Parathyroid Hormone (PTH) Homeostasis in Bartter Syndrome

NCT01021280 · Status: UNKNOWN · Type: OBSERVATIONAL · Enrollment: 15

Last updated 2012-06-14

No results posted yet for this study

Summary

Parathyroid hormone (PTH) gland calcium sensing receptor (CASR) regulates PTH secretion. CASR is also expressed in nephron thick ascending limb (TAL). Bartter syndrome (BS), a normotensive hypokalemic tubulopathy, may be due to mutations in different TAL channels, including the potassium channel ROMK. Mutations in CASR may also cause BS through its effects on ROMK function. However, it is unknown whether ROMK mutations exert any effects on CASR function and PTH physiology. Preliminary data from our center shows that PTH levels were specifically elevated in type II (where ROMK is mutated) and not in type IV (where another gene, Barttin is defective) BS, without a common explanation. We assume that the mutation in ROMK may cause a dysregulation of PTH secretion via possible interaction with CASR.

The purpose of this study is: to investigate the PT-gland function and regulation in BS.

Methods: Patients with BS type II and IV and normal controls will undergo a standard protocol of controlled ionic hypo- and hypercalcemia, during which PTH secretion, phosphate balance and calcium excretion will be followed. Calcium Vs PTH response curves will be generated and compared.

Expected impact and benefit: the results of this study will help understand the mechanisms of PTH regulation beyond CASR.

Conditions

Sponsors & Collaborators

  • Ben-Gurion University of the Negev

    collaborator OTHER
  • Soroka University Medical Center

    lead OTHER

Eligibility

Min Age
14 Years
Max Age
35 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2013-01-31
Primary Completion
2013-12-31
Completion
2014-06-30

Countries

  • Israel

Study Locations

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Entities

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT01021280 on ClinicalTrials.gov