinine levels (expressed as dl/mg/wk) was compared before and after the surgical procedure.

Assays
Total serum calcium [normal range: 8.9–10.5 mg/dl (2.22–2.62 mmol/l)], phosphate [normal range: 2.3–4.7 mg/dl (0.74–1.52 mmol/l)], alkaline phosphatases (normal range: 90–260 U/l) and creatinine were measured using a computerized autoanalyser. Creatinine clearance was calculated according to the Cockcroft–Gault equation.

Serum concentrations of PTH were determined by an IRMA, as described elsewhere [6]. In contrast to most other commercially available IRMAs for PTH, this assay detects full-length human PTH but not N-terminal truncated fragments, and thereby resembles recently introduced third-generation PTH IRMAs (biointact PTH or whole PTH). This also explains its lower normal range of 3–40 pg/ml(ng/l) [6]. A comparison with the PTH 1–84 assay from Scantibodies Inc. in a large cohort of haemodialysis patients (n = 98) showed a good correlation (R2 = 0.92, y = 0.91x, data not shown). Specific guidelines on the target range of PTH in renal transplant recipients are currently lacking. Applying current Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines for bone metabolism and disease in chronic kidney disease (CKD) [7] and assuming a conversion factor of 2 between intact and biointact PTH [8], target ranges for PTH were defined as follows: CKD stages 1 and 2: 3–40 pg/ml; CKD stage 3: 20–40 pg/ml; CKD stage 4: 40–60 pg/ml and CKD stage 5: 80–160 pg/ml.

Statistics
Parameters with normal distribution are expressed as mean ± SD, whereas parameters with skewed distribution are expressed as median and interquartile range (IQR). Differences between groups and periods were analysed using the Mann–Whitney U-test or Wilcoxon Signed rank test for continuous variables and the chi-square tests for discrete variables. Actuarial analysis of survival was performed using the Kaplan–Meier method, with P-values generated by the Wilcoxon test and log-rank test. To identify independent determinants of post-transplant PTX, present at the time of transplantation, multivariate logistic regression was performed, including all univariately associated variables (P < 0.2). After excluding colinearity, the best subset of variables was selected by backward elimination on P < 0.2. This subset was then subjected to a final backward elimination procedure on P < 0.05. The SAS version 9.1 (SAS Institute, Cary, NC) software program was used for the statistical analysis. P values <0.05 were considered significant.



   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Acknowledgements
 References
 
Incidence
A total of 1743 renal transplant procedures were performed at the University of Leuven between 1 January 1989 and 1 January 2004. Only 15 out of the 1743 patients (0.9%) received a graft from a living donor. One hundred and fifty-two renal recipients had a history of PTX prior to transplantation, corresponding to a baseline prevalence of 8.7%. The mean post-transplant follow-up per patient was 62.6 (25.9–107.4) months. Ninety subjects required a PTX in the post-transplant period. This corresponds to an overall PTX rate of 8.89 per 1000 person-years at risk. Figure 1 shows the Kaplan–Meier survival curve of renal recipients with PTX as endpoint. Patients were censored at the time of death, graft failure, loss of follow-up or end of follow-up.


Figure 1
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  		Fig. 1. Kaplan–Meier survival curve of renal recipients (1989–2004) using parathyroidectomy as the end point. The patients were censored at the time of death, graft failure, loss of follow-up or end of follow-up (1 January 2004).

 
Demographics
Patient demographics and clinical characteristics are summarized in Table 1. The mean age at the time of the PTX was 50.9 ± 12.6 years. There was an even distribution of men and women (45:45). Most patients were recipients of primary transplants. Primary renal disease was diabetes (n = 6), glomerulonephritis/vasculitis (n = 23), interstitial nephritis (n = 11), hypertensive/large-vessel disease (n = 5), cystic/hereditary/congenital (n = 26), miscellaneous (n = 3) and unknown or missing (n = 16). Time on dialysis was 47.7 ± 37.8 months. Eighty-two of the cases received haemodialysis, while eight were on peritoneal dialysis at the time of transplantation.


