Background Elevated calcium and phosphorus levels after therapywith injectable vitamin D for secondary hyperparathyroidismmay accelerate vascular disease and hasten death in patientsundergoing long-term hemodialysis. Paricalcitol, a new vitaminD analogue, appears to lessen the elevations in serum calciumand phosphorus levels, as compared with calcitriol, the standardform of injectable vitamin D.
Methods We conducted a historical cohort study to compare the36-month survival rate among patients undergoing long-term hemodialysiswho started to receive treatment with paricalcitol (29,021 patients)or calcitriol (38,378 patients) between 1999 and 2001. Crudeand adjusted survival rates were calculated and stratified analyseswere performed. A subgroup of 16,483 patients who switched regimenswas also evaluated.
Results The mortality rate among patients receiving paricalcitolwas 3417 per 19,031 person-years (0.180 per person-year), ascompared with 6805 per 30,471 person-years (0.223 per person-year)among those receiving calcitriol (P<0.001). The differencein survival was significant at 12 months and increased withtime (P<0.001). In the adjusted analysis, the mortality ratewas 16 percent lower (95 percent confidence interval, 10 to21 percent) among paricalcitol-treated patients than among calcitriol-treatedpatients. A significant survival benefit was evident in 28 of42 strata examined, and in no stratum was calcitriol favored.At 12 months, calcium and phosphorus levels had increased by6.7 and 11.9 percent, respectively, in the paricalcitol group,as compared with 8.2 and 13.9 percent, respectively, in thecalcitriol group (P<0.001). The two-year survival rate amongpatients who switched from calcitriol to paricalcitol was 73percent, as compared with 64 percent among those who switchedfrom paricalcitol to calcitriol (P=0.04).
Conclusions Patients who receive paricalcitol while undergoinglong-term hemodialysis appear to have a significant survivaladvantage over those who receive calcitriol. A prospective,randomized study is critical to confirm these findings.
The one-year mortality rate among patients undergoing hemodialysisin the United States approaches 20 percent, and mortality ratesamong patients undergoing hemodialysis at every age exceed therates among those not undergoing hemodialysis.1,2 Methods toimprove survival include increased doses of dialysis,3,4 improvednutrition,5 and management of anemia,6 but the mortality ratesremain high, despite considerable efforts targeting these factors.7Cardiovascular disease is the predominant cause of dialysis-relatedmortality.2 Recently, the effect of secondary hyperparathyroidismand its management on vascular disease has garnered substantialattention.8,9,10,11,12 Parenteral vitamin D effectively suppressesparathyroid hormone secretion and is therefore standard therapyfor secondary hyperparathyroidism.13,14 Yet such vitamin D administrationoften results in elevated calcium and phosphorus levels, whichmay accelerate vascular disease and hasten death.9,12,15,16
In 1998, paricalcitol (19-nor-1,25-dihydroxyvitamin D2) wasapproved for the treatment of hyperparathyroidism due to chronicrenal failure. Paricalcitol suppresses parathyroid hormone fasterthan calcitriol.17 When the appropriate dose is used, paricalcitolis associated with smaller changes in serum calcium and phosphorusthan is calcitriol (1,25-dihydroxyvitamin D3),18 the standardform of injectable vitamin D used worldwide. Paricalcitol alsosuppresses parathyroid hormone levels in patients with substantiallyelevated phosphorus levels, a subgroup typically resistant tocalcitriol.14,18 Given the differences between these formulationsand the associations of hyperparathyroidism, hyperphosphatemia,hypercalcemia, and an elevated calcium–phosphate product(the product of the calcium and phosphorus concentrations) withvascular disease and death,8,9,11,19,20 we examined the survivalrate at 36 months among 67,399 patients undergoing long-termhemodialysis who were treated with paricalcitol or calcitriol.
