NEPHROLOGY 2009; 14, 488492 doi:10.1111/j.1440-1797.2008.01058.

Original Article

Intravenous calcitriol versus paricalcitol in haemodialysis

patients with severe secondary hyperparathyroidism
ABDUL HALIM ABDUL GAFOR,1 RASHIDI SAIDIN,1 LOO CHEE YEAN,1 ROZITA MOHD,1
SOEHARDY ZAINUDIN,1 SHAMSUL AZHAR SHAH2 and NORELLA KONG CHIEW TONG1

1
Departments of Medicine and 2Public Health, Faculty of Medicine, Universiti Kebangsaan Malaysia,
Kuala Lumpur, Malaysia

SUMMARY:
Aim: Secondary hyperparathyroidism (SHPT) is common among haemodialysis patients. Intensive treatment
with calcitriol is often complicated by hypercalcaemia, hyperphosphataemia and elevated calcium phosphorus
(Ca X PO4) product. Paricalcitol is a vitamin D analogue developed to overcome some of the limitations of
calcitriol therapy. The study objectives were to compare the response of intact parathyroid hormone (iPTH) and
the incidence of hypercalcaemia, hyperphosphataemia and elevated Ca X PO4 product in patients with severe
SHPT treated with either i.v. calcitriol or i.v. paricalcitol.
Methods: This was a single centre randomized open label study. Patients with serum intact iPTH of 50 pmol/L
or more were randomized to receive either i.v. calcitriol (0.01 ug/kg) or i.v. paricalcitol (0.04 ug/kg) during every
haemodialysis treatment. Serum iPTH, calcium, phosphorus and alkaline phosphatase were measured at the
beginning of the study and every 3 weeks for 12 weeks. nep_1058 488..492

Results: Twenty-five patients were enrolled into the study 12 were randomized into the calcitriol group and
13 into the paricalcitol group. There were no differences in the baseline study parameters between both groups.
Serum iPTH levels were significantly reduced (P = 0.003) only in the paricalcitol group but not in the calcitriol
group (P = 0.101). On the other hand, serum calcium levels were significantly increased only in the calcitriol group
(P = 0.004 vs P = 0.242). Serum phosphorus, alkaline phosphatase and Ca X PO4 product were not different.
Conclusion: Intravenous paricalcitol may be superior to i.v. calcitriol for the treatment of severe SHPT in our
chronic haemodialysis population. A larger randomized controlled trial is indicated to confirm these initial findings.

KEY WORDS: calcium, calcium phosphorus product, haemodialysis, parathyroid hormone, phosphate.

