CIN is defined as an elevation of serum creatinine (Scr) of more than 25% or ≥0.5 mg/dl (44 μmol/l) from baseline within 48 h after excluding other factors that may cause nephropathy, such as nephrotoxins, hypotension, urinary obstruction, or atheromatous emboli. It is self-limited in most instances, with Scr levels peaking in 3-5 days and gradually returning to baseline levels within 7-10 days.
Prevalence
CIN is one of the major causes of hospital-acquired acute kidney injury (AKI) and represents about 12% of the cases. It is the third most common cause after renal hypoperfusion (42%) and postoperative renal injury (18%).
The reported incidence of CIN after percutaneous coronary intervention (PCI) varies between 0 and 24%, depending on the prevalence of associated risk factors, with the higher incidence being reported after emergency PCI.
A meta-analysis that included 40 studies, found a 6% incidence of CIN after contrast enhanced computed tomography (CT), 9% after peripheral angiography, and 4% after intravenous pyelography.
The incidence of CIN is low in patients with normal renal function (0-5%).However, several prospective controlled trials reported an incidence of 12-27% in patients with preexisting renal impairment. Furthermore, in one study, an incidence as high as 50% was reported in patients with diabetic nephropathy undergoing coronary angiography in spite of the use of low-osmolar CM (LOCM) and adequate hydration. Notably, up to 15% of them required dialysis. Development of CIN is associated with a longer hospital stay, an increased morbidity and mortality, in addition to a higher cost.
Pathophysiology
Although the definite mechanism of CIN is not well-understood, several mechanisms have been proposed
• Renal medullary hypoxia due to either a decrease in vasodilators (nitric oxide or prostaglandins), or an increase in vasoconstrictors (adenosine and endothelin).
• Direct toxicity of CM which could be related to harmful effects of free radicals and oxidative stress. It is thought that activation of cytokine-induced inflammatory mediators by reactive free radicals is the responsible mechanism. Conversely, the inhibition or reduction of free radicals formation might reduce CIN by alkalinizing tubular cells.
• In addition, apoptosis may also play a role in the development of CIN
Risk factors
Multiple risk factors may contribute to the development of CIN; these factors are divided into two groups; patient- and procedure-related.
Preexisting renal insufficiency (estimated glomerular filtration rate (eGFR) <60 ml/min) and diabetes mellitus are the most important patient-related risk factors. Others, include age >75 years, uncontrolled hypertension, hypotension requiring inotropes, congestive heart failure (CHF), use of intra-aortic balloon pump (IABP), anemia, hypoalbuminemia, and liver cirrhosis.
Procedure-related factors include high contrast volume, osmolality or viscosity, and repeated exposures to CM within 72 h. Other factors that may increase the risk of CIN include the concomitant use of diuretics or nephrotoxic drugs (nonsteroidal anti-inflammatory drugs (NSAIDs) and aminoglycosides).
Treatment
There is no definitive treatment available for established CIN; therefore, the benefit for CM-based diagnostic studies or interventional procedures should always be weighed against the risk of CIN. In addition, repeated exposure to CM within a short period of time should be avoided whenever possible.
Prevention strategies
Several pharmacological and nonpharmacological approaches have been evaluated for the prevention of CIN. The prevention strategies are most important in patients at high risk for CIN, such as those with AKI or preexisting chronic kidney disease (CKD). It is well established that minimizing the volume of CM, preventing volume depletion and avoiding activation of renal vasoconstriction are the most effective measures to prevent CIN. In addition, the concomitant use of diuretics or nephrotoxins (e.g. nonsteroidal anti-inflammatory drugs (NSAIDs), cytotoxic drugs, and aminoglycosides) should be avoided