Ignite Creation Date:
2024-05-05 @ 11:22 AM
Last Modification Date:
2024-10-26 @ 9:04 AM
Study NCT ID:
NCT00005261
Status:
COMPLETED
Last Update Posted:
2016-01-21
First Post:
2000-05-25
Brief Title:
Urinary Kallikrein and Hypertension A Prospective Study
Sponsor:
University of Utah
Organization:
University of Utah
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2016-01
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
To determine whether low total urinary kallikrein activity was prospectively associated with new hypertension onset or elevated blood pressures
Detailed Description:
BACKGROUND
Statistical evidence had been found for a dominant major gene segregating in large pedigrees for high urinary kallikrein levels protecting against hypertension which explained 51 percent of the variance of total urinary kallikrein TUK In normotensive adult and pediatric pedigree members low urinary kallikrein activity was associated with a positive family history of hypertension stroke andor coronary disease
DESIGN NARRATIVE
The presence of a previously reported dominant major gene inferred from segregation analysis of total urinary kallikrein activity TUK in selected pedigrees was verified on already collected frozen urine specimens Subjects were rescreened to obtain measured nine year follow-up blood pressure data Individuals were classified by assigned baseline TUK genotype and tested to determine whether low TUK was prospectively associated with new hypertension onset or elevated blood pressures Because a major gene effect was implicated available probes for the structural kallikrein gene or other related products regulating kallikrein were tested for genetic linkage to TUK levels Correlations with over 600 variables measured at baseline in pedigrees and twins were tested to analyze the strong familiality of environment refine the genetic analyses to better assign genotypes and detect gene-environment interactions All baseline variables except kallikrein aldosterone and prostaglandin measurements on frozen urine and follow-up blood pressure had already been collected
TUK may be a marker for a renal cellular or other physiological abnormality influencing both TUK expression and susceptibility to hypertension Therefore the relationship of TUK to urinary aldosterone prostaglandin E excretion and already measured urinary electrolytes plasma renin activity and baseline and reactive blood pressures was determined Genetic segregation analyses were performed of the urinary variables and other variables closely associated with TUK
Statistical evidence had been found for a dominant major gene segregating in large pedigrees for high urinary kallikrein levels protecting against hypertension which explained 51 percent of the variance of total urinary kallikrein TUK In normotensive adult and pediatric pedigree members low urinary kallikrein activity was associated with a positive family history of hypertension stroke andor coronary disease
DESIGN NARRATIVE
The presence of a previously reported dominant major gene inferred from segregation analysis of total urinary kallikrein activity TUK in selected pedigrees was verified on already collected frozen urine specimens Subjects were rescreened to obtain measured nine year follow-up blood pressure data Individuals were classified by assigned baseline TUK genotype and tested to determine whether low TUK was prospectively associated with new hypertension onset or elevated blood pressures Because a major gene effect was implicated available probes for the structural kallikrein gene or other related products regulating kallikrein were tested for genetic linkage to TUK levels Correlations with over 600 variables measured at baseline in pedigrees and twins were tested to analyze the strong familiality of environment refine the genetic analyses to better assign genotypes and detect gene-environment interactions All baseline variables except kallikrein aldosterone and prostaglandin measurements on frozen urine and follow-up blood pressure had already been collected
TUK may be a marker for a renal cellular or other physiological abnormality influencing both TUK expression and susceptibility to hypertension Therefore the relationship of TUK to urinary aldosterone prostaglandin E excretion and already measured urinary electrolytes plasma renin activity and baseline and reactive blood pressures was determined Genetic segregation analyses were performed of the urinary variables and other variables closely associated with TUK
Study Oversight
Has Oversight DMC:
Is a FDA Regulated Drug?:
Is a FDA Regulated Device?:
Is an Unapproved Device?:
Is a PPSD?:
Is a US Export?:
Is an FDA AA801 Violation?:
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| R01HL044738 | NIH | None | httpsreporternihgovquickSearchR01HL044738 |