Contrast-induced nephropathy in invasive cardiology

Abstract

Contrast-induced nephropathy (CIN) is an acute renal injury due to the renal toxicity of iodinated contrast media. It is classically defined as a relative (≥25%) or absolute (≥0.5 mg/dl; 44 μmol/l) increase in serum creatinine from baseline value. CIN accounts for 10 to 15% of hospital-acquired acute renal failure and may rarely lead to irreversible renal function loss. Following percutaneous coronary intervention, reported incidence of CIN varies between 0 to more than 20%, depending on the prevalence of risk factors and used definition. Nowadays, the diagnosis of CIN relays on serum creatinine monitoring, although it is a late marker of acute kidney injury. Given the expanding number of percutaneous coronary interventions made in outpatient settings and the morbidity and mortality associated with CIN, early detection of CIN is of utmost clinical relevance. Several plasmatic and urinary biomarkers have been studied in that view, with plasmatic cystatine-C and urinary NGAL being the most promising. As no treatment specifically targets CIN once it develops, the main goal for clinicians remains prevention, with hydration status optimisation being the only proven strategy to date. Here, we will review the recent evidence concerning CIN, its incidence, proposed early diagnostic biomarkers, as well as its treatment and prognostic implication.

A Comparison of Nephrotoxicity of Contrast Medium in Elderly Patients who Underwent Renal or Peripheral Arterial Vascular Intervention

“…This suggests that the application of iodixanol was safe in the study population. This is consistent with previous reports indicating that iodixanol has a good safety profile, which is similar or superior to low-osmolar CM (23,24) and superior to high-osmolar CM (25).…”

The Incidence of Contrast-Induced Nephropathy in Saudi Population after Cardiac Catheterization

“…Contrast-induced nephropathy is one of the most common causes of hospital-acquired acute kidney injury. The incidence of CIN varies between 0 and 24% according to multiple risk factors [5]. It is a transient and reversible form of acute kidney injury.…”

Is Melatonin Protective in Contrast Material Related Renal Failure?

“…Under normal situations, it is freely filtered by the glomeruli and totally reabsorbed in the proximal tubule. In the absence of tubular dysfunction, its serum level reflects glomerular filtration and can be used as a functional marker for acute and chronic changes in GFR (12,13) Melatonin and its metabolites force the antioxidant system to work through free radicals. An antioxidant enhances the synthesis of enzymes and increases the efficiency of other antioxidants (14).…”

“…Melatonin and its metabolites possess free radical scavenging activities (11). Melatonin has both receptor-mediated and receptor-independent actions and is believed to affect all cells (12,13). Melatonin increases mRNA and protein levels of antioxidant enzymes.…”