Secondary hyperparathyroidism (SHPT) affects approxi-
mately 75% of patients on haemodialysis.1 Multiple factors
are involved and work in concert in the development of
parathyroid hyperplasia and SHPT. Bricker and Slatopolsky2
in their early work emphasized the importance of hypocal-
caemia and phosphorus retention in patients with chronic
kidney disease in the pathophysiology of this entity. Other
important factors are impaired calcaemic response to par-
athyroid hormone, altered vitamin D metabolism and
resistance to calcitriol. Due to the end-organ resistance to
parathyroid hormone in uraemic patients, some degree of
Correspondence: Dr Abdul Halim bin Abdul Gafor, Nephrology
Unit, Department of Medicine, Universiti Kebangsaan Malaysia
Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras,
Kuala Lumpur, Malaysia. Email: halimgafor@gmail.com
Accepted for publication 19 October 2008.
2009 The Authors
Journal compilation 2009 Asian Pacific Society of Nephrology
hyperparathyroidism is needed to maintain normal bone
metabolism in patients with end-stage renal disease
(ESRD). Many experts consider the optimal levels of intact
parathyroid hormone (iPTH) associated with normal bone
histology are 1.52.5-times the upper reference limit of
normal subjects.3 Inadequate treatment of SHPT can
cause skeletal abnormalities,4 cardiovascular complications,5
infection and immunoregulatory dysfunction.6 Medical
treatment of SHPT relies on the control of hyperphospha-
taemia, adequate dosing of calcitriol and the use of recently
available calcimimetic agents. Phosphorus control is accom-
plished by phosphate-restricted diets and the use of oral
phosphate binders.7
The use of calcitriol to suppress excess iPTH in dialyzed
patients has been highly successful.8 Whereas this approach
prevents parathyroid gland hyperplasia, intensive treatment
with calcitriol is often complicated with hypercalcaemia and
hyperphosphataemia9 and may be associated with the devel-
opment of adynamic bone disease.10 The use of intermittent
i.v. calcitriol vs paricalcitol in HD with SHPT
(pulse) oral calcitriol therapy has been demonstrated to have
a greater incidence of hypercalcaemia and hyperphospha-
taemia in controlled studies that compared oral with i.v.
calcitriol therapy.8
Paricalcitol is a vitamin D analogue developed to over-
come some of the limitations of calcitriol therapy. Parical-
citol differs from calcitriol in that it lacks a carbon moiety at
the 19th position of its molecular structure.11 Initial studies
have shown that paricalcitol was efficacious and safe in
ESRD.12 It has been proven to lower serum iPTH as early as
12 weeks while providing an incidence of hypercalcaemia
and hyperphosphataemia comparable to placebo. Sprague
et al.13 had shown that paricalcitol treatment reduced serum
iPTH concentrations more rapidly and with fewer sustained
episodes of hypercalcaemia and increased calcium phospho-
rus (Ca X PO4) product compared to calcitriol therapy.
This study aimed to compare the response of iPTH and
the incidence of hypercalcaemia, hyperphosphataemia and
elevated Ca X PO4 product in chronic haemodialysis (HD)
patients with severe SHPT treated with either i.v. calcitriol
or i.v. paricalcitol. This study was unique as the patients
had severe SHPT and the use of newer agents such as non-
calcium containing phosphate binders and calcimimetics
agents were not available.
METHODS
Study population and design
This was a single centre randomized open-label study comparing i.v.
calcitriol and paricalcitol in chronic HD patients attending our HD
clinic. This study was approved by the Ethics Committee of the
Medical Faculty of this university. Informed consent was obtained from
the patient or their immediate relatives. Medically-stable adult ESRD
patients with SHPT on chronic HD three times a week for at least
3 months were enrolled into the study. Patients who were on calcitriol
(i.v. or p.o.), 1-a calcidol, bisphosphonate and calcitonin prior to
enrolment underwent a 2 week washout period. Patients with serum
iPTH levels of 50 pmol/L or more (normal range, 1.57.6) were ran-
domized (using blocks of three) to receive either i.v. paricalcitol or i.v.
calcitriol. The treatment lasted for 12 weeks and the dose ratio between
paricalcitol and calcitriol was 4:1 as recommended.12,13 Both drugs were
given in the last 0.5 h of every HD treatment. During the study,
patients were advised not to change their eating habits, oral calcium-
based phosphate binders and dialysate calcium concentration.
Doses of i.v. vitamin D were escalated every 3 weeks to achieve
at least 50% reduction in serum iPTH. Initial paricalcitol dose was
0.04 ug/kg and the increment was 0.04 ug/kg every 3 weeks. The initial
calcitriol dose was 0.01 ug/kg and the increment was 0.01 ug/kg every
3 weeks. The dose was reduced if serum iPTH levels decreased to less
than 10 pmol/L or when serum calcium was more than 2.8 mmol/
L(normal range, 2.142.58).
Outcome measures
Serum for iPTH, corrected serum calcium, phosphorus and alkaline
phosphatase (ALP) were sent to a single laboratory for measurement.
Serum iPTH levels were measured using chemiluminescence assay and
other parameters were measured using standard laboratory techniques.
The measurements were taken at the beginning of the study (baseline)
2009 The Authors
Journal compilation 2009 Asian Pacific Society of Nephrology
489
and every 3 weeks. Aluminium toxicity was excluded by a desferriox-
amine test prior to the study in high-risk patients. All patients had a
baseline ultrasound of the neck to exclude transformation of parathy-
roid nodules into nodular hyperplasia (possible tertiary hyperparathy-
roidism) and obvious parathyroid carcinoma.
Statistical analysis
An earlier study13 had shown that patients on paricalcitol achieved
approximately 50% (18% vs 33%) fewer episodes of two consecutive
hypercalcaemia (defined as a normalized serum total calcium
311.5 mg/dL (= 2.9 mmol/L)) and/or elevated Ca X PO4 product
(defined as 375 mg2/dL2 (= 6 mmol2/L2)) compared to i.v. calcitriol.
Based on these findings, it was calculated that 10 patients were needed in
each arm for a power of study of 80% and confidence interval of 95%. To
provide a slight margin of error given the possibility of subject attrition,
12 patients were recruited in each treatment group and were randomized
in blocks of three to receive either i.v. calcitriol or paricalcitol.
Results were expressed as mean 1 standard deviation or median and
interquartile range for continuous data. The changes in serum iPTH,
serum calcium, phosphorus, ALP and Ca X PO4 product within each
group were analysed using a repetitive anova test. The comparison
between baseline and end of study (week 12) blood parameters were
done using an unpaired Students t-test for parametric data and Mann
Whitney U-test for non-parametric data. P < 0.05 was taken as signifi-