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  		Table 1. Demographics and laboratory data

 
Signs and symptoms
HPT with hypercalcaemia persisting for more than 3 months after transplantation was the main indication for PTX. Laboratory data at the time of the PTX are summarized in Table 2. The mean serum level of calcium before surgery was 10.8 ± 0.8 mg/dl, which was significantly higher than at the time of transplantation. Sixty-one per cent of the cases were hypercalcaemic before the surgery. The mean serum PTH at the time of PTX was 107.1 pg/ml (76.0–160.8) [median (iqr)].


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  		Table 2. Impact of PTX on renal function and mineral metabolism

 
Most of the patients were asymptomatic. Bone pain and muscle weakness were recorded in five and one patient(s), respectively. Ultrasonographic data were available for 61 patients. In 44 of these patients, at least one enlarged parathyroid could be visualized. The maximal diameter of the largest gland visualized was 12.6 ± 5.0 mm (range 6–26 mm). In 32 out of the 44 patients, the maximal diameter was ≥10 mm.

Surgical treatment
The median time to PTX after transplantation was 11 months (range 1–167 months). Information concerning the operative procedure was available in 80 cases. The operative technique of choice was subtotal PTX (33/4 resection of the glands) (n = 74). Total PTX with parathyroid autograft and adenomectomy were performed in four and two cases, respectively. Pathology reports of surgically removed parathyroid tissue were reviewed in 62 patients. The histological diagnoses were diffuse hyperplasia (n = 33), nodular hyperplasia (n = 17) and parathyroid adenoma (n = 12).

Risk factors for post-transplant PTX, present at the time of transplantation
No difference between cases and controls A was observed with reference to gender, age, renal diagnosis, time on dialysis and type of dialysis (Table 1). Laboratory data obtained at the time of transplantation showed significant higher serum concentrations of calcium (10.7 ± 0.9 vs 9.9 ± 1.0 mg/dl, P < 0.0001), phosphorus (5.6 ± 1.5 vs 5.1 ± 1.6 mg/dl, P < 0.01), alkaline phosphatases (183.2 ± 91.2 vs 142.9 ± 120.1 U/l, P < 0.05) and PTH (218.0 vs 59.9 pg/ml, P < 0.05) in the cases as compared with the controls A. Of the cases and controls A, 54% and 27%, respectively, were hypercalcaemic at the time of transplantation, respectively (P < 0.0001). Based on the findings of the univariate analysis, the following parameters were entered in the multivariate logistic regression model: pre-transplant serum level of calcium, albumin, phosphorus, PTH, gender and history of PTX before transplantation (Table 3). Female gender [odds ratio (OR), 1.79; 95% confidence interval (95% CI), 1.09–2.93; P < 0.05] and higher pre-transplant serum concentrations of PTH (OR per 1 ng/l increase, 1.003; 95% CI, 1.002–1.004; P < 0.0001) and calcium (OR per 1 mg/dl increase, 2.58; 95% CI, 1.97–3.38; P < 0.0001) were identified as independent predictors of post-transplant PTX.


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  		Table 3. Univariate logistic regression analysis for association of variables with post-transplant parathyroidectomy

 
Outcome
There were no operative deaths. Data regarding the length of hospital stay were available for 58 cases. The mean hospital stay was 9.7 ± 4.9 days. The PTX was successful in 95% of the patients (n = 86), at least when considering the following criteria: normalization of serum calcium level and/or decrease of serum PTH level by at least 50%. A re-PTX was performed in three patients.

The evolution of the parathyroid function and mineral metabolism after PTX is shown in Table 2. A significant decrease of the serum level of PTH (11.5 vs 107.1 pg/ml, median, P < 0.0001) and calcium (9.0 ± 0.9 vs 10.8 ± 0.8 mg/dl, P < 0.0001) was observed shortly after the surgical procedure. Serum phosphorus level, conversely increased significantly (3.2 ± 0.8 vs 2.5 ± 0.6 mg/dl, P < 0.0001) after PTX. The PTH level reached the target range in only a minority (14.3–34.1%) of the patients. Post-PTX hypoparathyroidism was much more prevalent than HPT. The percentage of patients treated with calcium salts increased from 11.1% before PTX to 77.8% after PTX. The percentage of patients on active vitamin D treatment (calcitriol or 1-{alpha}-OHD3) increased from 11.1% before to 72.2% after PTX. The daily dose of active vitamin D and elementary calcium shortly after PTX amounted to 1.25 ± 0.98 µg and 3.30 ± 2.20 g, respectively. The dose of both supplements decreased over time.