Methods
Study Population
We performed a historical cohort study of patients undergoinglong-term hemodialysis at the U.S.-based dialysis facilitiesof Fresenius Medical Care North America. The primary study populationconsisted of all patients who started receiving treatment withparicalcitol (Zemplar, Abbott Laboratories) or calcitriol (Calcijex,Abbott Laboratories) on or after January 1, 1999, and who weretreated exclusively with that injectable vitamin D formulationuntil they died, their data were censored (when they switchedto another vitamin D formulation, underwent renal transplantation,or transferred to another facility), or the end of the studyperiod on December 31, 2001. Patients who had received any formof injectable vitamin D before January 1, 1999, were excluded.Among those who switched formulations during the study period,survival after switching was also examined. During the studyperiod, Fresenius Medical Care distributed management guidelinesthat included a target value for intact parathyroid hormoneof less than 300 pg per milliliter and a target value for thecalcium–phosphate product of less than 70. Specific therapiesto achieve these goals were not suggested, no policy was inplace to use one vitamin D formulation preferentially, and clinicaldata had not suggested a survival benefit for any one formulation.Just before this study, a 4:1 dosing ratio of paricalcitol tocalcitriol had been suggested in the literature.21 This studymet the privacy standards implemented by Fresenius. It was approvedby the institutional review board of the Massachusetts GeneralHospital with a waiver for informed consent.
Ascertainment of Exposures, Outcomes, and Covariates
During the study period, demographic and laboratory informationwas collected prospectively and entered into a central database updated and stored by Fresenius. No additional data wereretrospectively abstracted from medical records. On a patient'sadmission to a dialysis facility, demographic information, includingage, sex, race, date of first dialysis session, primary causeof renal failure, and diabetes status, was recorded. Data werecollected on the hemodialysis prescription, laboratory tests,hospitalization, death, and medications administered duringeach hemodialysis session (name, date, dose, and route of administration).Test results from a central laboratory were automatically downloadedto the data base, minimizing data-entry errors. Records of allmedications administered during each hemodialysis session undergoregular quality assessment and control measures because of theirlink with billing systems. All missed hemodialysis treatments,whether expected (e.g., because of hospitalization) or unexpected(e.g., because of noncompliance) and all permanent discharges(e.g., because of transplantation or death), together with diagnosescoded according to the International Classification of Diseases,9th Revision, Clinical Modification (ICD-9-CM),22 were recordedto complete the daily reconciliation of prescribed and administeredtreatments.
Base-line laboratory values were obtained by averaging all valuesobtained within three months before the date of evaluation.Quintiles of serum calcium and phosphorus levels were determinedby aggregating the values for all patients. Fresenius used thesame assay for intact parathyroid hormone measurements (NicholsAdvantage Chemiluminescence) throughout the study period. Becauseof known lot-to-lot drifts in this assay, serum levels of parathyroidhormone were categorized according to yearly quintiles, andcomparative quintiles across years were combined for the analysis.
The duration of dialysis was defined as the number of days fromthe initiation of long-term hemodialysis to the starting dateof treatment with paricalcitol or calcitriol. To adjust forcenter-specific effects that may have contributed to survivaldifferences, the models included the standardized mortalityrates for each dialysis center.1,7 The standardized mortalityrate was defined as a facility-specific, case-mix–adjustedmortality rate relative to all Fresenius dialysis centers throughoutthe United States. The standardized mortality rate was usedto adjust for between-center variations in survival that werenot accounted for by the typical explanatory variables, suchas differences in nutritional status and adequacy of dialysis.In this study, more than 1000 dialysis centers were represented.The study entry period, defined as the calendar quarter duringwhich a patient initiated vitamin D therapy, was examined asa measure of unknown confounding related to improvements inclinical practice over time.