cant. All statistical analyses were performed using the Statistical
Package for the Social Sciences ver. 11.0 (SPSS, Chicago, IL, USA).
RESULTS
A total of 25 patients were enrolled. Twelve were random-
ized into receiving i.v. calcitriol and 13 i.v. paricalcitol. All
the patients were on a calcium-containing phosphate binder
(calcium carbonate) on recruitment and their doses were
not adjusted throughout the study period. Eight patients in
the calcitriol group and five from the paricalcitol group were
already on oral Vitamin D (calcitriol or 1-a calcidol) prior
to enrolment of the study. All of them had undergone a
2 week washout period before the randomization. None of
the patients were on existing calcitonin or bisphosphonate.
The patients demographic data are as shown in Table 1.
Blood parameters within both treatment groups through-
out the study period are as tabulated in Table 2. During the
12 week study period, serum iPTH levels in the paricalcitol
group were significantly reduced from 136.78 1 57.32 to
77.72 1 52.16 pmol/L (P = 0.003) but this was not the case
in the calcitriol group, where the iPTH levels reduced from
128.12 1 52.45 to 74.30 1 105.21 pmol/L (P = 0.101). Con-
current serum calcium levels increased significantly in the
calcitriol group from 2.30 1 0.19 to 2.50 1 0.23 mmol/L
(P = 0.004), but did not change in the paricalcitol group
from 2.29 1 0.22 to 2.34 1 0.24 mmol/L (P = 0.242). Other
blood parameters of bone metabolism did not show any
changes.
The blood investigations between both groups at base-
line and at the end of the study period (week 12) are shown
in Table 3. There were no differences between the two
groups. There was only a trend of higher serum calcium
levels in the calcitriol group compared to the paricalcitol
group (2.50 1 0.23 vs 2.33 1 0.24 mmol/L; P = 0.09).
490
Table 1 Patient demographics at baseline
Age (years)
Sex Male
Female
Race Malay
Chinese
Indian
Years on HD
Causes of ESRD Diabetes mellitus
Hypertension
Glomerulonephritis
Calculi
NSAIDs
Unknown
ESRD, end-stage renal disease; HD, haemodialysis; NSAIDs, non-steroidal anti-inflammatory drugs.
DISCUSSION
Our study found that serum calcium levels were significantly
increased in the calcitriol group (P = 0.004) but not in the
paricalcitol group (P = 0.242). These findings were sup-
ported by a trend of higher serum calcium levels at end-
study in the calcitriol group compared to those in the
paricalcitol group, although this did not reach significance
(P = 0.09). These findings are similar to that reported by
Sprague et al.13 This can be explained by the high potency
of calcitriol on calcium absorption from the gut. Brown
et al. have demonstrated that paricalcitol had a lower
potency in stimulating intestinal calcium and phosphate
absorption.14 Paricalcitol does not upregulate intestinal
vitamin D receptors15 and does not stimulate intestinal
calcium transport proteins.14
Hypercalcaemia is frequently seen in the treatment of
SHPT with vitamin D compounds and calcium-containing
phosphate binders. Although isolated hypercalcaemia has
not been shown to be a direct cause for mortality of HD
patients, it poses a cardiovascular risk as an increased Ca X
PO4 product may predispose to soft tissue and vascular cal-
cification thus contributing to increased cardiovascular mor-
bidity and mortality.16 Block et al. found that, in a cohort of
40 000 haemodialysis patients, each 1 mg/dL (0.25 mmol/L)
increment in serum calcium was associated with a 16%
increase in 1 year mortality.17 Hence, hypercalcaemia
should be avoided in these patients at high risk of cardio-
vascular death by using non calcium-based phosphorus
binders and vitamin D analogues.
The iPTH levels were only significantly suppressed in
the paricalcitol group (P = 0.003) but not in the calcitriol
group (P = 0.101). Previous studies by Lindberg et al.12 and
Sprague et al.13 have reported the successful use of parical-
citol versus calcitriol in treating HD patients with moder-
ately severe SHPT with mean baseline of 6070 pmol/L,
whereas our study patients had more severe SHPT with
mean baseline serum iPTH levels of more than 100 pmol/L.
Although there were no differences in serum iPTH levels at
the end of study period between calcitriol and paricalcitol
AG Halim et al.
Calcitriol Paricalcitol P-value
47.8 1 16.4 48.2 1 14.1 0.96
8 6
4 7
8 8
3 3
1 2
5.3 1 2.4 4.4 1 2.3 0.35
1
4 6
2 4
1
3 1
2 1
groups (74.3 1 105.2 vs 77.7 1 52.2 mmol/L respectively),
our study suggested that paricalcitol may be preferable to
calcitriol when a rapid reduction of serum iPTH is necessary
in severe SHPT.
The degree of severity of SHPT in our patients can be
explained by the paucity of nephrologists (~70) for a dialysis
population of approximately 15 000 patients (acceptance
rate of 118 and prevalence rate of 550 per million population/
year) in this country.18 The majority of HD patients
are dialysed in government-run satellite units or non-
government/charity-run centres. Up to recently, regular
nephrological reviews were not generally available. Patient
compliance with diet, medications and fluid are also a major
factor as occur elsewhere. Calcium carbonate is the universal
phosphate binder as newer agents such as lanthanum carbon-
ate, sevelamer hydrochloride and calcimimetic agents have
only recently become available but costs are prohibitive.
Additionally, patients and their families are also reluctant to
accept parathyroidectomy even when medically indicated.
There were no differences between baseline and end-
study serum phosphorus, Ca X PO4 product and serum ALP in
between both groups. There were also no significant changes
in serum phosphorus, Ca X PO4 product and serum ALP
within each group throughout the study period. Our findings
on serum phosphorus levels were similar to those of Sprague
et al. who found no differences in the episodes of hyperphos-
phataemia between the two groups.13 However, the same
author also reported that the incidence of elevated Ca X PO4
product (and/or hypercalcaemia) for four consecutive labo-
ratory draws was higher in the calcitriol group compared to
the paricalcitol group. Surprisingly, there were no significant
changes in the Ca X PO4 product in the calcitriol group in
our study, when in fact the serum calcium rose significantly.
This observation can be partly explained by the fact that,
in clinical practice, serum phosphorus levels are usually
increased by a higher factor compared to serum calcium
levels and are therefore the greater culprit in causing the
higher Ca X PO4 product in chronic kidney disease patients.16
The paricalcitol doses in our study were based on the
patients bodyweight as recommended by earlier studies.12,13,19
2009 The Authors
Journal compilation 2009 Asian Pacific Society of Nephrology
 Table 2 The changes in blood parameters within each group over the duration of study
Blood parameters Medication Baseline Week 3 Week 6 Week 9 Week 12 P-value

