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NDT Advance Access published online on June 27, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm370
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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

Are PTH serum levels predictive of coronary calcifications in haemodialysis patients?

Giorgio Coen1, Micaela Manni2, Daniela Mantella3, Andrea Pierantozzi4, Alessandro Balducci2, Stefano Condò4, Salvatore DiGiulio3, Lijljana Yancovic5, Basilio Lippi1, Simone Manca6, Massimo Morosetti5, Luigi Pellegrino7, Giovanni Simonetti7, Massimo Taccone Gallucci6 and Giorgio Splendiani4

1Ospedale Israelitico, 2SanGiovanni-Addolorata Hospital, 3SanCamillo-Forlanini Hospital, 4TorVergata University Hospital, 5G.B.Grassi Hospital, 6Policlinico Casilino and 7Department of Radiology, TorVergata Hospital, Rome, Italy

Correspondence and offprint requests to: Giorgio Coen, MD, Via Dandolo 75 00153 Rome. Email: giorgio.coen{at}fastwebnet.it



   Abstract
Top
 Abstract
Introduction
 Patients and methods
 Results
 Discussion
 References
 
Background. Cardiac calcifications are a frequent occurrence in uraemic subjects and are probably connected to the increased cardiovascular mortality of haemodialysis patients. There is substantial support to the hypothesis that low levels of serum PTH in haemodialysis patients are associated with increased vascular and cardiac calcium deposits, due to decreased buffering capacity of bone in low turnover osteodystrophy. The present study has been carried out on a cohort of patients on haemodialysis, with exclusion of previously parathyroidectomized patients, with the aim to evaluate the association between PTH serum levels and coronary calcifications.

Methods. The study has been carried out in a cohort of 197 haemodialysis patients. There were 133 males and 64 females. Twenty-two patients had diabetes mellitus. Average age was 58.6 ± 12.9 years. Patients were divided into groups of intact PTH levels, 0–150 (A), 150–300 (B), 300–600 (C) and >600 (D) pg/ml.

Results. The values of coronary scores in the PTH groups were as follows: (A) 624.7 ± 939, (B) 866.4 ± 1080, (C) 1202.8 ± 1742.3 and (D) 1872.7 ± 2961.9. The difference between coronary calcium scores was significant (P < 0.01). A general linear model identified serum calcium and dialysis age as independent factors of calcium deposits in the high PTH group.

Conclusions. No prominent association between low PTH serum levels and the severity of coronary calcium deposits in haemodialysis patients was found while increased levels of PTH, with special regard to very elevated levels, associated with more frequent hypercalcaemia and hyperphosphataemia, should be considered a major risk factor of coronary calcifications and cardiac events.

Keywords: calcium coronary score; chronic kidney disease; haemodialysis; low bone turnover; serum iPTH



   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Discussion
 References
 
Cardiac calcifications are a frequent occurrence in uraemic subjects and are probably connected to the increased cardiovascular mortality of haemodialysis patients [1,2].

Many risk factors of vascular and cardiac calcifications have been found, such as age, dialysis age, serum calcium, phosphate and Ca x P serum levels. Also inflammatory markers and calcium–phosphate solubilizing agents, like serum fetuin-A [3–5] and matrix GLA protein [6], have a role. Among the risk factors, bone turnover as well has been included, a role that requires a better definition.

The issue whether there is an association between PTH serum levels, cardiac calcifications and cardiovascular death in chronic renal failure has been considered in the last few years in several publications [7–9]. There is a general opinion that low levels of serum PTH in haemodialysis patients are associated with increased vascular and cardiac calcium deposits [10–12]. This opinion is based on the concept that low bone turnover, associated with low serum PTH levels, is a condition of decreased calcium phosphate buffering capacity of bone [13], causing more hectic serum levels of these substances following intestinal absorption and also dialysis sessions with both calcium concentrations able to produce a positive calcium balance. Therefore, increased serum levels of calcium and phosphate, associated with low bone turnover, may induce increased severity of vascular calcifications.

It is known that in haemodialysis patients, the extent of coronary and valvular cardiac calcifications is connected to decreased survival [14–16]. Therefore, one might expect that patients with low serum PTH levels, in case of increased risk of vascular calcifications, have a higher risk of cardiovascular mortality and sudden death. Yet, data in favour of the association of low PTH levels and increased cardiovascular mortality are of difficult interpretation, since low levels of PTH may also be associated to malnutrition and inflammation, known causes of vascular damage, anaemia and cardiovascular death [17,18]. One of the most quoted contributions is by Coco and Rush [19]. They have found an association between decreased PTH serum levels, bone fractures, and general mortality. However, there were problems with the composition of their patient cohort, being inhomogeneous and probably unfitting the aim of the protocol, since part of it was of Afro-American descent, known to have less frequent fractures and higher PTH serum levels.