Statistical Analysis
Standard univariate analyses (chi-square and t-tests) were performed,and values are reported as means ±SD for descriptivepurposes. Mortality rates were calculated by dividing the numberof patients who died during the follow-up period by the numberof person-years of observation. The Kaplan–Meier methodwas used to examine crude survival, and Cox proportional-hazardsregression analysis was used to adjust for potential confounders.The primary analysis of survival included all patients; datawere censored at the time of transfer to a non-Fresenius facility,kidney transplantation, or switch to another vitamin D formulation.Hazard ratios for death with 95 percent confidence intervalswere calculated for patients treated with paricalcitol; patientstreated with calcitriol served as the reference category inall analyses. Stratum-specific hazard ratios were examined totest for effect modification. Treatment-specific hazard ratioswere calculated according to quintiles of base-line serum calcium,phosphorus, and parathyroid hormone levels. Follow-up analysesincluded laboratory values and data on subsequent survival forpatients who switched from one vitamin D formulation to theother. All reported P values are based on two-sided tests.
Results
Base-Line Characteristics
Between January 1, 1999, and December 31, 2001, treatment withinjectable vitamin D was initiated in 69,492 patients undergoingdialysis in Fresenius facilities. Of these, 67,399 (97 percent)were initially treated with paricalcitol or calcitriol and servedas the primary study population (Table 1). Patients receivingparicalcitol were more likely than those receiving calcitriolto be black and to have arteriovenous fistulas for vascularaccess, and they were less likely to have diabetes. Patientsreceiving paricalcitol also had higher base-line serum levelsof calcium, phosphorus, and parathyroid hormone. Base-line measuresof glucose control (for patients with diabetes), systolic bloodpressure, lipids, and the adequacy of dialysis (as indicatedby the urea reduction ratio) were similar in the two groups.The rate of hospitalization in the year before vitamin D therapywas started was similar in the two groups (28.1 percent in theparicalcitol group and 27.9 percent in the calcitriol group,P=0.38), whereas the percentage of patients with unexpectedabsences from dialysis differed significantly (8.2 percent inthe paricalcitol group vs. 7.3 percent in the calcitriol group,P<0.001).
Table 1. Base-Line Characteristics According to Vitamin D Therapy.
Crude and Adjusted Survival Rates
During the 36-month follow-up period, the mortality rates differedbetween the groups: among patients receiving paricalcitol, therewere 3417 deaths during a total of 19,031 person-years of observation(0.180 per person-year), as compared with 6805 deaths during30,471 person-years (0.223 per person-year) among those receivingcalcitriol (rate ratio, 0.80; 95 percent confidence interval,0.77 to 0.84; P<0.001). The differences in survival wereapparent within 12 months and continued to increase with time(P<0.001) (Figure 1A). Analysis of survival differences accordingto the year of study entry showed similar results (data notshown). The rates of death from specific causes (according tothe ICD-9-CM classification) among patients receiving calcitrioland paricalcitol, respectively, were 0.128 and 0.106 per person-yearfrom cardiovascular disease, 0.021 and 0.016 per person-yearfrom infection, and 0.075 and 0.057 per person-year from othercauses. Cox proportional-hazards regression analyses demonstratedthat a notable change in the effect estimate occurred afteradjustment for the period of study entry (Table 2). After furtheradjustments, the survival advantage associated with paricalcitoltreatment was 16 percent (95 percent confidence interval, 10to 21 percent). In the final model, in addition to therapy withparicalcitol, independent predictors of survival included serumalbumin, calcium, and phosphorus levels (P<0.001 for eachvariable).
Figure 1. Kaplan–Meier Analysis of Survival According to the Type of Vitamin D Therapy.
Panel A shows the survival of patients treated with either paricalcitol or calcitriol who received the same therapy for the duration of the follow-up. Panel B shows the survival of patients who switched from calcitriol to paricalcitol or from paricalcitol to calcitriol during the follow-up period. The time of switching was approximately 900 days after the initiation of dialysis for both groups. P values were calculated with the use of the log-rank test.
Table 2. Multivariable Cox Proportional-Hazards Models Examining Hazard Ratios Associated with Paricalcitol Treatment as Compared with Calcitriol Treatment.
