Statins for Prevention of Contrast-Associated Acute Kidney Injury: Is the Debate a Moot Point?

摘要

Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI) was first reported in the 1950s as a fatal AKI that occurred after intravenous pyelography in a patient with myeloma kidney. Since then, CIN has been plagued with controversy. There is controversy in the medical literature regarding its incidence, with reported rates ranging from as low as <1% to >30%. Moreover, there is controversy regarding the prognosis of patients who develop CIN, with reported rates of requiring dialysis varying from <0.5% to >5% [1-4]. Even the term CIN is controversial, with strong advocates for the term contrast "associated" AKI (CA-AKI) rather than "induced" given a lack of robust data to support a causal relationship, as most studies on CI-AKI did not include a comparable no-contrast control group. In fact, studies of contrast-enhanced computed tomography (CT) versus non-contrast CT show no difference in the incidence of AKI, suggesting perhaps differences in the incidence of AKI when iodinated contrast media is administered via the intravenous route rather than intra-arterial route [5]. The diagnosis is controversial, with some definitions using absolute increase in creatinine (from 0.3 to 0.5 mg/dL) and others using a relative increase in creatinine (from 25% to 50%), and few others using a relative decrease in estimated glomerular filtration rate (>50%) within 48-72 hours from baseline.