2009 The Authors

iPTH (pmol/L) (NR, 1.57.6) Calcitriol 128.12 1 52.45 92.55 1 39.33 100.15 1 70.79 96.47 1 82.24 74.30 1 105.21 0.101
Paricalcitol 136.78 1 57.32 123.73 1 61.18 139.75 1 80.02 98.85 1 69.15 77.72 1 52.16 0.003
Serum Calcium (mmol/L) Calcitriol 2.30 1 0.19 2.37 1 0.30 2.38 1 0.23 2.40 1 0.29 2.50 1 0.23 0.004
(NR, 2.142.58) Paricalcitol 2.29 1 0.22 2.26 1 0.21 2.25 1 0.21 2.37 1 0.30 2.34 1 0.24 0.242
Serum Phosphorus (mmol/L) Calcitriol 1.65 1 0.28 1.54 1 0.36 1.47 1 0.36 1.66 1 0.36 1.54 1 0.29 0.442
(NR, 0.711.36) Paricalcitol 1.58 1 0.40 1.73 1 0.44 1.84 1 0.30 1.62 1 0.50 1.53 1 0.50 0.088
ALP (IU/L) (NR, 32104) Calcitriol 137.5 (107296) 137.5 (106.25370.5) 136.0 (101.5303.0) 115.5 (93.75220.00) 118.0 (83.25245.50) 0.069
Paricalcitol 195.0 (116.0371.0) 186.0 (117.0278.5) 159.0 (117.5299.0) 149.0 (100.5259.0) 123.0 (91.0258.0) 0.265
Ca X PO4 product (mmol2/L2) Calcitriol 3.80 1 0.67 3.65 1 0.98 3.47 1 0.80 3.95 1 0.89 3.85 1 0.78 0.449
i.v. calcitriol vs paricalcitol in HD with SHPT