Stratified Models
On formal testing for effect modification, the survival benefitof paricalcitol did not vary with any of the covariates tested.Nonetheless, we performed stratified analyses to determine whetherthe effect estimate was consistent across multiple strata (Figure 2).In 28 of 42 strata, paricalcitol conferred a significantsurvival benefit, and in no stratum was calcitriol therapy favored.
Figure 2. Hazard Ratios for Death Associated with Paricalcitol Treatment, as Compared with Calcitriol Treatment, with Stratification According to the Characteristics of the Patients.
The percentages represent the fractions of patients within each stratum who died, the boxes represent point estimates, and the horizontal lines represent 95 percent confidence intervals. The reference category for each analysis is the corresponding group receiving calcitriol. Data on the duration of dialysis were missing for one patient. To convert values for calcium to millimoles per liter, multiply by 0.250, and to convert values for phosphorus to millimoles per liter, multiply by 0.3229.
The hazard ratios for death according to base-line quintilesof calcium, phosphorus, and parathyroid hormone differed betweenthe groups (Figure 3). The Cox models were adjusted for potentialconfounders (Table 2), and within each model, nine (n–1)covariates for the interaction between treatment and quintilewere included. Within each quintile, the risk of death was lowerin the paricalcitol group. Most notable was a significantlylower risk of death at all levels of serum calcium and parathyroidhormone.
Figure 3. Hazard Ratios for Death According to Quintiles of Serum Calcium, Phosphorus, and Parathyroid Hormone at Base Line.
Dark bars represent the effect of paricalcitol, and light bars represent the effect of calcitriol. R denotes the reference category for all analyses. The asterisks denote P<0.05.
Follow-Up Analysis
During 12 months of follow-up, the mean hemoglobin levels andurea reduction ratios were similar in the two groups (data notshown). The mean percent changes from base line in the levelsof calcium, phosphorus, and parathyroid hormone are shown inTable 3. Three, 6, and 12 months after the initiation of vitaminD therapy, the mean (±SD) doses of paricalcitol per administrationwere 4.2±2.5, 4.3±2.7, and 4.3±2.8 µg,respectively, and the average doses of calcitriol per administrationwere 1.0±0.7, 1.1±1.0, and 1.3±1.2 µg,respectively. In a multivariate analysis stratified accordingto the vitamin D formulation, an increase in the dose of eitherformulation was not associated with a significant survival advantageor disadvantage (data not shown).
Table 3. Mean Percentage Changes in Calcium, Phosphorus, and Parathyroid Hormone Levels after Initiation of Vitamin D Therapy.
During the follow-up period, the frequency of unexpected absencefrom dialysis was similar in the two groups (16.1 percent inthe paricalcitol group and 15.9 percent in the calcitriol group,P=0.35); however, the rates of transplantation differed (3.8percent in the paricalcitol group and 3.3 percent in the calcitriolgroup, P<0.001). Ten percent of patients (6684 patients)terminated their initial vitamin D therapy more than one monthbefore leaving the study (data censored or patient died) anddid not initiate treatment with another injectable formulation.Removing these patients from the analysis did not appreciablychange the effect estimates (data not shown). Finally, in asubgroup of patients who switched formulations, the 14,862 patientswho switched from calcitriol to paricalcitol had a higher subsequentrate of two-year survival than the 1621 who switched from paricalcitolto calcitriol (73 percent vs. 64 percent, P=0.04) (Figure 1B).Multivariate analysis of this population was not performed becauseof incomplete data and the small number of patients who switchedfrom paricalcitol to calcitriol.
Discussion
In this historical cohort study of 67,399 patients undergoinghemodialysis in whom injectable vitamin D therapy was initiatedbetween 1999 and 2001, the patients treated with paricalcitolhad a significant survival advantage as compared with thosetreated with calcitriol. This advantage appeared to be independentof base-line calcium, phosphorus, and parathyroid hormone levelsand other potential confounders. The benefit of paricalcitolwas suggested in several subgroups of patients, including blacksand patients with diabetes. In addition, those who switchedfrom calcitriol to paricalcitol appeared to have a significantsurvival advantage over those who switched from paricalcitolto calcitriol.
