Contrast-induced nephropathy: definition, epidemiology, and patients at risk

Radiological procedures utilizing intravascular iodinated contrast media injections are being widely applied for both diagnostic and therapeutic purposes. This has resulted in an increasing incidence of procedure-related contrast-induced nephropathy (CIN). The definition of CIN includes absolute (> or = 0.5 mg/dl) or relative increase (> or = 25%) in serum creatinine at 48-72 h after exposure to a contrast agent compared to baseline serum creatinine values, when alternative explanations for renal impairment have been excluded. Although the risk of renal function impairment associated with radiological procedures is low (0.6-2.3%) in the general population, it may be very high in selected patient subsets (up to 20%), especially in patients with underlying cardiovascular disease. This review provides information on the known risk factors for the development of CIN, and completes with describing user-friendly CIN risk score based on the readily available information.     

Contrast-induced nephropathy

Interventional radiological procedures involving anaesthesiaare generally increasing. Contrast-induced nephropathy (CIN),usually defined as an increase in serum creatinine of 44 µmollitre^–1 (0.5 mg dl^–1) or a 25% increase from thebaseline value 48 h after intravascular injection of contrastmedia, is a common and potentially serious complication of theuse of iodinated contrast media in patients at risk of acuterenal injury. It is an important cause of hospital-acquiredrenal failure, may be a difficult differential diagnosis andthe incidence does not appear to have changed over the lastfew decades. In the general population, the incidence of CINis estimated to be 1–2%. However, the risk for developingCIN may be as high as 50% in some patient subgroups, such asthose with diabetes mellitus and pre-existing renal impairment.The impact of CIN on clinical outcomes has been evaluated mostextensively in patients undergoing percutaneous coronary interventionwhere it is associated with increased mortality both in hospitaland at 1 yr. As treatment is limited to supportive measureswhile awaiting the resolution of the renal impairment, emphasisneeds to be directed at prevention.     

Contrast-induced nephropathy

Contrast-induced nephropathy (CIN) has been extensively studied since the 1950s due, in part, to its devastating adverse events. The intellectual push for additional investigation into pathogenesis and prevention has heightened in recent years due to increased utilization of contrast enhanced imaging studies. Lack of a universal CIN definition and varied glomerular filtration rate markers have resulted in a varied reported incidence. Risk assessment and risk reduction strategies have evolved over the past several years. Current evidence supports volume supplementation before the administration of intravascular contrast to reduce the hazard of CIN. Other strategies to reduce the risk of CIN, including low osmolar contrast media, N-acetylcysteine, and intrarenal fenoldopam therapy, have variable levels of evidence, and further randomized trials are necessary.     

Breast cancer risk assessment and risk reduction

Until recently, the primary message of breast health awareness programs was that early detection is a woman's best protection against breast cancer, because there was no way to prevent it. Currently, however, tamoxifen is approved for chemoprevention of breast cancer in high-risk women, and studies are underway evaluating other medications that may decrease breast cancer risk. Data have also become available regarding the efficacy of surgical strategies to reduce breast cancer risk. Any prevention method, however, will have associated risk of complications or adverse effects, and determining the net risk/benefit ratio depends on the ability to accurately quantify a woman's baseline likelihood of developing breast cancer. This article reviews available methods for assessing and reducing breast cancer risk.     

Contrast-induced nephropathy: pathogenesis and prevention

Contrast-induced nephropathy (CIN) is the third most common cause of acute kidney injury in hospitalized patients. Diagnostic and interventional cardiovascular procedures generate nearly half the cases. Elderly patients and those with chronic kidney disease, diabetes, and cardiovascular disease are at greatest risk. Procedure-related risk factors include large volumes of contrast and agents with a high osmolality. Renal medullary ischemia arising from an imbalance of local vasoconstrictive and vasodilatory influences coupled with increased demand for oxygen-driven sodium transport may be the key to its pathogenesis. Contrast agents may also have a direct cytotoxic effect that operates through the generation of reactive oxygen species. Pre- and post-procedure administration of normal saline, isotonic sodium bicarbonate, N-acetylcysteine, and a variety of other pharmacologic agents have been used to prevent or mitigate CIN. While normal saline is generally accepted as protective against CIN, uncertainty still surrounds the role of sodium bicarbonate and N-acetylcysteine. Dialytic therapies before, during, and after exposure to contrast have been tested with mixed results. Logistical and economic disincentives argue against these modalities.     

