Introduction:
TNF-alpha (tumor necrosis factor-alpha) is a pro-inflammatory cytokine that is a key mediator involved in regulating the immune system’s response to infection, injury, or inflammation. During infection and/or states of inflammation, TNF-alpha up-regulates other pro-inflammatory cytokines such as IL-1 and IL-6 which in turn cause immune cell migration to the damaged tissue. TNF-alpha can lead to phagocytosis of foreign molecules during acute inflammatory states, but also lead to tissue damage in states of chronic inflammation. There is interplay between TNF-alpha and Tissue Factor, as tissue damage during inflammatory states leads to TNF-alpha activating Tissue Factor as to help initiate the extrinsic pathway of the coagulation cascade and form a blood clot. This relationship between the two molecules is deemed thromboinflammation, and unfortunately can lead to pathologic hypercoagulable states in patients who are suffering from chronic inflammatory states, such as end stage renal disease (ESRD) patients due to the accumulation of toxic metabolic waste products. ProBNP is a precursor molecule that is cleaved to BNP (brain natriuretic peptide) during times of cardiac stress, such as heart failure, left ventricular dysfunction, or chronic hypertension, all of which tend to affect ESRD patents. In these patients, elevated Tissue Factor and proBNP reflect increased risk of cardiovascular disease, with thromboembolic events and fluid overload due to heart failure, respectively, being the primary risk factors. Patients with ESRD are in a chronic inflammatory state with increased TNF-alpha levels, leading to pathologic activation of tissue factor and subsequent thromboembolic risk, leading to cardiovascular disease/ fluid overload reflected by increased proBNP levels.
Methods:
This study aimed to look at the regulatory role between Tissue Factor, TNF-alpha, and proBNP in a 2023 cohort of 70 ESRD patients. The controls represent normal plasma from 10 healthy volunteers. Pearson correlation curves were generated which aimed to look at the correlation between either Tissue Factor and TNF-alpha or between Tissue Factor and proBNP.
Results:
All three of the biomarkers in the ESRD patients were statistically significantly elevated when compared to the controls with average values for Tissue Factor = 341.9285714 (controls = 60.1875), TNF-alpha = 2.619587 (controls = 0.610973), and proBNP = 23.0823 (controls = 19.31928). The results showed that Tissue Factor and TNF-alpha had a statistically significant (p = 0.00711) positive correlation with an r value of 0.319003, while Tissue Factor and proBNP had a statistically non-significant (p = 0.094241) positive correlation with an r value of 0.201585.
Conclusions:
These studies show that both proBNP and TNF-alpha are upregulated in ESRD and tissue factor may have a regulatory role.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.