Renal osteodystrophy encompasses a spectrum of disorders ofbone and mineral metabolism, including secondary hyperparathyroidism,which is characterized by elevated parathyroid hormone levelswith high bone turnover; adynamic bone disease, which is characterizedby low bone turnover with parathyroid hormone levels of lessthan 150 pg per milliliter; and, in some patients, a combinationof the two.23,24 The development of renal osteodystrophy isrelated to the complex interaction among disordered mineral,bone, and parathyroid metabolism; calcium-based oral phosphatebinders; dialysate calcium levels; and vitamin D therapy.24The goal of vitamin D therapy is to prevent skeletal complicationsby suppressing serum parathyroid hormone levels in patientswith secondary hyperparathyroidism. However, vitamin D therapycan elevate calcium and phosphorus levels and oversuppress parathyroidhormone levels. Suppression of parathyroid hormone can leadto adynamic bone disease,25 which itself is associated withskeletal complications.26,27,28 Furthermore, emerging data suggestthat the adverse consequences of the management of renal osteodystrophyhave important roles in vascular calcification and the excessrisk of death from cardiovascular causes among patients undergoingdialysis.8,9,10,11,15,20,29 Few studies, however, have examinedthe independent effects of vitamin D therapy, and none, to ourknowledge, have compared survival among patients receiving differenttypes of vitamin D formulations.
Although our study is subject to the usual limitations of retrospectivestudies, including misclassification and bias, the prospectivecollection of data and contemporaneous comparison groups strengthenour findings.30 In addition, the inclusion of patients fromsuch a large number of dialysis facilities (more than 1000)probably minimized bias.30 Because all dialysis centers useda centralized standard data base that was linked to billingsystems, the primary exposure, treatment with injectable vitaminD, and the primary outcome, survival, were well documented.Certain base-line characteristics, however, did differ betweenthe groups.
Clinical data suggesting a survival benefit of paricalcitolover calcitriol have not been available. Nonetheless, in ourstudy nonrandom assignment of therapy could have led to unequalsusceptibility to the outcome.30 Adjustment for base-line differencesattenuated but did not eliminate the effect, the survival curvesseparated over time, and significant differences were notedwhen patients switched formulations; all of these observationsprovide support for a therapeutic effect. Although the exactduration of the effect of these medications and the specificreasons for switching are unknown, the survival curves of thetwo groups switching medication separated over time. The latterfinding suggests that an intention-to-treat analysis of theentire cohort would have misclassified patients. During thestudy period, most clinical nephrologists were aware that elevatedcalcium, phosphorus, and parathyroid hormone levels are associatedwith adverse consequences,29 that blacks with renal diseasein general have more severe secondary hyperparathyroidism,31and that diabetic patients undergoing dialysis tend to havelower parathyroid hormone levels than nondiabetic patients.32Therefore, given the data supporting the use of paricalcitol,17,18,33,34several base-line differences were expected. By comparison,base-line lipid profiles, glucose and blood-pressure control,and measures of the adequacy of dialysis were similar in thetwo groups, as were hemoglobin levels and the adequacy of dialysisat follow-up. However, with continued refinements in the analyticapproach that addressed a number of confounders, the benefitof paricalcitol diminished, leaving open the possibility thatunmeasured confounders (e.g., a specific "doctor effect") accountin part for the survival differences.
