The Calcemic Response to Continuous Parathyroid Hormone (PTH)(1-34) Infusion in End-Stage Kidney Disease Varies According to Bone Turnover: A Potential Role for PTH(7-84)

Context: Factors contributing to PTH resistance in dialysis patients remain elusive. Objectives: The study assessed the skeletal and biochemical response to 46 h of PTH(1-34) infusion in dialysis patients. Design: The study was a prospective, controlled assessment of response to PTH(1-34). Setting:...

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Published inThe journal of clinical endocrinology and metabolism Vol. 95; no. 6; pp. 2772 - 2780
Main Authors Wesseling-Perry, Katherine, Harkins, G. Chris, Wang, He-jing, Elashoff, Robert, Gales, Barbara, Horwitz, Mara J., Stewart, Andrew F., Jüppner, Harald, Salusky, Isidro B.
Format Journal Article
LanguageEnglish
Published Bethesda, MD Oxford University Press 01.06.2010
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Abstract Context: Factors contributing to PTH resistance in dialysis patients remain elusive. Objectives: The study assessed the skeletal and biochemical response to 46 h of PTH(1-34) infusion in dialysis patients. Design: The study was a prospective, controlled assessment of response to PTH(1-34). Setting: The study was performed at the University of California, Los Angeles, General Clinical Research Center. Participants: Nineteen dialysis patients and 17 healthy volunteers were studied. Intervention: PTH(1-34) was infused at a rate of 8 pmol/kg · h for 46 h. Bone biopsy was performed in all dialysis patients. Main Outcome Measures: Serum calcium, phosphorus, 1,25-dihydroxyvitamin D, PTH (four separate assays), and FGF-23 were determined at baseline and h 7, 23, 35, and 46 of the infusion. Results: Serum calcium levels rose in healthy volunteers (9.2 ± 0.1 to 11.9 ± 0.3 mg/dl; P < 0.01) and in dialysis patients with adynamic/normal bone turnover (9.0 ± 0.3 to 10.7 ± 0.7 mg/dl; P < 0.05) but did not change in dialysis patients with high bone turnover. Serum phosphorus levels declined in healthy volunteers (3.9 ± 0.1 to 3.5 ± 0.1 mg/dl; P < 0.05) but increased in all dialysis patients (6.7 ± 0.4 to 8.0 ± 0.3 mg/dl; P < 0.05). Full-length PTH(1-84) declined in all subjects; however, PTH(7-84) fragments declined only in healthy subjects and in dialysis patients with normal/adynamic bone but remained unchanged in dialysis patients with high bone turnover. Conclusions: The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH. PTH(7-84) may contribute to this phenomenon.The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH and PTH(7-84) may contribute to this phenomenon.
AbstractList CONTEXT:Factors contributing to PTH resistance in dialysis patients remain elusive. OBJECTIVES:The study assessed the skeletal and biochemical response to 46 h of PTH(1-34) infusion in dialysis patients. DESIGN:The study was a prospective, controlled assessment of response to PTH(1-34). SETTING:The study was performed at the University of California, Los Angeles, General Clinical Research Center. PARTICIPANTS:Nineteen dialysis patients and 17 healthy volunteers were studied. INTERVENTION:PTH(1-34) was infused at a rate of 8 pmol/kg · h for 46 h. Bone biopsy was performed in all dialysis patients. MAIN OUTCOME MEASURES:Serum calcium, phosphorus, 1,25-dihydroxyvitamin D, PTH (four separate assays), and FGF-23 were determined at baseline and h 7, 23, 35, and 46 of the infusion. RESULTS:Serum calcium levels rose in healthy volunteers (9.2 ± 0.1 to 11.9 ± 0.3 mg/dl; P < 0.01) and in dialysis patients with adynamic/normal bone turnover (9.0 ± 0.3 to 10.7 ± 0.7 mg/dl; P < 0.05) but did not change in dialysis patients with high bone turnover. Serum phosphorus levels declined in healthy volunteers (3.9 ± 0.1 to 3.5 ± 0.1 mg/dl; P < 0.05) but increased in all dialysis patients (6.7 ± 0.4 to 8.0 ± 0.3 mg/dl; P < 0.05). Full-length PTH(1-84) declined in all subjects; however, PTH(7-84) fragments declined only in healthy subjects and in dialysis patients with normal/adynamic bone but remained unchanged in dialysis patients with high bone turnover. CONCLUSIONS:The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH. PTH(7-84) may contribute to this phenomenon.
