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Published on: June 18, 2020
Plasma Cell-Free DNA and Caspase-3 Levels in Patients with Chronic Kidney Disease
Anna Clementi1,2, Grazia Maria Virzì2,3, Sabrina Milan Manani2,3
1Department of Nephrology and Dialysis, Santa Marta and Santa Venera Hospital, 95024 Acireale, Italy.
Insights
Cell-free plasma DNA (cfDNA) and caspase-3 levels are elevated in chronic kidney disease (CKD) patients, particularly those with advanced disease. These findings suggest a role for inflammation and apoptosis in CKD progression.
Area of Science:
- Biochemistry
- Nephrology
- Molecular Biology
Background:
- Cell-free plasma DNA (cfDNA) is extracellular DNA released during cell death.
- Elevated cfDNA levels are observed in various clinical conditions, including chronic kidney disease (CKD).
- Caspase-3 is a key mediator of apoptosis, a process implicated in CKD pathogenesis.
Purpose of the Study:
- To evaluate cfDNA and caspase-3 levels in CKD patients.
- To investigate the association of these molecules with CKD stage and progression.
- To explore the potential role of inflammation and apoptosis in renal damage.
Main Methods:
- Compared cfDNA and caspase-3 levels in 25 CKD patients and 10 healthy controls.
- Assessed biomarker levels across different CKD stages.
- Correlated cfDNA and caspase-3 levels with serum creatinine and urea.
Main Results:
- cfDNA and caspase-3 levels were significantly higher in CKD patients versus controls.
- Elevated levels were particularly pronounced in advanced CKD (stage 5).
- Positive correlations were found between cfDNA, caspase-3, creatinine, and urea.
Conclusions:
- CKD patients exhibit increased cfDNA and caspase-3 levels.
- These findings suggest inflammation and apoptosis may contribute to CKD progression.
- Higher cfDNA and caspase-3 may reflect worsening renal damage and uremic toxin levels.
Background:
Cell-free plasma DNA (cfDNA) is circulating extracellular DNA arising from cell death mechanisms (apoptosis, necrosis, etc.). It is commonly existent in healthy individuals, but its ranks increase in diverse clinical circumstances, such as kidney disease, sepsis, myocardial infarction, trauma and cancer. In patients with advanced chronic kidney disease, cfDNA is connected to inflammation, and it has been associated with higher mortality. Caspase-3 plays a dominant role in apoptosis, a mechanism of programmed cell death involved in the pathogenesis and progression of chronic kidney disease (CKD). The aim of this pilot study was the evaluation of cfDNA levels and caspase-3 concentrations in patients with chronic kidney disease, in order to investigate the potential role of these molecules, deriving from inflammatory and apoptotic mechanisms, in the progression of renal damage.
Methods:
We compared cfDNA and caspase-3 levels in 25 CKD patients and in 10 healthy subjects, evaluating their levels based on CKD stage. We also explored correlations between cfDNA and caspase-3 levels in CKD patients and between cfDNA and caspase-3 levels and serum creatinine and urea in this population.
Results:
We observed that cfDNA and caspase-3 levels were higher in patients with CKD compared to healthy subjects, in particular in patients with advanced renal disease (CKD stage 5). A positive correlation between cfDNA and caspase-3 levels and between cfDNA and caspase-3 and creatinine and urea were also noticed.
Conclusions:
Patients with chronic kidney disease show higher levels of cfDNA and caspase-3 levels compared to the control group. Based on these preliminary results, we speculated that the worsening of renal damage and the increase in uremic toxin concentration could be associated with higher levels of cfDNA and caspase-3 levels, thus reflecting the potential role of inflammation and apoptosis in the progression of CKD. Future studies should focus on the validation of these promising preliminary results.
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