Ignite Creation Date:
2025-12-25 @ 12:00 AM
Ignite Modification Date:
2026-01-05 @ 6:09 PM
Study NCT ID:
NCT06591858
Status:
NOT_YET_RECRUITING
Last Update Posted:
2024-09-19
First Post:
2024-09-05
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Evaluation of Renal Function in Patients With Hyperthyroidism
Sponsor:
Assiut University
Organization:
Study Overview
Official Title:
Evaluation of Renal Function in Patients With Subclinical and Overt Hyperthyroidism
Status:
NOT_YET_RECRUITING
Status Verified Date:
2024-09
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 evaluate the effect of subclinical and overt Hyperthyroidism in renal function
Detailed Description:
* Thyroid disorders are very common with a high prevalence among the general population. Thyroid diseases are associated with many detrimental effects that have a serious impact on various body systems.(1)
* Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low serum thyroid stimulating hormone (TSH) and elevated serum thyroxin (T4), tri-iodothyronine (T3), or both. Whereas subclinical hyperthyroidism (SCH) is defined as low serum TSH level with normal serum levels of T3 and T4.(2)
* The relationship between thyroid hormones and kidney function is well-known for many years. Thyroid diseases adversely affect renal physiology; meanwhile, kidney diseases could result in thyroid dysfunction.
* Thyroid hormones contribute to the maintenance of water and electrolyte balance, and participate in the renal transport system. Hyperthyroidism results in an increased glomerular filtration rate (GFR) by about 18-25%. due to increased renal blood flow and activation of renin angiotensin-aldosterone system (RAAS). Also, these changes have been reported in patients with hyperthyroidism.(3-5)
* Several mechanisms were found playing roles on increasing both the size and functional capacity of kidney:
1. Thyroid hormone directly influences the expression and activity of most of renal transporters by direct binding of thyroid hormone to the promoter region of a transporter gene (6)
2. In hyperthyroid state beta-adrenergic receptors in kidney cortex, and synthesis and secretion of renin by juxtaglomerular cells are increased, which in turn enhance angiotensin-converting enzyme activity.(7)
3. Increased RAAS activity results in afferent arteriolar vasodilatation and efferent arteriolar vasoconstriction with a consequent increase in the filtration pressure...(8) D) Hyperthyroidism increases systolic blood pressure by increasing heart rate, decreasing systemic vascular resistance, raising cardiac output, and increases nitric oxide production which all contributes to the hyper dynamic circulation. Hyperthyroidism results in increased renal blood flow.(7)
* Observed that both BUN and creatinine levels increased significantly after euthyroidism was achieved in hyperthyroid patients, these findings point out to true decline in renal function rather than a mere adaptation to hemodynamic changes.
Although the mechanistic link between thyroid and kidney disease remains unclear, hyperthyroidism may have significant effect on renal function
* Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low serum thyroid stimulating hormone (TSH) and elevated serum thyroxin (T4), tri-iodothyronine (T3), or both. Whereas subclinical hyperthyroidism (SCH) is defined as low serum TSH level with normal serum levels of T3 and T4.(2)
* The relationship between thyroid hormones and kidney function is well-known for many years. Thyroid diseases adversely affect renal physiology; meanwhile, kidney diseases could result in thyroid dysfunction.
* Thyroid hormones contribute to the maintenance of water and electrolyte balance, and participate in the renal transport system. Hyperthyroidism results in an increased glomerular filtration rate (GFR) by about 18-25%. due to increased renal blood flow and activation of renin angiotensin-aldosterone system (RAAS). Also, these changes have been reported in patients with hyperthyroidism.(3-5)
* Several mechanisms were found playing roles on increasing both the size and functional capacity of kidney:
1. Thyroid hormone directly influences the expression and activity of most of renal transporters by direct binding of thyroid hormone to the promoter region of a transporter gene (6)
2. In hyperthyroid state beta-adrenergic receptors in kidney cortex, and synthesis and secretion of renin by juxtaglomerular cells are increased, which in turn enhance angiotensin-converting enzyme activity.(7)
3. Increased RAAS activity results in afferent arteriolar vasodilatation and efferent arteriolar vasoconstriction with a consequent increase in the filtration pressure...(8) D) Hyperthyroidism increases systolic blood pressure by increasing heart rate, decreasing systemic vascular resistance, raising cardiac output, and increases nitric oxide production which all contributes to the hyper dynamic circulation. Hyperthyroidism results in increased renal blood flow.(7)
* Observed that both BUN and creatinine levels increased significantly after euthyroidism was achieved in hyperthyroid patients, these findings point out to true decline in renal function rather than a mere adaptation to hemodynamic changes.
Although the mechanistic link between thyroid and kidney disease remains unclear, hyperthyroidism may have significant effect on renal function
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?: