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Completed No phase listed Observational

FGF23 and Angiotensin-(1-7) in Hypophosphatemia (GAP)

ClinicalTrials.gov ID: NCT03489993

Public ClinicalTrials.gov record NCT03489993. Field values are reproduced from the official study page; the official ClinicalTrials.gov record remains the source of truth for eligibility, enrollment, and contact information.

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Data is sourced from official ClinicalTrials.gov public API records. Always review the official ClinicalTrials.gov record for the latest information.

Official title

Interplay of FGF23 and Angiotensin-(1-7) in Hypophosphatemia (GAP)

Brief summary

Reproduced verbatim from the official ClinicalTrials.gov record. Not medical advice.

Hereditary hypophosphatemia encompasses rare genetic conditions characterized by renal phosphate wasting. Increased circulating levels of fibroblast growth factor 23 (FGF23), a key regulator of phosphorus metabolism, are critical to the pathophysiology of these diseases, most notably in X-linked hypophosphatemia (XLH). Increased FGF23 induces hypertrophy and scarring in the heart in part via stimulating the traditional renin-angiotensin system (RAS) pathway, angiotensin-converting enzyme (ACE)/angiotensin (Ang ll), particularly in patients with chronic kidney disease, but the effect of FGF23 on the heart in patients with FGF23-related hypophosphatemic diseases is unknown. In addition, the relationship between FGF23 and the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) (Ang-(1-7) pathway of the RAS is unknown. The objective of this study is to describe the relationship between FGF23, which causes low phosphorus levels, and components of the RAS in the blood and urine to help the investigators understand why the disease occurs and how to better treat it. Subjects will be identified by querying the Electronic Medical Record according to medical diagnosis. Thirty subjects, 2-24 years of age, will be recruited from the tertiary care Pediatric Endocrinology and Pediatric Nephrology clinics at Brenner Children's Hospital. Inclusion criteria include a confirmed diagnosis of hereditary FGF23-related hypophosphatemia. Clinical data will be obtained from the Electronic Medical Record. Each subject will undergo study assessments at baseline, 6 months and 1 year that include blood work, an echocardiogram, and blood pressure measurements. The primary hypothesis is that subjects with higher Ang-(1-7) levels have lower rates of cardiac hypertrophy and thus are protected against high FGF23 levels. The secondary hypothesis is that subjects with higher Ang-(1-7) levels have lower systolic blood pressure.

Study identification

NCT ID
NCT03489993
Recruitment status
Completed
Study type
Observational
Phase
Not listed
Enrollment
8 participants

Conditions and interventions

Eligibility (public fields only)

Age range
2 Years to 24 Years
Sex
All
Healthy volunteers
Healthy volunteers not accepted

This page does not interpret eligibility. Detailed inclusion and exclusion criteria are on the official ClinicalTrials.gov record.

Study timeline

Start date
Dec 5, 2018
Primary completion
Dec 22, 2020
Completion
Dec 22, 2020
Last update posted
Aug 4, 2022

2018 – 2020

United States locations

U.S. sites
1
U.S. states
1
U.S. cities
1
Facility City State ZIP Site status
Wake Forest University Health Sciences Winston-Salem North Carolina 27157

Site contact phone numbers, emails, and investigator names are intentionally not displayed here. Open the official ClinicalTrials.gov record for site contact information.

About this trial record page

What this page shows
Public field values for ClinicalTrials.gov record NCT03489993, including study identification, conditions, interventions, eligibility (age, sex, healthy volunteer), timeline, and U.S. site list.
What this page does not do
No medical advice, eligibility judgments, treatment recommendations, study quality scoring, or AI-generated medical summaries. No site contact phone numbers, emails, or investigator names.
Where the data comes from
Sourced from the official ClinicalTrials.gov public API. The official record is the source of truth.
Last refresh
Last update posted Aug 4, 2022 · Synced Sep 10, 2026

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