Inflammation and hypoalbuminemia mediate the association between CKD and contrast-associated AKI

Chronic kidney disease (CKD) is associated with an increased risk of contrast-associated acute kidney injury (CA-AKI), but the pathways underlying this relationship, including the contribution of intermediate factors, are not well characterized. We investigated the association between CKD and CA-AKI in patients undergoing coronary angiography or percutaneous coronary intervention and evaluated the potential mediating roles of serum albumin and high-sensitivity C-reactive protein (hsCRP) in this association.

During the study period, a total of 13,024 patients underwent coronary angiography of these, 3740 met the predefined inclusion criteria and formed the final study cohort. Multivariable logistic regression and formal mediation analyses were subsequently employed to evaluate the associations of interest.

Among the 3740 patients, 414 (11.1%) developed CA-AKI. Lower pre-procedural serum albumin and higher log-transformed hsCRP (LnhsCRP) were independently associated with increased CA-AKI risk (OR [95% CI] 0.730 [0.583-0.913], P = 0.006, and 1.385 [1.215-1.579], P < 0.001, respectively). The initial association between CKD and CA-AKI (OR 1.906 [1.552-2.342]) was attenuated after adjustment for albumin and hsCRP (OR 1.253 [0.975-1.609]). Subsequent mediation analysis indicated that serum albumin and hsCRP statistically accounted for approximately 31.3% and 56.6% of the attenuation in the association between CKD and CA-AKI, with an additional co-mediation effect of 12.1%.

Systemic inflammation and hypoalbuminemia, beyond reduced kidney function, may help explain CA-AKI risk in CKD and could inform risk stratification strategies using inflammatory and nutritional biomarkers.