Uric Acid and Pentraxin-3 Levels Are Independently Associated with Coronary Artery Disease Risk in Patients with Stage 2 and 3 Kidney Disease

Abstract

Background and Objectives: Cardiovascular disease is prevalent in chronic kidney disease (CKD). Uric acid is increased in subjects with CKD and has been linked with cardiovascular mortality in this population. However, no study has evaluated the relationship of uric acid with angiographically proven coronary artery disease (CAD) in this population. We therefore investigated the link between serum uric acid (SUA) levels and (i) extent of CAD assessed by the Gensini score and (ii) inflammatory parameters, including C-reactive protein (CRP) and pentraxin-3, in patients with mild-to-moderate CKD. Material and Methods: In an unselected population of 130 patients with estimated glomerular filtration rate (eGFR) between 90 and 30 ml/min/1.73 m², we measured SUA, serum pentraxin-3, CRP, urinary protein-to-creatinine ratio, lipid parameters and the severity of CAD as assessed by coronary angiography and quantified by the Gensini lesion severity score. Results: The mean serum values for SUA, pentraxin-3 and CRP in the entire study population were 5.5 ± 1.5 mg/dl, 6.4 ± 3.4 ng/ml and 3.5 ± 2.6 mg/dl, respectively. The Gensini scores significantly correlated in univariate analysis with gender (R = –0.379, p = 0.02), uric acid (R = 0.42, p = 0.001), pentraxin-3 (R = 0.54, p = 0.001), CRP (R = 0.29, p = 0.006) levels, eGFR (R = –0.33, p = 0.02), proteinuria (R = 0.21, p = 0.01), and presence of hypertension (R = 0.37, p = 0.001), but not with smoking status, diabetes mellitus, and lipid parameters. After adjustments for traditional cardiovascular risk factors, only uric acid (R = 0.21, p = 0.02) and pentraxin-3 (R = 0.28, p = 0.01) remained significant predictors of the Gensini score. Conclusions: SUA and pentraxin-3 levels are independent determinants of severity of CAD in patients with mild-to-moderate CKD. We recommend a clinical trial to determine whether lowering uric acid could prevent progression of CAD in patients with CKD.

Correlation between arterial stiffness and inflammatory markers in autosomal dominant polycystic kidney disease patients with preserved renal function

“…However, lack of correlation between arterial stiffness, as assessed by artery elasticity, and PTX3 levels in our cohort seems not consistent with previously reported associations between elevated PTX3 and surrogate markers of ED such as VCAM-1 [24], flow-mediated dilatation [21,33] as well as cardiovascular outcomes and severity of CAD in CKD patients [12,19,21].…”

“…Systemic inflammation is considered among the potential dysregulated pathways underlying CKDassociated ED [12]. CKD patients seem to be particularly prone to develop a state of persistent microinflammation, potentially due to raised production as well as decreased renal clearance of pro-inflammatory cytokines [13,14].…”

Multifactorial treatment for improvement of renal function and cardiovascular risk: an ATTEMPT for patients with metabolic syndrome and chronic kidney disease

“…These findings were also confirmed in meta-analyses 25,26 . Interestingly, similar results have been reported in patients with renal dysfunction [27][28][29][30] , thus highlighting the role of SUA as a possible CVD risk factor in these patients. Furthermore, hyperuricemia has been suggested as a risk factor for CKD development 31,32 and progression 33,34 .…”

Potential serum biomarkers in the pathophysiological processes of stroke

“…Therefore, the release of PTX3 may reflect vascular damage. Recently, several studies suggested that PTX3 might be associated with increased mortality in patients with vascular diseases [85]. A recent study in 376 patients with ischemic stroke showed that higher levels of PTX3 were independently associated with increased mortality in ischemic stroke patients [86].…”