Context: Factors contributing to PTH resistance in dialysis patients remain elusive. Objectives: The study assessed the skeletal and biochemical response to 46 h of PTH(1-34) infusion in dialysis patients. Design: The study was a prospective, controlled assessment of response to PTH(1-34). Setting: The study was performed at the University of California, Los Angeles, General Clinical Research Center. Participants: Nineteen dialysis patients and 17 healthy volunteers were studied. Intervention: PTH(1-34) was infused at a rate of 8 pmol/kg · h for 46 h. Bone biopsy was performed in all dialysis patients. Main Outcome Measures: Serum calcium, phosphorus, 1,25-dihydroxyvitamin D, PTH (four separate assays), and FGF-23 were determined at baseline and h 7, 23, 35, and 46 of the infusion. Results: Serum calcium levels rose in healthy volunteers (9.2 ± 0.1 to 11.9 ± 0.3 mg/dl; P < 0.01) and in dialysis patients with adynamic/normal bone turnover (9.0 ± 0.3 to 10.7 ± 0.7 mg/dl; P < 0.05) but did not change in dialysis patients with high bone turnover. Serum phosphorus levels declined in healthy volunteers (3.9 ± 0.1 to 3.5 ± 0.1 mg/dl; P < 0.05) but increased in all dialysis patients (6.7 ± 0.4 to 8.0 ± 0.3 mg/dl; P < 0.05). Full-length PTH(1-84) declined in all subjects; however, PTH(7-84) fragments declined only in healthy subjects and in dialysis patients with normal/adynamic bone but remained unchanged in dialysis patients with high bone turnover. Conclusions: The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH. PTH(7-84) may contribute to this phenomenon.
Context: Factors contributing to PTH resistance in dialysis patients remain elusive. Objectives: The study assessed the skeletal and biochemical response to 46 h of PTH(1-34) infusion in dialysis patients. Design: The study was a prospective, controlled assessment of response to PTH(1-34). Setting: The study was performed at the University of California, Los Angeles, General Clinical Research Center. Participants: Nineteen dialysis patients and 17 healthy volunteers were studied. Intervention: PTH(1-34) was infused at a rate of 8 pmol/kg · h for 46 h. Bone biopsy was performed in all dialysis patients. Main Outcome Measures: Serum calcium, phosphorus, 1,25-dihydroxyvitamin D, PTH (four separate assays), and FGF-23 were determined at baseline and h 7, 23, 35, and 46 of the infusion. Results: Serum calcium levels rose in healthy volunteers (9.2 ± 0.1 to 11.9 ± 0.3 mg/dl; P < 0.01) and in dialysis patients with adynamic/normal bone turnover (9.0 ± 0.3 to 10.7 ± 0.7 mg/dl; P < 0.05) but did not change in dialysis patients with high bone turnover. Serum phosphorus levels declined in healthy volunteers (3.9 ± 0.1 to 3.5 ± 0.1 mg/dl; P < 0.05) but increased in all dialysis patients (6.7 ± 0.4 to 8.0 ± 0.3 mg/dl; P < 0.05). Full-length PTH(1-84) declined in all subjects; however, PTH(7-84) fragments declined only in healthy subjects and in dialysis patients with normal/adynamic bone but remained unchanged in dialysis patients with high bone turnover. Conclusions: The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH. PTH(7-84) may contribute to this phenomenon. The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH and PTH(7-84) may contribute to this phenomenon.