Contrast-induced nephrotoxicity: the effects of vasodilator therapy.

The increasingly frequent use of contrast-enhanced imaging for diagnosis or intervention in patients with peripheral vascular disease has generated concern about the incidence and avoidance of contrast-induced nephrotoxicity (CIN). In this prospective study, we sought to identify those patients at greater risk of developing CIN and to evaluate the efficacy of vasodilator therapy with dopamine in limiting this complication. Baseline serum creatinine (Cr) concentrations were obtained on admission and daily for up to 72 hr after angiography in 222 patients undergoing 232 angiographic procedures. The preangiographic treatment was varied at 2-month intervals for 1 year. All patients received an intravenous infusion of 5% dextrose and 0.45% normal saline at a rate of 75 to 125 ml/hr. During the first interval patients received 12.5 g of 25% mannitol immediately prior to their contrast load, in addition to intravenous fluids. During the next 2-month period the patients were given renal dose dopamine intravenously (3 micrograms/kg/min) commencing the evening before angiography and continued to the next morning. During the latter half of the study the treatment regimens were modified so that the use of mannitol was restricted to patients with diabetes mellitus and dopamine to patients with serum creatinine concentrations of > or = 2 mg/dl. Postangiographic elevation in Cr occurred in 2, 10.4, and 62% of studies in patients with baseline creatinine levels of < or = 1.2 mg/dl, 1.3 to 1.9 mg/dl, and > or = 2.0 mg/dl, respectively. None of the patients receiving dopamine experienced an elevation in creatinine. There was no statistical correlation between age, diabetes, or medication with calcium channel blockers and CIN.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evidence-based perioperative risk reduction

Canadian Journal of Anesthesia/Journal canadien d'anesthésie -     

造影剂肾病的防治进展

造影剂肾病（Contrast—induced nephropathy,CIN）的发病率逐年攀升,已经成为医源性急性肾功能衰竭的重要原因之一。因此,CIN近年来备受关注。关于CIN的研究工作,目前主要集中在危险因素、发病机制及防治措施等方面,其防治主要集中于水化疗法、N-乙酰半胱氨酸、钙离子拮抗剂以及干预肾小管上皮细胞凋亡等防治措施的研究。本文将就近年来CIN的防治进展作一综述。     

Contrast-induced nephrotoxicity: clinical landscape

Over 80 million doses of iodinated intravascular contrast media (CM) were administered in the most recent tabulations of 2003, corresponding to approximately 8 million liters, making it one of the highest volume medical drugs used compared to any other pharmaceutical. The evolution of CM has focused on minimizing adverse events by eliminating ionicity, increasing hydrophilicity, lowering osmolality and increasing the number of iodine atoms per molecule. Contrast media are classified into three general categories based on their osmolality relative to blood: high osmolar (5 times or greater than blood), low osmolar (2-3 times blood) and iso-osmolar (the same as blood). All imaging modalities that employ CM, especially computerized tomography (CT), have shown rapid growth. In the last two decades, the use of CT scanning has increased by 800%. From 1979 to 2002, the number of cardiac catheterization procedures in the USA increased by 390% and in Europe from 1992 to 1999 by 112%. There is a general consensus that renal insufficiency and diabetes are major risk factors for contrast-induced nephropathy (CIN), particularly when co-existing. The US Renal Data System documents a 'relentless' increase in kidney failure, projecting a 90% increase by 2010. Diabetes affects 194 million people worldwide and the number is anticipated to increase by 75% by 2025. The unavoidable conclusion is that patient exposure and prevalence of risk factors for CIN will continue to increase.     

