Acute kidney injury represents an important clinical problem in hospitalized patients, with persistently high rates of mortality and morbidity. With an ever-increasing number of patients receiving intravascular injection of iodinated contrast media worldwide, contrast induced nephropathy (CIN) has become the third leading cause of hospital-acquired AKI. Approximately half of these cases are in patients undergoing cardiac catheterization procedures.~The prevention and early intervention of CIN has been hampered mainly by the lack of a consensus definition and the paucity of early predictive biomarkers to accurately identify high-risk patients. CIN is most frequently defined as an increase in serum creatinine (sCr) by 25-50% above the baseline, generally occurring within the first 24 h after contrast exposure, in the absence of other causes. However, sCr is an unreliable indicator during acute changes in kidney function, and alterations in sCr levels are not particularly sensitive or specific for small changes in the glomerular filtration rate (GFR)e, gender, race and intravascular volume. Biomarkers such as kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) have been used for the early diagnosis of AKI, although with no definitive results.
Biomarkers such as kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) have been used for the early diagnosis of AKI, although with no definitive results. The investigators explored the association between plasma aging biomakers such as sklotho and contrast induced nephropathy in patients undergoing percutaneous coronary intervention (PCI) with contrast injection.