Factors contributing to PTH resistance in dialysis patients remain elusive. The study assessed the skeletal and biochemical response to 46 h of PTH(1-34) infusion in dialysis patients. The study was a prospective, controlled assessment of response to PTH(1-34). The study was performed at the University of California, Los Angeles, General Clinical Research Center. Nineteen dialysis patients and 17 healthy volunteers were studied. PTH(1-34) was infused at a rate of 8 pmol/kg x h for 46 h. Bone biopsy was performed in all dialysis patients. Serum calcium, phosphorus, 1,25-dihydroxyvitamin D, PTH (four separate assays), and FGF-23 were determined at baseline and h 7, 23, 35, and 46 of the infusion. Serum calcium levels rose in healthy volunteers (9.2 +/- 0.1 to 11.9 +/- 0.3 mg/dl; P < 0.01) and in dialysis patients with adynamic/normal bone turnover (9.0 +/- 0.3 to 10.7 +/- 0.7 mg/dl; P < 0.05) but did not change in dialysis patients with high bone turnover. Serum phosphorus levels declined in healthy volunteers (3.9 +/- 0.1 to 3.5 +/- 0.1 mg/dl; P < 0.05) but increased in all dialysis patients (6.7 +/- 0.4 to 8.0 +/- 0.3 mg/dl; P < 0.05). Full-length PTH(1-84) declined in all subjects; however, PTH(7-84) fragments declined only in healthy subjects and in dialysis patients with normal/adynamic bone but remained unchanged in dialysis patients with high bone turnover. The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH. PTH(7-84) may contribute to this phenomenon.
Factors contributing to PTH resistance in dialysis patients remain elusive.CONTEXTFactors contributing to PTH resistance in dialysis patients remain elusive.The study assessed the skeletal and biochemical response to 46 h of PTH(1-34) infusion in dialysis patients.OBJECTIVESThe study assessed the skeletal and biochemical response to 46 h of PTH(1-34) infusion in dialysis patients.The study was a prospective, controlled assessment of response to PTH(1-34).DESIGNThe study was a prospective, controlled assessment of response to PTH(1-34).The study was performed at the University of California, Los Angeles, General Clinical Research Center.SETTINGThe study was performed at the University of California, Los Angeles, General Clinical Research Center.Nineteen dialysis patients and 17 healthy volunteers were studied.PARTICIPANTSNineteen dialysis patients and 17 healthy volunteers were studied.PTH(1-34) was infused at a rate of 8 pmol/kg x h for 46 h. Bone biopsy was performed in all dialysis patients.INTERVENTIONPTH(1-34) was infused at a rate of 8 pmol/kg x h for 46 h. Bone biopsy was performed in all dialysis patients.Serum calcium, phosphorus, 1,25-dihydroxyvitamin D, PTH (four separate assays), and FGF-23 were determined at baseline and h 7, 23, 35, and 46 of the infusion.MAIN OUTCOME MEASURESSerum calcium, phosphorus, 1,25-dihydroxyvitamin D, PTH (four separate assays), and FGF-23 were determined at baseline and h 7, 23, 35, and 46 of the infusion.Serum calcium levels rose in healthy volunteers (9.2 +/- 0.1 to 11.9 +/- 0.3 mg/dl; P < 0.01) and in dialysis patients with adynamic/normal bone turnover (9.0 +/- 0.3 to 10.7 +/- 0.7 mg/dl; P < 0.05) but did not change in dialysis patients with high bone turnover. Serum phosphorus levels declined in healthy volunteers (3.9 +/- 0.1 to 3.5 +/- 0.1 mg/dl; P < 0.05) but increased in all dialysis patients (6.7 +/- 0.4 to 8.0 +/- 0.3 mg/dl; P < 0.05). Full-length PTH(1-84) declined in all subjects; however, PTH(7-84) fragments declined only in healthy subjects and in dialysis patients with normal/adynamic bone but remained unchanged in dialysis patients with high bone turnover.RESULTSSerum calcium levels rose in healthy volunteers (9.2 +/- 0.1 to 11.9 +/- 0.3 mg/dl; P < 0.01) and in dialysis patients with adynamic/normal bone turnover (9.0 +/- 0.3 to 10.7 +/- 0.7 mg/dl; P < 0.05) but did not change in dialysis patients with high bone turnover. Serum phosphorus levels declined in healthy volunteers (3.9 +/- 0.1 to 3.5 +/- 0.1 mg/dl; P < 0.05) but increased in all dialysis patients (6.7 +/- 0.4 to 8.0 +/- 0.3 mg/dl; P < 0.05). Full-length PTH(1-84) declined in all subjects; however, PTH(7-84) fragments declined only in healthy subjects and in dialysis patients with normal/adynamic bone but remained unchanged in dialysis patients with high bone turnover.The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH. PTH(7-84) may contribute to this phenomenon.CONCLUSIONSThe skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH. PTH(7-84) may contribute to this phenomenon.
