Atorvastatin facilitates protection against contrast-induced nephropathy in patients undergoing coronary angiography via humoral mediators rather than altered renal hemodynamics

Introduction

Contrast-induced acute kidney injury (CI-AKI) represents a frequently neglected complication of contrast agent use, which is associated with suboptimal treatment outcomes in the subset of patients with coronary artery disease (CAD) [1]. Despite the use of several well-established preventive measures [2], including peri-procedural hydration, limitation of contrast agent dose and the cessation of potentially nephrotoxic agents, the onset of CI-AKI is still common [3]. Recently, numerous studies have lent support to the notion that pre-procedural use of high-dose statins is associated with decreased risk of CI-AKI development [2, 4, 5]. Further reports exploring surrogate endpoints provided insight into the anti-apoptotic effect of statins towards renal tubular cells [6]. Although several molecular pathways have been suggested [6, 7], the effect of both atorvastatin and rosuvastatin on renal hemodynamics remains unknown. Also, the interplay between statins and humoral mediators of cell survival, including anti-apoptotic renalase [8], has not been investigated so far.

Aim

Therefore, the aim of the study was to evaluate the impact of a loading dose of atorvastatin on post-procedural renal hemodynamics and urinary renalase concentration in patients with CAD submitted to coronary angiography.

Material and methods

In this prospective, randomized, single-blind study, 67 statin-naive patients with stable angina scheduled for coronary angiography were randomized to atorvastatin at a dose of 80 mg administered 24 h prior to the procedure (study group; n = 33) or placebo (control group; n = 34). The research complied with the Declaration of Helsinki and was authorized by the local Ethics Committee. All the study participants gave their written informed consent to study enrollment. The primary inclusion criterion was the diagnosis of stable angina with either high pre-test probability of CAD or a positive treadmill electrocardiographic stress test or echocardiographic dobutamine test. The exclusion criteria included cardiogenic shock, pulmonary edema, acute or chronic respiratory failure (blood oxygen saturation < 90%), advanced heart failure with left ventricular ejection fraction (LVEF) < 35%, evidence of renal artery stenosis or hydronephrosis, severe valvular heart disease of any kind, high pulse pressure > 80 mm Hg, tachycardia > 100 bpm or bradycardia < 50 bpm, severe obesity (body mass index > 40 kg/m2), active...


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