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Updated: Mar 18, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Determinants of thromboxane biosynthesis in patients with moderate to severe chronic kidney disease
Natale Vazzana1, Francesca Santilli1, Stefano Lattanzio1
1Internal Medicine and Center of Excellence on Aging, "G. d'Annunzio" University Foundation, Chieti, Italy.
Insights
Platelet activation and oxidative stress increase with chronic kidney disease (CKD) progression. Anemia in CKD is linked to this platelet activation, potentially increasing cardiovascular risk.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Biochemistry
Background:
- Accelerated atherothrombosis is a complication in chronic kidney disease (CKD).
- Mechanisms underlying this complication are not fully understood.
- Thromboxane (TX)-dependent platelet activation and its determinants in CKD require further investigation.
Purpose of the Study:
- To assess thromboxane (TX)-dependent platelet activation in CKD patients.
- To identify factors influencing TX biosynthesis in CKD, including oxidative stress, inflammation, and anemia.
- To explore the relationship between kidney function, anemia, and platelet activation.
Main Methods:
- Cross-sectional study comparing urinary 8-iso-PGF2α (oxidative stress marker) and 11-dehydro-TXB2 (platelet activation marker).
- Included 115 patients with stage 1-4 CKD.
- Multivariate analysis to identify independent predictors of TX biosynthesis.
Main Results:
- Urinary 11-dehydro-TXB2 and 8-iso-PGF2α levels increased with CKD stage.
- Both markers were inversely associated with estimated glomerular filtration rate (eGFR) and hemoglobin levels.
- Urinary 8-iso-PGF2α, hemoglobin, and eGFR were independent predictors of urinary 11-dehydro-TXB2.
Conclusions:
- Patients with CKD exhibit persistent platelet activation, even in early stages.
- This activation is linked to kidney function and oxidative stress.
- Anemia in CKD is independently associated with TX-dependent platelet activation, suggesting a link to cardiovascular risk.
Background:
Mechanisms of accelerated atherothrombosis in patients with chronic kidney disease (CKD) are only partly characterized. The aims of this study were to evaluate the extent of thromboxane (TX)-dependent platelet activation in patients with CKD, and to characterize the determinants of altered TX biosynthesis in this setting, with particular reference to enhanced lipid peroxidation, low grade inflammation and CKD-related anemia.
Patients And Methods:
A cross sectional comparison between urinary 8-iso-PGF2α and 11-dehydro-TXB2, in vivo markers of oxidative stress and platelet activation, respectively, was performed in 115 patients with stage 1-4 CKD.
Results:
Levels of both urinary 11-dehydro-TXB2 and 8-iso-PGF2α increased sequentially across the four CKD stages (P<0.0001, Kruskal-Wallis test). Both urinary prostanoids were inversely associated with either estimated glomerular filtration rate (eGFR, P<0.0001) or hemoglobin levels (P<0.0001). A significant direct correlation was also observed between urinary 11-dehydro-TXB2 and 8-iso-PGF2α (Rho=0.620, P<0.0001). On multivariate analysis, urinary 8-iso-PGF2α (β=0.459, P<0.0001), hemoglobin levels (β=- 0.261, P=0.002) and eGFR (β=-0.172, P=0.032) were independent predictors of urinary 11-dehydro-TXB2 (adjusted R(2)=0.488).
Conclusions:
This study provides biochemical evidence of persistent platelet activation in patients with CKD. This condition occurs early in the natural history of the disease and is related to kidney function and oxidative stress. Moreover, we found an independent inverse relationship between hemoglobin levels and TX-dependent platelet activation. This finding may provide a mechanistic link between CKD-related anemia and increased cardiovascular risk.
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