Although base-line measurements (e.g., values for serum lipids,glycosylated hemoglobin, and blood pressure) suggested thatthe use of oral medications was similar in the groups, incompleteinformation about oral medications is a limitation of this study.For example, accurate information about the use of calcium-basedor non-calcium-based phosphate binders was unavailable. Duringthe study period, most patients used calcium-based phosphatebinders, and although aluminum-based binders were available,their use was limited because of known adverse events associatedwith aluminum accumulation. The use of sevelamer, a non-calcium-basedbinder introduced in October 1998, probably increased in thispopulation. Although sevelamer use was recently associated withreduced vascular calcification as compared with the use of calcium-basedbinders,10 it is unlikely that use of this medication explainedour findings. The nationwide prescription of sevelamer amongpatients undergoing dialysis was approximately 10 percent in1999, 20 percent in 2000, and 30 percent in 2001 (Burke S, Genzyme:personal communication), and our results remain significanteven when each study year is analyzed separately. Furthermore,paricalcitol appeared to be beneficial among patients with low-to-normalmineral levels — the groups least likely to have receivednon-calcium-based binders.
The mechanism by which paricalcitol exerts its potential beneficialeffect remains to be determined. Differential effects of paricalcitoland calcitriol on mineral metabolism suggest that the primarymechanism involves mineral and parathyroid hormone metabolism.The blunted effect of paricalcitol on gut absorption and boneresorption of minerals, as compared with that of calcitriol,17,18,35may lead to lower mineral loads, which could reduce the riskof vascular calcification and death from cardiovascular causes.8,10The relative survival advantage with paricalcitol, however,was largely consistent across strata of base-line mineral andparathyroid hormone levels (Figure 3), suggesting a benefitthat may extend beyond these base-line levels. Indeed, vitaminD receptors are ubiquitous throughout the body and, when activated,modify inflammation, immune function, cell growth, and celldifferentiation.36 Slight modifications of the parent compound(D-1,25-dihydroxyvitamin D3) dramatically affect cellular responses.33,34,37,38In vitro studies suggest that calcitriol, unlike paricalcitol,sensitizes cells to energy depletion and iron-mediated injury,39and data from animal models suggest that hydroxyvitamin D2 compoundsare much less toxic than hydroxyvitamin D3 compounds.40 In thepresent study, the use of paricalcitol was associated with areduction in the rate of death from cardiovascular, infectious,and other causes. Elevated phosphorus and parathyroid hormonelevels have been associated with increased mortality from vascularand nonvascular causes, including infection.20 For data on causesof death, we used ICD-9-CM codes, whose accuracy has been questioned,41and therefore further studies are needed to identify the exactmechanisms involved.
The patients in our study represented a broad spectrum of diseaseseverity, and thus were representative of patients seen in routineclinical practice between 1999 and 2001, a period when clinicaldata did not suggest a difference in survival between patientsusing different vitamin D formulations. Before conclusions canbe drawn about the role of paricalcitol in the management ofsecondary hyperparathyroidism, additional research is required.First, clinical conclusions should not be drawn until our findingshave been confirmed by a prospective, randomized trial. Second,if these results are confirmed, the mechanisms that underliethem should be elucidated to determine whether they are explainedby a protective effect of paricalcitol, a harmful effect ofcalcitriol, or both. For example, although we did not observea dose–response effect on mortality associated with calcitriol,an increased dose of calcitriol relative to the dose of paricalcitolmight explain our findings. Finally, further studies shouldaddress the question of whether therapy initiated before theonset of hemodialysis or after renal transplantation also affectssurvival.
Drs. Teng, Lazarus, and Ofsthun are employees of Fresenius MedicalCare North America. Dr. Lowrie reports having served as a consultantto Fresenius Medical Care North America.
We are indebted to Drs. Carlos Camargo, Jr., Meir Stampfer,and Tom Greene for their suggestions and support and to Mr.Ishwar Thadhani for his inspiration.
Source Information
From Fresenius Medical Care North America, Lexington, Mass. (M.T., E.L., N.O., J.M.L.); and the Renal Unit, Massachusetts General Hospital, Harvard Medical School, Boston (M.W., R.T.).
Address reprint requests to Dr. Thadhani at Bullfinch 127, 55 Fruit St., Massachusetts General Hospital, Boston, MA 02114, or at thadhani.r{at}mgh.harvard.edu.