A significant increase of serum creatinine from 1.76 ± 0.63 to 1.91 ± 0.72 mg/dl (P < 0.0001) was noted within the first month after the PTX. On the long-term, renal function stabilized (Table 2). There was no significant difference in the slope of the 1/serum creatinine curve before and after the surgical procedure [–0.025 (–0.11 to 0.11) vs –0.038 (–0.23 to 0.10) dl/mg/year]. Figure 2 shows the Kaplan–Meier graft survival curve in cases and controls B. Patients were censored at loss of follow-up or end of follow-up. Serum creatinine at the time of PTX (and an equivalent time point in the controls) did not differ between cases and controls B (1.76 ± 0.63 vs 1.71 ± 0.60 mg/dl, P = NS). Graft survival in both groups was almost identical (log-rank P = 0.92; Wilcoxon P = 0.95). Censoring for death revealed similar findings. No differences in patient survival (both censored and uncensored for graft survival) were observed either (data not shown).


Figure 2
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  		Fig. 2. Comparison of graft survival between patients requiring parathyroidectomy (n = 90) and a matched cohort of renal allograft recipients (n = 180).

 


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Acknowledgements
 References
 
In order to gain insight into the incidence and risk factors of post-transplant PTX, we performed a retrospective observational and case-controlled study, including 1743 recipients of a kidney allograft, transplanted between 1989 and 2004 in the renal transplant unit of the University hospital Leuven. Of the patients with a functioning renal graft 5% had a history of PTX because of persistent HPT. This corresponds to an overall PTX rate of 8.89 per 1000 person-years at risk. The Kaplan–Meier PTX-free survival curve suggests that the ‘risk’ of being referred for PTX declines with time after transplantation. This evolution opposes what is observed in renal failure patients following the start of maintenance dialysis and suggests that persistent rather than de novo HPT urged the surgery [9]. Prevalence rates of post-transplant PTX reported in recent literature range from 0.6% to 5.6% (Table 4) [7–15]. Such a large variation has also been observed in dialysis patients [16]. The lack of unequivocal indications and thresholds for PTX, as well as registration bias, case-mix and differences in duration of follow-up represent plausible explanations.


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  		Table 4. Epidemiology of parathyroidectomy in patients with a functioning renal transplant

 
The decision to recommend parathyroid surgery after kidney transplantation is a difficult one. Evidence-based guidelines are currently lacking. Laboratory data, clinical symptoms and imaging data should all be taken into account. For most clinicians, persistent HPT with hypercalcaemia represents the main indication. The calcaemia threshold for referral to a surgeon varies across different transplantation centres (Table 4). In the present series, the pre-PTX calcium level was 10.8 mg/dl, reflecting a rather liberal approach. Besides elevated serum levels of PTH and calcium, increased alkaline phosphatase activity, indicating high bone turnover, and clinical symptoms such as bone pain and pruritus may serve as additional indications. Imaging procedures may not only be helpful in locating parathyroid glands but also in assessing the parathyroid glandular weight [20].

The median time to PTX in the present study was 11 months, which is shorter as compared with the interval reported in previous studies (Table 4). In a recent protocol biopsy study, Gwinner et al. [17,21] demonstrated that persistent HPT is associated with nephrocalcinosis, which in turn, is independently associated with chronic allograft nephropathy. Whether a PTX will result in the disappearance of the interstitial calcium deposits remains to be investigated.

Because of the lack of clear recommendations in literature, the choice of operative procedure is to date related more to personal preference than to objective criteria [10,11,13]. A subtotal PTX was the procedure of choice in our patients. More specifically, the procedure comprised the removal of the three largest glands and a three-fourths resection of the remaining gland.