Context: Factors contributing to PTH resistance in dialysis patients remain elusive. Objectives: The study assessed the skeletal and biochemical response to 46 h of PTH(1-34) infusion in dialysis patients. Design: The study was a prospective, controlled assessment of response to PTH(1-34). Setting: The study was performed at the University of California, Los Angeles, General Clinical Research Center. Participants: Nineteen dialysis patients and 17 healthy volunteers were studied. Intervention: PTH(1-34) was infused at a rate of 8 pmol/kg · h for 46 h. Bone biopsy was performed in all dialysis patients. Main Outcome Measures: Serum calcium, phosphorus, 1,25-dihydroxyvitamin D, PTH (four separate assays), and FGF-23 were determined at baseline and h 7, 23, 35, and 46 of the infusion. Results: Serum calcium levels rose in healthy volunteers (9.2 ± 0.1 to 11.9 ± 0.3 mg/dl; P < 0.01) and in dialysis patients with adynamic/normal bone turnover (9.0 ± 0.3 to 10.7 ± 0.7 mg/dl; P < 0.05) but did not change in dialysis patients with high bone turnover. Serum phosphorus levels declined in healthy volunteers (3.9 ± 0.1 to 3.5 ± 0.1 mg/dl; P < 0.05) but increased in all dialysis patients (6.7 ± 0.4 to 8.0 ± 0.3 mg/dl; P < 0.05). Full-length PTH(1-84) declined in all subjects; however, PTH(7-84) fragments declined only in healthy subjects and in dialysis patients with normal/adynamic bone but remained unchanged in dialysis patients with high bone turnover. Conclusions: The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH. PTH(7-84) may contribute to this phenomenon.The skeleton of dialysis patients with high bone turnover is resistant to the calcemic actions of PTH and PTH(7-84) may contribute to this phenomenon.
Author Harkins, G. Chris
Elashoff, Robert
Jüppner, Harald
Wang, He-jing
Salusky, Isidro B.
Wesseling-Perry, Katherine
Stewart, Andrew F.
Gales, Barbara
Horwitz, Mara J.
AuthorAffiliation David Geffen School of Medicine at University of California, Los Angeles (K.W.-P., H.W., R.E., B.G., I.B.S.), Los Angeles, California 90095; Immutopics International (G.C.H.), San Clemente, California 92673; The University of Pittsburgh School of Medicine (M.J.H., A.F.S.), Pittsburgh, Pennsylvania 15213; and Massachusetts General Hospital and Harvard Medical School (H.J.), Boston, Massachusetts 02114
AuthorAffiliation_xml – name: David Geffen School of Medicine at University of California, Los Angeles (K.W.-P., H.W., R.E., B.G., I.B.S.), Los Angeles, California 90095; Immutopics International (G.C.H.), San Clemente, California 92673; The University of Pittsburgh School of Medicine (M.J.H., A.F.S.), Pittsburgh, Pennsylvania 15213; and Massachusetts General Hospital and Harvard Medical School (H.J.), Boston, Massachusetts 02114
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  surname: Wesseling-Perry
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  givenname: G. Chris
  surname: Harkins
  fullname: Harkins, G. Chris
  organization: 2Immutopics International (G.C.H.), San Clemente, California 92673
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  givenname: He-jing
  surname: Wang
  fullname: Wang, He-jing
  organization: 1David Geffen School of Medicine at University of California, Los Angeles (K.W.-P., H.W., R.E., B.G., I.B.S.), Los Angeles, California 90095
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  surname: Elashoff
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  organization: 1David Geffen School of Medicine at University of California, Los Angeles (K.W.-P., H.W., R.E., B.G., I.B.S.), Los Angeles, California 90095
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  surname: Gales
  fullname: Gales, Barbara
  organization: 1David Geffen School of Medicine at University of California, Los Angeles (K.W.-P., H.W., R.E., B.G., I.B.S.), Los Angeles, California 90095
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  givenname: Mara J.