On the contrary, in a study by Young et al. [20] on haemodialysis patients, PTH was found to be an independent risk factor of cardiovascular death. Also Ganesh et al. [8] have found an increased mortality risk associated to elevated PTH serum levels. However, there was a U-shaped relationship of log PTH, in quintiles, with sudden death reaching a statistical significance level only for PTH serum levels >495 pg/ml. Similar results were obtained by Slinin et al. [21]. Therefore, there are discordant data on the relationship between PTH serum levels and risk of death, which cannot be easily reconciled with the proposition that low levels of PTH are associated to increased cardiac calcifications, also a known risk factor of cardiac death.

Actually, evidence that low bone turnover is associated with increased arterial calcifications has been provided by London et al. [10]. They studied 58 haemodialysis patients subjected to bone biopsy and evaluated for arterial calcifications with an X-ray survey of some other indicative arterial sites. The extent of arterial calcifications was inversely related to histomorphometric bone turnover. However, the cohort of patients included a relatively large number of patients with aluminium deposition, and also a number of previously parathyroidectomized cases, with low turnover induced by surgery, possibly affected by calcifications generated prior to parathyroidectomy.

The present study has been carried out on a cohort of patients on haemodialysis, with exclusion of previously parathyroidectomized subjects, and unaffected by aluminium exposure. The results, aimed to evaluate the association between PTH serum levels and coronary calcifications, are in favour of a direct association between PTH serum levels and coronary calcium deposits.



   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Discussion
 References
 
This study has been carried out in a cohort of 197 patients on maintenance haemodialysis from six dialysis units of Rome. Patients were considered eligible for the study if dialysis duration was >6 months, their age was >18 years, the vascular access performance was satisfactory with a blood flow of at least 300 ml/min and a Kt/V >1.0, the heart rate <80 bpm, the voluntary apnoea was of at least 20 s and a written informed consent to participate in the study was given. The patients received neither steroids nor non-steroidal inflammatory drugs, or anticoagulant therapy. Parathyroidectomy and previous renal transplantation were exclusion criteria.

Mean age was 58.6 ± 12.9 years. There were 133 males and 64 females. Twenty-two patients had diabetes mellitus. Fifty-three percent of the patient cohort was affected by arterial hypertension and was treated with calcium channel blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists and {alpha}- and ß-blockers, achieving a satisfactory blood pressure control.

All the patients were treated with phosphate-binding agents, generally, sevelamer in 130 patients, calcium carbonate in 42 patients and both drugs in 40; 47 patients received aluminium-containing agents, usually associated to other phosphate binders, in limited doses (≤1.5 g/day) and for restricted periods of time in case of persistently elevated serum phosphate levels. Forty-eight patients were under treatment with IV calcitriol, which had been started at least 8–12 months prior to the enrollment.

Fifty-four percent of the patients were treated with standard bicarbonate dialysis using Cuprophan or Low-Flux-PolySulfone (LF-PS) membranes, 20% with acetate-free biofiltration (AFB) using Polyacrylonitrile-AN69 (PAN-AN69 ST) and the remaining patients with haemodiafiltration using Helixone (FX80) or Polycarbonate (Spiraflo SG 8 Plus). All patients underwent haemodialysis three times a week. The dialysis sessions lasted 4 h and were delivered at constant blood and dialysate flow rate values of 300 and 500 ml/min, respectively. Calcium concentration in the dialysate was 1.25, or 1.5 or 1.75 mmol/l, in 37, 39 and 24% of patients, respectively. Calcium concentration was 1.75 mM when required to favour a positive calcium balance.

Multislice computed tomography (MSCT) was performed with a 16-channel multidetector scanner (Light Speed 16, General Electric Medical Systems, USA). A retrospective gating technique was used to synchronize the data reconstruction with the ECG signal. Mean heart rate during MSCT was 70 ± 8 bpm (range 50–85). All scans were performed with the following parameters: detector collimation 4 x 2.5 mm, reconstruction interval 10 mm, gantry rotation time 0.5 s, tube voltage 120 Kv, tube current 300 mA, field of view (FOV) 25 cm, acquisition volume 12 cm (i.e. pulmonary artery bifurcation to diaphragm), caudo-cranial scan direction. Images were obtained during a single breath-hold of ~12–15 s.

EBCT is the classical technique for coronary calcium scoring, but in the last years MSCT has become the standard for evaluation of coronary calcium. The coronary calcium scores correlate well with those from EBCT [22] for a threshold of 130 Hounsfield units (HU). All the data were evaluated using the Agatston score that is the standard unit for reporting calcification. Informed consent was obtained from all patients.

