Coronary artery diseaseContrast-Induced nephropathy after percutaneous coronary interventions in relation to chronic kidney disease and hemodynamic variables
Section snippets
Study patients
The prospectively collected Cardiovascular Research Foundation angioplasty database was queried to identify a total of 7,230 consecutive patients who underwent first percutaneous coronary intervention (angioplasty, stenting, directional atherectomy, rotablation) over a period of 5 years; we excluded patients with acute ST-elevation myocardial infarction within 48 hours, cardiogenic shock, and baseline end-stage renal disease requiring dialysis. There were 1,980 patients (27.4%) with and 5,250
Baseline and procedural characteristics
Data on patients with or without baseline CKD, according to the development of CIN, are listed in Table 1.
Among patients with CKD, those who developed CIN were older and more often had diabetes, hypertension, hyperlipidemia, peripheral vascular disease, previous myocardial infarction and/or stroke, congestive heart failure (New York Heart Association class >II) with or without pulmonary edema, moderate/severe left ventricular dysfunction (ejection fraction <40%), and non–ST-elevation myocardial
Discussion
In the present study, we extended previous observations regarding CIN in patients with CKD and documented that this complication has prognostic importance even in patients without baseline CKD. We also found that decrements of baseline eGFR value convey incrementally higher mortality. This probably indicates the presence of various stages within the same pathophysiologic spectrum; abnormal periprocedural hemodynamic parameters were strongly associated with CIN in both patient subgroups.
In
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2022, International Journal of CardiologyCitation Excerpt :Besides the important diagnostic and therapeutic value of the procedures, potential harmful side-effects of intra-arterial CA administration are of significant healthcare concern. Side-effects of CA exposure range from mild inconveniences, such as flushing and headache, to allergic reactions as well as to contrast-induced thyroid dysfunction [1] and contrast-associated acute kidney injury (AKI) with association to increased morbidity and mortality [2–4]. Although, the temporal association between contrast exposition and death in AKI does not prove a causal relationship and other risk factors such as peri-procedural hemodynamic changes, ischemia and artheroembolic events may add to acute creatinine rise after cardiac catheterization [2,5], the amount of exposed contrast agent volume (CAV) was consistently identified as independent risk factor for AKI [4,6,7].