From the long-term follow-up data, it is obvious that presently recommended PTH target values are difficult to achieve with surgery. Persistent or transient hypoparathyroidism, a condition feared because of the associated risk of adynamic bone disease, was observed in up to 68.3% of the patients during prolonged follow-up. Hampi et al. [22], however, reported that even 20 years after total PTX without autograft a normal bone metabolism could be maintained in haemodialysis patients by adequate substitution with oral calcium and vitamin D despite almost undetectable PTH levels. This observation needs confirmation in the setting of renal transplantation.

Previously, we and others demonstrated a deterioration of renal function shortly after PTX [5]. In the present study, renal function was shown to stabilize after the initial deterioration. The slopes of the 1/serum creatinine curve were similar before and after the surgical procedure. In agreement with Kerby et al. [12], we moreover observed no difference in graft survival between patients requiring a PTX and a control group of non-parathyroidectomized renal transplant recipients. All together, these data indicate that in the long-term, a PTX has no detrimental impact on graft function

Female gender and a high serum level of PTH and calcium at the time of transplantation were independent predictors of post-transplant PTX. These findings support the notion that the setting for persistent HPT is at least partly established before transplantation. It is well known that women are more susceptible to parathyroid gland hyperactivity [3,5,9,23,24]. Estrogens are thought to play a pathogenic role since they have been demonstrated to activate the parathyroid gland both directly and indirectly (via altered calcium metabolism). The observation that female gender is a predictor of post-transplant PTX, independent from the severity of the HPT at the time of transplantation, is intriguing. This observation may reflect a referral bias. Indeed, when considering persistent HPT a risk factor for accelerated osteoporosis, the threshold for referring menopausal women for PTX may be hypothesized to be lower than for men. Our findings clearly demonstrate that renal transplantation is not necessarily the ‘ideal treatment’ that solves the problem of secondary HPT. Patients with severe secondary HPT and/or hypercalcaemia at the time of transplantation are moreover at high risk for delayed graft function [25,26]. For these reasons, control of secondary HPT before transplantation should be aimed at. Calcimimetic agents are increasingly used to achieve this goal [27]. To date, calcimimetics need to be interrupted at the time of transplantation, as they are not approved for use in renal transplant recipients. Cessation of calcimimetics may result in substantial rebound of the parathyroid function. It may therefore be hypothesized that a more widespread use of calcimimetics will result in a decline of the PTX rate in dialysis patients along with a parallel increase of the PTX rate in renal transplant recipients. Adequately powered clinical studies demonstrating that the safety and efficacy of calcimimetic agents in the setting of renal transplantation are urgently needed as anecdotal reports, so far, have yielded contradictory results [28,29]. We acknowledge that our study has several limitations that are mainly related to the retrospective design. It should however be stressed that our study—to the best of our knowledge—is the largest systematic study on the incidence and outcome of PTX in renal transplant recipients that is currently available. Additional strengths include the use of a uniform PTH (biointact-like) assay for the whole length of the study and the accurate (computerized) and long-term follow-up. Given the complexity of the issue of bone mineral metabolism in the kidney transplant recipient, some of which have become evident only in recent years (such as link between bone disease and vascular calcification), there is a clear need for prospective studies of surgery versus observation. Important outcome parameters to be addressed should include bone health, vascular calcifications and graft and patient survival. Only these studies will allow for the formulation of unequivocal recommendations concerning the indication and timing of PTX in the renal transplant recipient.

In conclusion, our study confirms that persistent HPT requiring PTX after successful renal transplantation is a common clinical problem. Female patients with a high pre-transplant level of PTH and calcium are especially at risk. Although graft function, overall, deteriorates shortly after parathyroid surgery, graft function on the long-term and graft survival are not different from controls.



   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
References
 
We would like to thank the members of the Leuven Collaborative group for Renal Transplantation for their continuous support and contribution to our renal data system.

Conflict of interest statement. None declared.



   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 

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Received for publication: 2. 9.06
Accepted in revised form: 16. 1.07


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