Blood samples for the biochemical evaluation were drawn prior to a dialysis session. Serum samples were stored at –30°C until the assays. The following assays were made: serum calcium, phosphorus, alkaline phosphatase and intact PTH.

Serum calcium, phosphorus and alkaline phosphatase were measured by colorimetric methods using a Roche autoanalyzer. Total calcium was corrected for serum albumin using the equation: Calcium = Ca + 0.8 (4.0 albumin). Normal values of these variables are: 8.5–10.2 mg/dl, 3.0–4.5 mg/dl and 35–125 mU/ml, respectively. Serum intact PTH was measured by an IRMA (Nichols Institute Diagnostic, San Juan Capistrano, CA, USA). The normal range of values is 10–65 pg/ml. Serum aluminium was assayed with atomic absorption technique [23], as part of an annual control.

The statistical evaluation was carried out using a personal computer equipped with the SPSS for Windows statistical package (Chicago, IL, USA, release 12.0). In addition to descriptive statistics for the selected variables, comparison of groups was also evaluated by parametric tests, such as Student's t test and ANOVA with post hoc test. The test of homogeneity of variances, the Levene's test, was used to choose between Bonferroni and Tamhane post hoc test. Correlation and linear regression analysis were performed to examine the relationship between the cardiac calcium scores and clinical and biochemical parameters. Multiple regression analysis was performed as well to assess the combined influence of variables on the calcification scores. A P-value <0.05 was considered statistically significant. The forward method was used, with criteria to enter in the model: F-probability <0.05. F-probability >0.10 to exit from the model. We also used the general linear model (dividing variables involved into groups, using quartile and median) to estimate the partial effect of each single variable taken into account in any analysed model.



   Results
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 Abstract
 Introduction
 Patients and methods
 Results
Discussion
 References
 
Average values of the studied parameters for the entire cohort are reported in Table 1, together with normal reference values. Serum aluminium levels were <0.8 µM/l. In addition, the patients were divided into groups of increasing intact PTH serum levels: A, 0–150 (40 patients, mean age 59.5 ± 11.9 years); B, 150–300 (51 patients, mean age 61.8 ± 12.4 years); C, 300–600 (54 patients, mean age 59.4 ± 12 years) and D, >600 pg/ml (52 patients, age 54 ± 14.2 years). The mean values of the studied variables for the PTH groups are reported in Table 2. Statistical differences (ANOVA) were found for age (P < 0.02), serum phosphate (P < 0.001), Ca x P (P < 0.0001), serum Ca (P < 0.05), alkaline phosphatase (P < 0.005) and BMI (P < 0.05). The difference in terms of coronary calcification scores among the groups of PTH was significant (P < 0.01). There was a progressive increase of the average value from group A to group D, with pathological, nevertheless lower levels, in the A group (PTH, 0–150 pg/ml) (Table 2, Figure 1). A significant difference was found among the coronary scores, while no difference was found among valvular calcification scores for the different groups of PTH serum levels. Post hoc analysis results are also reported in Table 2.


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  		Table 1. Descriptive statistics

 

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  		Table 2. ANOVA and post hoc test

 

Figure 1
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  		Fig. 1. Coronary score values (M ± SD) vs PTH groups.

 
Significant correlations were found between PTH serum levels and the following other variables: age (r = –0.177, P < 0.013), HD age (r = 0.176, P < 0.015), serum P (r = 0.203, P < 0.004), serum Ca (r = 0.198, P < 0.005), Ca x P (r = 0.263, P < 0.001), AP (r = 0.333, P < 0.001), coronary score (r = 0.240, P < 0.001).); and between coronary score and: age (r = 0.239; P = 0.001), HD age (r = 0.161; P = 0.026), serum Ca (r = 0.250; P < 0.000) and iPTH as reported above.

The results of multiple regression analysis, forward method (acceptance criteria for the model, F < 0.05), with coronary score as dependent variable, and serum Ca, age, iPTH, HD age, Ca x P and BMI as independent variables are reported in Table 3. Serum Ca, age, iPTH and HD age were found to be significant. Successively, multiple regression analysis, forward model, were employed with coronary score as dependent variable and the following significant independent variables: iPTH and age; iPTH and HD age; iPTH and serum Ca. The results are reported on the right side of Table 4. iPTH was constantly significant. Partial contribution of individual variables was analysed with a general linear model, with the median as cut-off for age and HD age (61.5 years and 50.5 months, respectively), and quartiles for serum Ca (8.9, 9.5, 10.2 mg/dl as cut-off values). Data shown on the left side of Table 4 indicate that significance for iPTH in the model with age is found, while in the models with HD age, and serum Ca, iPTH is no longer significant. Further application of the general linear model with HD age and serum Ca only showed variables to be significant. Therefore, while iPTH is certainly associated to coronary score, its contribution may be partly ascribed also to serum Ca and HD age.