(NR, <4.4) Paricalcitol 3.63 1 1.07 3.90 1 1.02 4.11 1 0.58 3.85 1 1.30 3.61 1 1.32 0.244

Median and interquartile range. ALP, alkaline phosphatase; Ca X PO4, calcium phosphorus; iPTH, intact parathyroid hormone; NR, normal range.

Journal compilation 2009 Asian Pacific Society of Nephrology

Table 3 Comparison between calcitriol and paricalcitol groups at baseline and at end of study
Baseline End of study
Calcitriol Paricalcitol P-value Calcitriol Paricalcitol P-value
iPTH (pmol/L) (NR 1.57.6) 128.1 1 52.4 136.8 1 7.3 0.7 74.3 1 105.2 77.7 1 52.2 0.92
Serum calcium (mmol/L) (NR 2.142.58) 2.30 1 0.19 2.29 1 0.26 0.84 2.50 1 0.23 2.33 1 0.24 0.09
Serum phosphorus (mmol/L) (NR 0.711.36) 1.65 1 0.28 1.58 1 0.40 0.64 1.54 1 0.29 1.53 1 0.50 0.95
ALP (IU/L) (NR 32104) 137.5 (107296) 195 (116371) 0.5 118.0 (83.25245.5) 123.0 (91.0258.0) 0.61
Ca X PO4 product (mmol2/L2) (NR < 4.4) 3.80 1 0.67 3.63 1 1.07 0.66 3.85 1 0.78 3.61 1 1.32 0.59

Median and interquartile range. ALP, alkaline phosphatase; Ca X PO4, calcium phosphorus; iPTH, intact parathyroid hormone; NR, normal range.
491
492
Recent data suggest that paricalcitol dosing should be based
on the degree of severity of SHPT. Martin et al. and Mitso-
poulos et al. proposed that the initial paricalcitol dose should
be calculated according to the formula of iPTH (pg/mL)/80
or iPTH (pg/mL)/120.20,21 These authors found that, with
these doses, the serum iPTH reduction was more rapid and
had less risk of hypercalcaemia or elevated Ca X PO4 prod-
uct.20,21 This approach was based on their observation of lack
of correlation between the patients bodyweight and parathy-
roid hormone levels. In practise, the patients true dry weight
is not easily assessed even by experienced clinicians. Further-
more, Fukuda et al. reported that higher doses of activated
vitamin D3 are required to suppress the large and hyperplastic
parathyroid glands. All these findings suggested that the early
administration of effective doses of vitamin D could delay or
prevent transformation of the parathyroid glands from diffuse
to nodular hyperplasia.22
As this was an open-labelled, single-centre study, albeit
randomized, it was still exposed to investigator bias.
Although the study showed some differences between the
two treatment arms, the number of subjects was small and
the study duration was too short to allow us to recommend
major changes to current clinical practice. Nevertheless, our
findings suggest that paricalcitol is preferable to calcitriol for
the treatment of HD patients with severe SHPT (iPTH,
>100 pmol/L) as it reduces serum iPTH significantly with
less risk of hypercalcaemia.
We conclude that paricalcitol is effective and may be
preferable to calcitriol for the treatment of haemodialysis
patients with severe SHPT (iPTH, >100 pmol/L). A larger
prospective, multicentre study with cost-analysis would be
ideal as this treatment is more expensive.
ACKNOWLEDGEMENTS
We would like to thank the Dean of the Faculty of Medicine,
Universiti Kebangsaan Malaysia, for allowing us to publish
these data. We also are grateful to Abbott (Malaysia) Sdn
Bhd for sponsoring the medications used in this study.
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2009 The Authors
Journal compilation 2009 Asian Pacific Society of Nephrology