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  fullname: Horwitz, Mara J.
  organization: 3The University of Pittsburgh School of Medicine (M.J.H., A.F.S.), Pittsburgh, Pennsylvania 15213
– sequence: 7
  givenname: Andrew F.
  surname: Stewart
  fullname: Stewart, Andrew F.
  organization: 3The University of Pittsburgh School of Medicine (M.J.H., A.F.S.), Pittsburgh, Pennsylvania 15213
– sequence: 8
  givenname: Harald
  surname: Jüppner
  fullname: Jüppner, Harald
  organization: 4Massachusetts General Hospital and Harvard Medical School (H.J.), Boston, Massachusetts 02114
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  surname: Salusky
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ID FETCH-LOGICAL-c5461-8b155fa5b9c5fc8115d43c8d36a68ce2251875c239e83a8aabbf29e7cc80347f3
ISSN 0021-972X
1945-7197
IngestDate Thu Aug 21 14:11:27 EDT 2025
Fri Jul 11 08:23:26 EDT 2025
Mon Jun 30 12:40:49 EDT 2025
Thu Apr 03 07:04:55 EDT 2025
Mon Jul 21 09:14:08 EDT 2025
Thu Apr 24 22:59:10 EDT 2025
Tue Jul 01 02:46:17 EDT 2025
Fri May 16 04:03:20 EDT 2025
Fri Feb 07 10:35:23 EST 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 6
Keywords Kidney disease
Obesity
Urinary system disease
Antiosteoporotic
Nutrition
Continuous
Peptide hormone
Nutrition disorder
Metabolic diseases
Osteoarticular system
Osteoforming
Parathyroid hormone
Perfusion
Renal failure
Turnover
Bone
Endocrinology
Nutritional status
Teriparatide
Language English
License CC BY 4.0
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c5461-8b155fa5b9c5fc8115d43c8d36a68ce2251875c239e83a8aabbf29e7cc80347f3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
Address all correspondence and requests for reprints to: Katherine Wesseling-Perry, Division of Pediatric Nephrology, A2-383 MDCC, 10833 LeConte Boulevard, Los Angeles, California 90095. E-mail: kwesseling@mednet.ucla.edu.
PMID 20382692
PQID 3164450161
PQPubID 2046206
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PublicationTitle The journal of clinical endocrinology and metabolism
PublicationTitleAlternate J Clin Endocrinol Metab
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Publisher Oxford University Press
Copyright by The Endocrine Society
Endocrine Society
The Endocrine Society
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Snippet Context: Factors contributing to PTH resistance in dialysis patients remain elusive. Objectives: The study assessed the skeletal and biochemical response to 46...
CONTEXT:Factors contributing to PTH resistance in dialysis patients remain elusive. OBJECTIVES:The study assessed the skeletal and biochemical response to 46 h...
Factors contributing to PTH resistance in dialysis patients remain elusive. The study assessed the skeletal and biochemical response to 46 h of PTH(1-34)...
Context: Factors contributing to PTH resistance in dialysis patients remain elusive. Objectives: The study assessed the skeletal and biochemical response to 46...
Factors contributing to PTH resistance in dialysis patients remain elusive.CONTEXTFactors contributing to PTH resistance in dialysis patients remain...
Context: Factors contributing to PTH resistance in dialysis patients remain elusive. Objectives: The study assessed the skeletal and biochemical response to 46...
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SubjectTerms Adolescent
Biological and medical sciences
Biopsy
Bone and Bones - drug effects
Bone and Bones - metabolism
Bone and Bones - pathology
Bone Development - drug effects
Bone turnover
Calcification, Physiologic - drug effects
Calcium - blood
Calcium - urine
Dialysis
Disease resistance
End-stage renal disease
Endocrinopathies
Feeding. Feeding behavior
Female
Fibroblast growth factor 23
Fibroblast Growth Factors - blood
Fundamental and applied biological sciences. Psychology
Hemodialysis
Humans
Kidney diseases
Kidney Failure, Chronic - drug therapy
Kidney Failure, Chronic - pathology
Male
Medical sciences
Original
Parathyroid hormone
Parathyroid Hormone - physiology
Parathyroid Hormone - therapeutic use
Peptide Fragments - physiology
Phosphorus
Phosphorus - blood
Renal Dialysis
Skeleton
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Vertebrates: endocrinology
Vitamin D
Young Adult
Title The Calcemic Response to Continuous Parathyroid Hormone (PTH)(1-34) Infusion in End-Stage Kidney Disease Varies According to Bone Turnover: A Potential Role for PTH(7-84)
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Volume 95
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