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International Journal of Clinical Biology and Biochemistry

Vol. 6, Issue 1, Part A (2024)

Thyroid hormone metabolism in renal disease

Author(s):

Kamal Ali Zalfo and Dr. Rojeen Rashid Sulieman

Abstract:

Introduction and research aim: Hyperthyroidism or hypothyroidism may play different important and regulatory roles in multiple organs of the body. The absence or excess of the TH hormone has harmful effects on all tissues of the body, so thyroid hormone (TH) is necessary for kidney function and development. The aim of the research: to evaluate the function of the thyroid gland and its relationship to kidney disease and to know its relationship to the severity of the disease.
Background: The hormone responsible for triggering the secretion of triiodothyronine (3T) is known as thyroid stimulating hormone. It has a significant function in regulating the body's metabolism, which encompasses several mechanisms that govern the pace of activity in cells and tissues. This includes the production of 4T by the thyroid gland. Thyroid hormone (T4) is one of the primary hormones released by the thyroid gland. Thyroid function is associated with alterations in renal function. Thyroid function indicators might differ depending on age, chronic illnesses, and genetic background. Hence, there exists a connection between thyroid function and reduced kidney function that can be attributed to both direct and indirect factors. Hormone receptors selectively bind to molecules that possess certain conformations and functional groups, hence only responding to the hormones that exhibit such characteristics. Cells from various tissues in the body may possess identical types of receptors. The levels of FT3 steadily declined, resulting in heightened kidney injury and the presence of albumin in the urine. Despite having regular thyroid function.
Methods: A group of solid methodological studies, published between the years 2017 to 2023, collected the relationship between thyroid hormones and natural and chronic kidney disease.
Results: Chronic kidney failure may be a condition resulting from hypothyroidism. It has become clear that iodine clearance takes place in the glomerular filtration in the kidneys, which is the cause of chronic kidney failure. Iodine secretion diminishes, leading to a rise in the plasma concentration of inorganic iodide and thus its absorption. A high concentration of inorganic iodide within the body may inhibit the formation of thyroid hormones. Iodine is filtered out in the glomerular filtration in the kidneys, which is the cause of kidney failure. Also, there was a difference in the severity of the infection between males and females with diabetes, and there was no difference between those without diabetes. People with diabetes with kidney tissue damage experienced an abnormal change in TSH secretions, and there was a direct relationship with the age of those affected, genetic history, and infections of the immune system.
Discussion: FT3 and FT4 exhibit a negative correlation with SCr and ACR, while showing a positive correlation with eGFR. Conversely, TSH showed a negative correlation with eGFR and a positive correlation with ACR. The cause is a disparity in the iodine concentration within thyroid secretions. Conversely, hypothyroidism can be associated with constriction of the blood arteries in the kidneys and a reduction in efficient blood flow to the kidneys, leading to kidney injury and the development of microalbuminuria.
Conclusion: Increased TSH was associated with a decrease in glomerular filtration rate (eGFR), especially in the reference range. The direct effect of increasing fT4 was a decrease in glomerular filtration rate (eGFR). There are significant differences between males and females in nephropathy due to increased TSH, while there are statistically significant differences in males, less than females, in cases of type 2 diabetes. It has also been shown that chronic nephropathy (CKD) and increased severity of hypothyroidism with gradual decline result from glomerular filtration rate (eGFR). On the other hand, patients may have hypothyroidism, which has led to a significant decrease in the number of white blood cells and hemoglobin levels, with a quarter of TSH increasing. In addition, this study demonstrated that kidney function in older individuals who had a low normal FT3 level and a high normal TSH level was impaired. It has also been shown that the lack of iodine secretion leads to an increase in the plasma concentration of inorganic iodide, and thus FT3 levels gradually decrease, causing an increase in the severity of kidney damage and albuminuria. Even with normal thyroid function.
 

Pages: 49-55  |  66 Views  24 Downloads

How to cite this article:
Kamal Ali Zalfo and Dr. Rojeen Rashid Sulieman. Thyroid hormone metabolism in renal disease. Int. J. Clin. Biol. Biochem. 2024;6(1):49-55. DOI: 10.33545/26646188.2024.v6.i1a.59
International Journal of Clinical Biology and Biochemistry

International Journal of Clinical Biology and Biochemistry

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