Abstract
Introduction:Studies have shown that the renin angiotensin aldosterone system (RAAS) and inflammation are related to kidney injury progression. The aim of this study was to evaluate RAAS molecules and chemokine (C-C motif) ligand 2 (CCL2) in 82 patients with chronic kidney disease (CKD).Methods:Patients were divided into two groups: patients diagnosed with CKD and patients without a CKD diagnosis. Glomerular filtration rate (GFR) and albumin/creatinine ratio (ACR) were determined, as well as plasma levels of angiotensin-(1-7) [Ang-(1-7)], angiotensin-converting enzyme (ACE)1, ACE2, and plasma and urinary levels of CCL2.Results:CCL2 plasma levels were significantly higher in patients with CKD compared to the control group. Patients with lower GFR had higher plasma levels of ACE2 and CCL2 and lower ratio ACE1/ACE2. Patients with higher ACR values had higher ACE1 plasma levels.Conclusion:Patients with CKD showed greater activity of both RAAS axes, the classic and alternative, and higher plasma levels of CCL2. Therefore, plasma levels of RAAS molecules and CCL2 seem to be promising prognostic markers and even therapeutic targets for CKD.
Highlights
Studies have shown that the renin angiotensin aldosterone system (RAAS) and inflammation are related to kidney injury progression
This study aimed to evaluate the association between plasma levels of the RAAS molecules and plasma and urinary levels of CCL2 with chronic kidney disease (CKD) markers in patients with and without CKD
Plasma levels of CCL2 were significantly higher in patients with CKD when compared to the control group (Table 1)
Summary
Studies have shown that the renin angiotensin aldosterone system (RAAS) and inflammation are related to kidney injury progression. The aim of this study was to evaluate RAAS molecules and chemokine (C-C motif) ligand 2 (CCL2) in 82 patients with chronic kidney disease (CKD). Results: CCL2 plasma levels were significantly higher in patients with CKD compared to the control group. Patients with lower GFR had higher plasma levels of ACE2 and CCL2 and lower ratio ACE1/ACE2. Conclusion: Patients with CKD showed greater activity of both RAAS axes, the classic and alternative, and higher plasma levels of CCL2. The assessment of kidney impairment is recommended by assessing albuminuria, mainly as spot urine albumin/creatinine ratio (ACR), and by assessing renal function with the estimated glomerular filtration rate (GFR) based on serum creatinine values or available equations. The main mechanisms of arterial hypertension in CKD are saline and volume overload, in addition to increased activity of renin angiotensin aldosterone system (RAAS), endothelial dysfunction, and inflammation
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