Radiocontrast media (RCM) are medical drugs used to improve the visibility of internal organs and structures in X-ray based imaging techniques. They may have side effects ranging from itching to a life-threatening emergency, known as contrast-induced nephropathy (CIN). We define CIN as acute renal failure occurring within 24–72 hrs of exposure to RCM that cannot be attributed to other causes. It usually occurs in patients with preexisting renal impairment and diabetes. The mechanisms underlying CIN include reduction in medullary blood flow leading to hypoxia and direct tubule cell damage and the formation of reactive oxygen species. Identification of patients at high risk for CIN is important. We have reviewed the risk factors and procedures for prevention, providing a long list of references enabling readers a deep evaluation of them both. The first rule to follow in patients at risk of CIN undergoing radiographic procedure is monitoring renal function by measuring serum creatinine and calculating the eGFR before and once daily for 5 days after the procedure. It is advised to discontinue potentially nephrotoxic medications, to choose radiocontrast media at lowest dosage, and to encourage oral or intravenous hydration. In high-risk patients N-acetylcysteine may also be given.

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Side Effects of Radiographic Contrast Media: Pathogenesis, Risk Factors, and Prevention

A recent report has suggested that contrast mediainduced nephropathy (CMIN) is the third highest cause of hospital-acquired acute renal failure [1]. In nearly half of these patients, CMIN occurred during cardiac diagnostic or interventional procedures such as percutaneous coronary intervention. However, considering the amount of contrast media (CM) used today in extracardiac diagnostic procedures, the incidence of nephropathy still remains relatively low. This low incidence may be attributed to the introduction and use of nonionic, lowor iso-osmolal compounds, to the use of smaller volumes of CM and to an increasing awareness of patients who may be at risk for impairment of renal function. The latter is especially true in patients with pre-existing renal failure, diabetes, or both. Understandably, the reason a number of patients develop acute renal failure following a cardiac procedure is the necessity to perform these procedures in the presence of pre-existing, and often non-modifiable, risk factors for renal impairment. Permanent impairment of renal function requiring dialysis can occur in up to 10% of patients with preexisting renal failure who develop further reduction in renal function after coronary angiography [2], or in <1% of all patients who undergo percutaneous coronary intervention using CM [3]. In-hospital mortality after acute renal failure requiring dialysis in these patients could reach 36% [3], even if this rate might be due to the effects of eventually coexisting comorbidities [4,5]. In most studies, CMIN is defined as an acute decrease in renal function after intravascular administration of CM in the absence of other causes. It is expressed as an increase in serum creatinine levels of 0.5mg/dl (or 44 mmol/l) or a 25% or greater relative increase from baseline 48–72 h after a diagnostic or interventional procedure [6], even if the clinical significance of this definition in the absence of preexisting chronic renal failure is questionable. Nonionic and ionic iodinated contrast media are currently classified, at the concentrations required for diagnostic or interventional radiologic and cardiac procedures, according to their osmolality compared with the osmolality of plasma. The high-osmolal contrast media (osmolality 1500–1800mOsm/kg) are first generation agents. In fact, the so-called low-osmolal contrast media still have an increased osmolality compared with plasma (600–850mOsm/kg), while the newest nonionic radiocontrast agents have a lower osmolality, 290mOsm/kg, iso-osmolal to plasma (Table 1).

Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art.

Contrast-induced nephropathy (CIN) is a serious complication of angiographic procedures resulting from the administration of contrast media (CM). It is the third most common cause of hospital acquired acute renal injury and represents about 12% of the cases. 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. More sensitive markers of renal injury are desired, therefore, several biomarkers of tubular injury are under evaluation. Multiple risk factors may contribute to the development of CIN; these factors are divided into patient- and procedure-related factors. Treatment of CIN is mainly supportive, consisting mainly of careful fluid and electrolyte management, although dialysis may be required in some cases. The available treatment option makes prevention the corner stone of management. This article will review the recent evidence concerning CIN incidence, diagnosis, and prevention strategies as well as its treatment and prognostic implications.

Contrast-induced Nephropathy.

During a 14-month period, 75 deaths occurring in relation to 53,581 cardiac catheterizations were consecutively and prospectively reported to the Registry Committee of the Society for Cardiac Angiography. Three of the patients died several days after their catheterization from an unrelated cause and are excluded from this analysis. There were 21 patients (group I) who arrived at the laboratory in extremis and whose deaths were expected irrespective of the catheterization. Most of these patients suffered from recent myocardial infarctions and cardiogenic shock, or had complex congenital malformations. In 35 patients (group II), a cardiovascular complication occurring during the catheterization resulted in death. In 16 patients (group III) catheterization seemed uneventful, but death occurred suddenly 10 min to 10 h after the procedure. Of these 16 patients, eight had left main coronary artery obstruction greater than or equal to 90%, five had three-vessel disease all with 90% obstructions, one had 2-vessel disease both with 90% obstructions, and who had critical aortic stenosis. The 51 unexpected deaths (groups II and III) were considered to be causally related to the procedure, a mortality rate of 0.10%. Subsets with an increased mortality rate (M), were patients with: a) left main disease greater than 50% (M = 0.94%); b) ejection fraction less than 30% (M = 0.54%); c) NYHA class III or IV (m = 0.24%); d) age over 60 years (M = 0.23%); or e) three-vessel disease (M = 0.13%). In conclusion, catheterization related mortality occurs mostly in patients with far advanced cardiac disease. Nearly 1/3 of the unexpected deaths occurred suddenly after a seemingly uneventful procedure. Close monitoring after catheterization of patients with similar characteristics (left main disease greater than or equal to 90%, or three-vessel disease all greater than or equal to 90%) might disclose avenues for reducing mortality occurring after catheterization.

Mortality related to cardiac catheterization and angiography.

Objective:Global incidence of contrast-induced nephropathy (CIN) is 2–5%, but a recent Kenyan study highlighted a local incidence of 12–14% without offering an explanation for the higher incidence. This study proposes that inflammatory states confer a higher relative risk for development of CIN. Our objective was to determine the risk of developing CIN given the presence of an inflammatory state in patients in Kenya.Methods:Prospective cohort study of patients undergoing a contrast-enhanced CT (CECT) scan in a private university teaching hospital in Kenya and having no known risk factors for CIN. 423 patients were recruited and grouped into those without inflammation (unexposed) having serum C-reactive protein (CRP) levels ≤5 mg dl−1 and those with evidence of inflammation having CRP levels >5 mg dl−1. Serum creatinine (SCr) was measured before the CECT and 48 h following the CECT with CIN diagnosed by an increase of >25% in the SCr from the baseline. Relative risk was determined and multiple logistic reg...

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G. T. Benness

Papers

Contrast media and the kidney.