Immune System May Provoke Salt Sensitive Hypertension in CDK

Chronic kidney disease commonly known as CDK is a type of kidney disorder in which there is a gradual loss of kidney function and develops complications of high blood pressure and may also lead to heart attacks if the pressure of blood against the walls of blood vessels is not controlled. The new research reveals that the immune system has some link with hypertension.

The research team from TMDU (Tokyo Medical and Dental University) found that in patients of chronic kidney disease, the Tumor Necrosis factor  (TNF- α ) signaling factor of the immune system may provoke hypertension.

The complete study results are published in the journal “Kidney International”.

The immune system works very efficiently to provide protection against any pathogen that permeates the body to sustain normal health by finding out all the health-related threats, delivering the immune cells and changing the expression of a gene.

But the researchers from Tokyo Medical and Dental University (TMDU), Japan have discovered that there is a link between salt-sensitive hypertension and the immune system in individuals suffering from CKD (chronic kidney disease).

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Chronic kidney disease is a fundamental cause of about million deaths and has influenced over eight hundred million individuals worldwide. The substantial intricacy of chronic kidney disease is hypertension or high blood pressure.

The researchers have found that the development of CKD can be controlled by regulating normal blood pressure. High blood pressure is the main cause of CKD. Many individuals suffering from CKD have shown an increased sensitivity to salt. Increased salt sensitivity is a condition that is very hard to control because the salt intake from the diet has an excessive impact on blood pressure.

Salt sensitive hypertension is caused by a pathway known as WNK-SPAK-NCC phosphorylation cascade if over activated unsuitably because it causes increased reabsorption of salts in the kidney. it has not been assured that WNK-SPAK-NCC causes high blood pressure in patients of CKD or not and the regulation of phosphorylation cascade is still unknown.

Researchers used a diseased mouse model and found high levels of lysine deficient protein kinase 1 protein (WNK1) in the kidneys of mice suffering from CKD. High levels of WNK 1 protein causes an elevated triggering of the proteins SPAK and NCC. In mice suffering from CKD, the WNK-SPAK-NCC pathway stayed triggered when fed a diet with a high amount of salt, causing salt-sensitive hypertension.

The investigators also studied recent researches indicating that the immune system has a great impact on salt sensitivity. High levels of TNF- α (a pro-inflammatory cytokine) were certain in the kidney of mice bearing CKD and stipulation of TNF- α causes and elevated levels of WNK 1.

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Dr. Eisei Sohara, the first author of this study says that the transcription of WNK1 was not increased by TNF- α but TNF- α controlled the degeneration of mature WNK1 protein.

Normally a protein NEDD4-2E3-ligase degenerates mature WNK1 and it was found that TNF- α increases the levels of WNK1 protein and prevents the transcription of protein that degenerates WNK1. Investigators confirmed the relation between salt sensitivity and immune system by restraining TNF- α and found that the salt sensitivity of mice bearing CKD fed a diet with a high amount of salt was reversed.

The widely used antihypertensive drugs are thiazide diuretics that are NCC inhibitors but the effectiveness of these drugs vary among chronic kidney disease patients. Considerable response to thiazide diuretics is usually observed from individuals with high activity of NCC. The results of this research play a significant role to choose better NCC inhibitors in the future