The primary focus of this study was the association between the uric acid-to-albumin ratio (UAR) and the development of contrast-induced nephropathy (CIN). A higher UAR was found to be associated with a higher likelihood of CIN, suggesting that it may serve as an indicator of risk. To the best of our knowledge, this is one of the few studies including all acute coronary syndrome (ACS) subtypes in this context. Contrast media (CM) are widely used in various imaging procedures, particularly in coronary angiography. They are eliminated exclusively via glomerular filtration. In individuals with normal renal function, CMs are typically cleared within 24 hours
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The pathophysiology of CIN involves three primary mechanisms: medullary ischemia, the generation of reactive oxygen species, and direct tubular toxicity. However, the exact contribution of each mechanism remains uncertain 13. CIN has been reported to account for approximately 11% of hospital-acquired acute kidney injury in previous studies 14. Once CIN develops, it is associated with increased morbidity and mortality over the subsequent two years 15. Established risk factors for CIN include hypertension, diabetes mellitus, atrial fibrillation, and chronic heart failure (CHF), all of which have been shown to increase susceptibility to acute kidney injury after cardiac catheterization 16. In the subgroup analysis of ACS types, the incidence of CIN was noticeably higher in patients presenting with STEMI compared with those with NSTEMI. This finding may be explained by the greater inflammatory burden, more pronounced ischemia–reperfusion injury, and increased hemodynamic instability typically associated with STEMI, all of which may exacerbate renal vulnerability to contrast exposure. Furthermore, STEMI procedures often require urgent and more extensive angiographic evaluation, which can lead to higher contrast volume and additional procedural stress. Previous studies have similarly reported higher rates of CIN in STEMI populations 1, supporting the notion that this subgroup carries an intrinsically elevated risk profile. The alignment of our results with existing evidence reinforces the importance of careful renal risk assessment in STEMI patients undergoing coronary angiography. CIN remains a major clinical concern in interventional cardiology due to its impact on long-term outcomes.
Serum uric acid (UA) may have prognostic value in ST-elevation myocardial infarction (STEMI), as elevated levels have been linked with adverse in-hospital events 17. Several studies have demonstrated a significant relationship between hyperuricemia and increased risk of CIN following coronary angiography 18. Experimentally, UA has been shown to precipitate as monosodium urate crystals, inducing local inflammation. Moreover, UA contributes to oxidative stress, inflammation, and endothelial dysfunction 19. Sanchez-Lozada et al. reported that hyperuricemia is an independent risk factor for AKI in critically ill patients, even after adjusting for hypertension, chronic kidney disease, and CHF 20. Hyperuricemia may lead to AKI via both crystalline and non-crystalline pathways, including renal vasoconstriction, inflammation, and apoptosis. In a long-term cohort study involving nearly 50,000 participants, hyperuricemia was significantly associated with all-cause mortality and progression to renal failure 21.
Albumin is known to play important roles in various physiological and pathological processes. It is the main determinant of intravascular oncotic pressure and serves as a carrier protein for various bioactive molecules, including hormones, drugs, and free fatty acids 22. Additionally, albumin has demonstrated anti-inflammatory, anti-oxidative, and anti-apoptotic properties 23. Hypoalbuminemia has been linked to coronary artery disease and increased all-cause mortality 24. Oxidative stress and inflammation, both of which are central to the pathogenesis of CIN, are exacerbated by hypoalbuminemia 25. It leads to increased blood viscosity, oxidative stress, and endothelial dysfunction 26. Additionally, decreased synthesis and increased serum albumin catabolism have been associated with an increased inflammatory response 7. In patients with ACS, elevated chemokine levels trigger systemic inflammation, reduce antioxidant capacity, increase lipid peroxidation, and promote oxidative stress 27. A meta-analysis confirmed that hypoalbuminemia is a significant predictor of AKI 28.
Considering the shared pathophysiological pathways of uric acid and albumin in inflammation and oxidative stress, their combined evaluation through UAR has shown superior predictive value compared to individual assessment. One study demonstrated that UAR >1.7 was significantly associated with AKI in critically ill patients 29. Recently, Faisal et al. reported that UAR >1.62 provided better predictive accuracy for CIN 30. It is important to note that the UAR values in those studies were calculated based on albumin levels measured in g/dL. The findings of our study appear to be consistent with these results.
Several findings of our study are consistent with previous reports evaluating predictors of contrast-induced nephropathy. Similar to earlier studies, elevated uric acid levels and reduced serum albumin-both indicators of heightened oxidative stress and systemic inflammation-were associated with a higher risk of CIN. The strong predictive performance of the uric acid-to-albumin ratio in our cohort also aligns with recent evidence demonstrating its prognostic value in patients with acute coronary syndromes and in those undergoing primary percutaneous coronary intervention. Nevertheless, the magnitude of the predictive strength observed in our study appears to be higher than that reported in earlier literature, which may be explained by differences in patient selection, inclusion of all ACS subtypes, and the larger sample size. These similarities and discrepancies suggest that UAR may be a robust biomarker across different clinical contexts, although further multicenter prospective studies are warranted to clarify its generalizability.
This study has several limitations. First, it was conducted at a single center and designed retrospectively, which may introduce selection bias. Second, the multifactorial nature of CIN pathogenesis limits the ability of our findings to explain all contributing mechanisms. Lastly, although mortality data were collected, the absence of a clear linear relationship with UAR limits further interpretation; therefore, mortality was only presented descriptively in the table. Future prospective and multicenter studies will be needed to clarify the extent to which UAR can be integrated into routine clinical practice.
In conclusion, combined evaluation of serum uric acid and albumin as UAR revealed significant results in predicting CIN following ACS. Given its accessibility and simplicity, UAR may serve as a useful marker and should be considered for routine laboratory assessment following coronary angiography.
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