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(2009). Calcitriol ameliorates capillary deficit and fibrosis of the heart in subtotally nephrectomized rats. Nephrol Dial Transplant
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Tentori, F., Albert, J. M., Young, E. W., Blayney, M. J., Robinson, B. M., Pisoni, R. L., Akiba, T., Greenwood, R. N., Kimata, N., Levin, N. W., Piera, L. M., Saran, R., Wolfe, R. A., Port, F. K.
(2009). The survival advantage for haemodialysis patients taking vitamin D is questioned: findings from the Dialysis Outcomes and Practice Patterns Study. Nephrol Dial Transplant
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Isakova, T., Gutierrez, O. M., Chang, Y., Shah, A., Tamez, H., Smith, K., Thadhani, R., Wolf, M.
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(2008). High-dose cholecalciferol to correct vitamin D deficiency in haemodialysis patients. Nephrol Dial Transplant
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Noonan, W., Koch, K., Nakane, M., Ma, J., Dixon, D., Bolin, A., Reinhart, G.
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Wolf, M., Betancourt, J., Chang, Y., Shah, A., Teng, M., Tamez, H., Gutierrez, O., Camargo, C. A. Jr., Melamed, M., Norris, K., Stampfer, M. J., Powe, N. R., Thadhani, R.
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Dobnig, H., Pilz, S., Scharnagl, H., Renner, W., Seelhorst, U., Wellnitz, B., Kinkeldei, J., Boehm, B. O., Weihrauch, G., Maerz, W.
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Bodyak, N., Ayus, J. C., Achinger, S., Shivalingappa, V., Ke, Q., Chen, Y.-S., Rigor, D. L., Stillman, I., Tamez, H., Kroeger, P. E., Wu-Wong, R. R., Karumanchi, S. A., Thadhani, R., Kang, P. M.
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Lamb, E. J, Hodsman, A., van Schalkwyk, D., Ansell, D., Warwick, G.
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Zierold, C., Mings, J. A., Deluca, H. F.
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Chertow, G. M., Blumenthal, S., Turner, S., Roppolo, M., Stern, L., Chi, E. M., Reed, J., on behalf of the CONTROL Investigators,
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Teng, M., Wolf, M., Ofsthun, M. N., Lazarus, J. M., Hernan, M. A., Camargo, C. A. Jr, Thadhani, R.
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Norman, P.E., Powell, J.T.
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Xiang, W., Kong, J., Chen, S., Cao, L.-P., Qiao, G., Zheng, W., Liu, W., Li, X., Gardner, D. G., Li, Y. C.
(2005). Cardiac hypertrophy in vitamin D receptor knockout mice: role of the systemic and cardiac renin-angiotensin systems. Am. J. Physiol. Endocrinol. Metab.
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Sambrook, P. N., Chen, J. S., March, L. M., Cameron, I. D., Cumming, R. G., Lord, S. R., Schwarz, J., Seibel, M. J.
(2004). Serum Parathyroid Hormone Is Associated with Increased Mortality Independent of 25-Hydroxy Vitamin D Status, Bone Mass, and Renal Function in the Frail and Very Old: A Cohort Study. J. Clin. Endocrinol. Metab.
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Jorna, F. H., Tobe, T. J. M., Huisman, R. M., de Jong, P. E., Plukker, J. T. M., Stegeman, C. A.
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Dobrez, D. G., Mathes, A., Amdahl, M., Marx, S. E., Melnick, J. Z., Sprague, S. M.
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Vattikuti, R., Towler, D. A.
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Curhan, G.
(2004). Fooling the Parathyroid Gland -- Will There Be Health Benefits?. NEJM
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Andreucci, V. E., Kerr, D. N. S., Kopple, J. D.
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Shoji, T., Shinohara, K., Kimoto, E., Emoto, M., Tahara, H., Koyama, H., Inaba, M., Fukumoto, S., Ishimura, E., Miki, T., Tabata, T., Nishizawa, Y.
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