Statins in the Prevention of Contrast-Induced Nephropathy

Abstract

Coronary angiography and percutaneous coronary interventions are common procedures that utilize iodinated contrast medium to visualize the coronary arterial tree and treat stable and unstable ischemic heart syndromes. Exposure to contrast agents can cause acute and persistent worsening of renal function leading to increased morbidity and mortality. Certain patient characteristics such as age, presence of diabetes, congestive heart failure, chronic kidney disease, hemodynamic instability on presentation, and type and volume of contrast used can increase the risk of developing contrast-induced nephropathy (CIN) and its subsequent complications. Despite the lack of a universal definition, CIN is typically defined as an increase in serum creatinine ≥0.5 mg/dL or 25 % above baseline 48 to 72 h after contrast exposure. Previous research has shown the benefits of adequate intravenous hydration with iso-osmolar crystalloids and the importance of limiting the amount of low-osmolar and iso-osmolar contrast used to prevent the development of CIN. 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have anti-inflammatory and anti-apoptotic properties with few side effects, making it an attractive therapeutic option for prevention of CIN. A number of trials have examined the benefit of different types of statins, high-dose versus low-dose statins, loading versus chronic dosing of statins, in various clinical presentations including acute coronary syndromes and elective procedures, and in those with associated comorbidities such as anemia and chronic kidney disease. In this review, we will summarize recent data regarding statin therapy for prevention of contrast-induced nephropathy.

Efficacy of nicorandil treatment for prevention of contrast-induced nephropathy in high-risk patients undergoing cardiac catheterization: A prospective randomized controlled trial

“…In this study, Iohexol (low-osmolar, non-ionic contrast medium) was also used to reduce complications and CIN incidence. Although, the exact pathophysiology of CIN remains unclear, the possible direct and indirect pathophysiologic effects of contrast exposure that have been suggested include renal vasoconstriction, which leads to decreased oxygenation of the medulla causing ischemia and renal injury, direct tubular toxicity due to the creation of oxygen free radicals, causing acute tubular necrosis, and a decrease in glomerular filtration due to the alterations of tubulo-glumeral regulatory mechanisms [4,8,20,21]. Nicorandil, a K-ATP channel opener and a NO donor, is currently used in the treatment of angina and acute heart failure.…”

“…Contrast-induced nephropathy (CIN), also known as contrast-induced acute kidney injury (CI-AKI) is a well-known, prevalent and serious side effect of the administration of iodine contrast medium after angiocardiography or radiological procedures [1,2]. In clinical studies, CIN is defined as an elevation of serum creatinine level 44.2 µmol/L (0.5 mg/dL) or 25% above the baseline within 48-72 h after contrast administration without an alternative cause [3][4][5]. The exact pathophysiological mechanisms of CIN are complex and remain unclear.…”

Do statins induce or protect from acute kidney injury and chronic kidney disease: An update review in 2018

“…Advanced age, diabetes, congestive heart failure, CKD, hemodynamic instability, and type and volume of contrast may all precipitate the development of CIN. [17] Previous research accentuated that adequate intravenous hydration with iso-osmolar crystalloids and limiting the amount of low-osmolar and iso-osmolar contrast are crucial for prevention of CIN. Several trials in various clinical conditions, including acute coronary syndromes, examined the effect of different types of statins, high-versus low-dose statins and loading versus chronic dosing of statins.…”

Statins role in preventing contrast-induced acute kidney injury: a scoping review

“…Advanced age, type and volume of contrast, pre-existing disease such as congestive heart failure and CKD, and haemodynamic instability are reportedly more likely to influence the development of CI-AKI. 11 Chyou et al 45 demonstrated that increased age, diabetes mellitus, acute coronary syndrome, and CKD are the factors responsible for precipitating the hazard for contrast-induced nephropathy. Further, Chung et al 46 confirmed that there is a 13% increased risk of developing severe renal failure with statin treatment among the highrisk population.…”