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  		Table 3. Regression analysis, forward model

 

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  		Table 4. General linear model and regression, forward analysis

 


   Discussion
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
References
 
In the only study available showing an association between bone turnover and arterial calcifications, performed with bone biopsies and histomorphometric evaluation, a statistical association was found between low PTH serum levels with low bone turnover and arterial calcium deposits. However, the study was questionable since the patients had been evidently exposed to aluminium and, furthermore, at least 23 of 58 had been in the past subtotally parathyroidectomized. Therefore, their current low bone turnover could be possibly associated to elevated calcification scores due to previous arterial damage and calcium deposits. In our patient cohort, there were no cases of aluminium toxicity and no previously parathyroidectomized patients. With this patient cohort, the study, based on the evaluation of coronary calcification with MSCT in a sizeable number of haemodialysis patients, divided up in ranks of PTH serum levels, is not in agreement with outstandingly increased coronary calcium deposits in the patients with lower PTH levels, known to be associated to decreased bone turnover to the level of adynamic bone disease (ABD). On the contrary, more elevated coronary score values were associated with PTH serum levels above 600 pg/ml.

Actually, our previously published data [24], obtained in a substantial number of patients from the same dialysis units, subjected to bone biopsy, all with a negative aluminium histochemistry, are clearly indicative that PTH serum levels <150 pg/ml, are associated with ABD in at least half of the cases and normal turnover histologically related to mixed osteodystrophy or normal bone in at least another 50%. These results are in agreement with other publications [25–27]. Therefore, patients in the low PTH category (0–150 pg/ml), in the case of association between extent of vascular calcifications and low bone turnover, should show higher values of coronary scores compared with the other groups. On the contrary, a progressive increase of calcium coronary score was present with increasing PTH serum levels. Multiple regression analysis with a forward approach showed age, PTH, serum Ca and, at a lower significance level, haemodialysis age, as significant independent variables. Therefore, PTH was selected as an independent risk factor, while Ca x P and phosphate were excluded from the model. The same results, even if simply by comparison of low (<250 pg/ml) and high (>250 pg/ml) serum levels of PTH were reported by Oh et al. [28] in a cohort of young adult patients. Also of some support to our findings are the results of a recently published study [29]. Uraemic rats raised on a low protein diet were able to develop extensive medial artery calcifications, associated to increased bone turnover. The calcifications were prevented by ibandronate administration, known to slow bone turnover.

Our results do not exclude the observation that some categories of patients, like diabetes mellitus in haemodialysis, may combine low levels of PTH, with low bone turnover, and increased risk of arterial calcium deposits while treated with calcium salts for phosphate chelation [30]. However, further analysis with a general linear model identified serum calcium as the major determinant of calcium deposits in the high PTH group. High PTH levels associated with the lower quartile of serum calcium levels, on average, were not associated to increased coronary score values (Figure 2).


Figure 2
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  		Fig. 2. Coronary score vs quartiles (1–4) of serum calcium in the PTH groups.

 
Our results are more in line with the evidence that high PTH serum levels in haemodialysis patients are associated with increased mortality, due to sudden death and cardiovascular and general mortality. The association of elevated PTH serum levels with cardiovascular mortality is in agreement with the finding of increased coronary and arterial calcium deposits. Probably, there might be a difference between different studied populations according to the type of treatment with vitamin D or the intake of calcium and dialysis bath calcium concentration utilized. However, in our cases the groups were comparable for what concerns calcium intake and vitamin D treatment.

The study has some obvious limitations due to its cross-sectional nature, with patients selected from different dialysis units, with possibly somewhat different therapeutic approaches, and due to single biochemical assays being related to long-term arterial lesions.

However, the finding of no major association between low turnover bone disease and the severity of coronary calcium deposits in haemodialysis patients bears practical implications, since more than the low levels of PTH and their associated low bone turnover states, increased levels of PTH, with special regard to very elevated levels, associated with more frequent hypercalcaemia and hyperphosphataemia and should be considered a major risk factor of coronary calcifications and cardiac events. Therefore, special attention should be paid to the control of elevated levels of secondary hyperparathyroidism and the related calcium phosphate derangements.

Conflict of interest statement. None declared.



   References
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 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 

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Received for publication: 29. 1.07
Accepted in revised form: 15. 5.07


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