Introduction:
Several factors relate to the kidney's function and thyroid hormone levels. The level of thyroid hormones directly or indirectly affects the development and function of the kidneys, mainly because the thyroid hormones affect both the pre and intrinsic renal blood flow by increasing it and the GFR (glomerular filtration rate). GFR is the capacity of the kidneys to filter the blood and it is altered with the thyroid levels. Thyroid dysfunction is frequently related to glomerulonephritis by an autoimmune pathogenesis. Many medications have the potential to impair thyroid and renal function, and studies have shown connections between thyroid and renal cancers.
What Is the Relationship Between Thyroid Disease and Kidney?
Thyroid and renal disorders can occur together with common etiological causes. Furthermore, treatment options for one disease may impact those for another organ. Thyroid dysfunction impacts renal physiology and development, whereas kidney illness can cause thyroid dysfunction. Primary hypothyroidism and subclinical hypothyroidism are more common in CKD patients.
The physiological benefits of hypothyroidism in CKD, as well as the risk of CKD progression with hyperthyroidism, show the importance of taking a careful approach to treating thyroid hormone abnormalities in CKD. Thyroid dysfunction is also linked to glomerulonephritis, and an autoimmune process causes both. Thyroid hormones influence cell growth and protein synthesis. Thyroid hormone status affects the functioning renal mass, expressed as the kidney-to-body mass ratio. Hyperthyroidism raises the functioning renal mass, whereas hypothyroidism lowers it.
On the other hand, severe hyperthyroidism results in the disintegration of proteins and, ultimately, renal atrophy. Moreover, congenital kidney abnormalities are more likely to occur in children with congenital hypothyroidism. Thyroid hormones also influence the kidney function of newborns. The thyroid hormone status in the congenital period impacts the mitochondrial energy metabolism enzymes in the proximal convoluted tubule (PCT) cells.
How Does Thyroid Hormone Act on the Kidney?
By their effects on the GFR, thyroid hormones influence the renal expulsion of the water load. It is commonly recognized that sodium (Na) or potassium (K)'s ATP enzymes (ATPase) play an important role in the transportation of solutes within the PCTs. Thyroid hormones mainly affect tubular potassium permeability and sodium or potassium ATPase activity to increase sodium reabsorption at the PCT. Similar effects are seen in tubular calcium reabsorption but not magnesium. The adrenergic receptors and dopaminergic activation of renal tubular cells are also similarly regulated by thyroid hormones. Adrenergic modulation, renin release, and angiotensinase activity have been demonstrated to impact the renin-angiotensin-aldosterone axis.
How Does Thyroid Hormone Impact Kidney Function?
In which thyroid hormones impact renal function, prerenal and direct renal influences are involved. Here, thyroid hormones' effects on the cardiovascular system and renal blood flow (RBF) modulate the pre-renal effects. Thyroid hormone impacts the glomerular filtration rate (GFR), tubular secretory and re-absorptive processes, and hormonal effects on the physiological functioning of the renal tubular, showing the direct effects on the kidneys. RBF, GFR, tubular function, electrolyte homeostasis, and kidney shape are all impacted by thyroid disease. The numerous impacts on renal function of hypothyroidism and hyperthyroidism and they are:
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Hyperthyroidism and Its Influence on Kidney Function: GFR and RBF are elevated in hyperthyroidism. Thyroid hormones have a multifaceted impact on RBF and GFR. Thyroid hormones are pre-renal agents that raise cardiac output through decreased systemic vascular resistance and favorable chronotropic and inotropic effects. This increases renal blood flow (RBF) indirectly. In the renal cortex and medulla, there is an increase in endothelial production of nitric oxide (NO) due to the stimulation of nitric oxide synthase (NOS), which is caused by thyroid hormones directly and endothelial shear stress related to high arterial pressure indirectly. An opposite relation between renal vasoconstrictor endothelium is observed. As a result, there is a net increase in RBF due to increased intrarenal vasodilatation and decreased vasoconstriction.
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Hypothyroidism and Its Influence on Kidney Function: In general, the consequences of hyperthyroidism on the kidney are the opposite of those of hypothyroidism. Reduced renal response to vasodilators, such as vascular endothelial growth factor (VEGF) and insulin-like growth factor-1, decreased cardiac output (adverse chronotropic and inotropic effects), increased peripheral vascular resistance, intrarenal vasoconstriction, and decreased expression of renal vasodilators all contribute to hypothyroidism's reduced RBF. Reduced RBF may also be caused by pathologic alterations in the glomerular structure associated with hypothyroidism, such as thickening of the glomerular basement membrane and expansion of the mesangial matrix. In many cases, there are several causes. The GFR is reversibly lowered (by roughly 40 percent) in over 55 percent of adult hypothyroidism cases.
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Thyroid Impairment in Kidney Transplantation and Dialysis: Individuals with CKD undergoing hemodialysis (HD) have an increased TSH and low thyroid hormone levels. Even when total T4 levels are low, heparin increases the free T4 fraction in patients with chronic kidney disease (CKD) following heparin dialysis by blocking the binding of T4 to protein. Despite decreased blood thyroid hormone levels, there is a compensating influence on the cellular transport of thyroid hormones among CKD patients on hemodialysis that helps preserve the euthyroid state (a state where the kidney shows minimal functioning). As a result of reversing the CKD syndrome, kidney transplantation affects multiple thyroid profiles caused by CKD. After transplantation of the kidneys, the low T3 and T4 levels gradually improve throughout the first three to four months. Kidney transplant recipients typically have a decline in T4 levels during the first few months following transplantation, which is lower than the pre-transplant level until it steadily returns to normal.
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Thyroid Dysfunction and Chronic Kidney Disease: Among CKD patients, primary hypothyroidism (non-autoimmune) is frequently seen. In particular, there is a constant increase in the incidence of subclinical hypothyroidism with a drop in GFR. Low T3 levels, particularly total T3 rather than free T3, are the first and most prevalent thyroid function anomaly in patients with chronic kidney disease. There are various reasons why a low T3 syndrome arises in CKD patients. The iodothyronine deiodination and T3 protein binding are impacted by fasting, long-term metabolic acidosis, and long-term protein deficiency. These conditions also decrease T4's peripheral conversion to T3 and T3's protein binding.
Conclusion:
Different pathways are seen for the relation between kidney and thyroid functions when each organ is affected. These interactions have structural correlates in addition to functional changes. In CKD, TSH increases are typical but may not always indicate hypothyroidism. Thyroid function is also significantly impacted by CKD treatment options such as kidney transplantation, HD, and Parkinson's disease. Medication used to treat thyroid problems may cause renal failure or necessitate lowering CKD dosages. To understand the nature of the disease and the patient's condition and to come up with an appropriate treatment plan, it is crucial to be acquainted with both the problem and the science behind these conditions.