Contrast-induced nephropathy: pharmacological prophylaxis

Contrast media-associated acute renal failure represents the third most common cause of in-hospital renal function deterioration after decreased renal perfusion and post-operative renal insufficiency. Although generally benign, this complication is associated with a mortality rate ranging from 3.8 to 64%, depending on the increase of creatinine concentration. Multiple drugs have been tested in an attempt to prevent this complication. Central to the pathophysiology of contrast-induced nephrotoxicity (CIN) is an alteration in renal hemodynamics. In an effort to reverse these hemodynamic changes, vasodilators and diuretics have been tested as prophylactic drugs. However, their effectiveness has not been confirmed. Recently, considerable interest has resulted from the initial positive data on the effectiveness of prophylactic administration of antioxidant compounds, such as acetylcysteine and ascorbic acid. In this review, we focus on the effectiveness of pharmacologic therapies for preventing CIN.     

Contrast-induced nephropathy after peripheral vascular intervention: Long-term renal outcome and risk factors for progressive renal dysfunction

Objective

Contrast-induced nephropathy (CIN) is a frequently used quality outcome marker after peripheral vascular interventions (PVIs). Whereas the factors associated with CIN development have been well documented, the long-term renal effects of CIN after PVI are unknown. This study was undertaken to investigate the long-term (1-year) renal consequences of CIN after PVI and to identify factors associated with renal function deterioration at 1-year follow-up.

Contrast-induced nephropathy and endovascular aortic aneurysm repairs

Editor—We read with interest the review of contrast-inducednephropathy (CIN) by Wong and Irwin.¹ The authors should becommended for an excellent article, but we would like to commentupon CIN and endovascular aortic aneurysm repairs (EVARs).     

Contrast-induced nephrotoxicity in renal allograft recipients

BACKGROUND: Intravenous administration of radiographic contrast agents is an important cause of acute renal failure, accounting for one third of the cases of hospital-acquired acute renal failure in patients with native kidneys. The safety of intravenous contrast has not been studied in renal allograft recipients since the availability of cyclosporine as a maintenance immunosuppressive therapy. As patients with renal transplantation may be at a higher risk of contrast-induced nephrotoxicity (CIN) due to concomitant use of cyclosporine and higher prevalence of diabetes and renal insufficiency, we retrospectively studied development of CIN in these patients. PATIENTS AND METHODS: We identified 44 patients (1988 1997) with functioning renal allograft who underwent different intravenous or intraarterial contrast studies (ICS). Pre- and post-ICS renal function tests were done in 35 of these patients. The following were the various ICS done in these patients: coronary angiogram (6), CT scan with intravenous contrast ( 11), angiogram for evaluation of peripheral vascular disease (11), allograft angiogram with angioplasty (5), pulmonary angiogram (1) and intravenous pyelogram (1). The mean age of the patients was 42 +/- 2.1 years and the mean serum creatinine was 2.3 +/- 0.25 mg/dl (mean +/- SEM). Fourty percent of patients (14 of 35) had diabetes, and 25.7% (9 of 35) had chronic rejection. Ninety four percent (33 of 35) of the patients were taking cyclosporine at the time of ICS. RESULTS: Nine patients had > or = 25% increase in serum creatinine from baseline after ICS. Two of these patients were excluded from the analysis as renal functions in these patients had deteriorated prior to ICS and renal failure was attributed to sepsis. Of the remaining 7 patients, 5 had diabetes and 2 had chronic rejection. Only 4 of these 7 patients with CIN received prophylaxis (I/V hydration) prior to ICS. The baseline serum creatinines were not different in patients who had no change in renal function to those who developed CIN (1.97 +/- 0.20 vs 1.54 +/- 0.17 mg/dl, p = 1.5, mean +/- SEM). More than 50% increase in baseline serum creatinine was seen in only 3 of these 7 patients, 2 of these patients had diabetes and third had chronic rejection and congestive heart failure. None of these patients received prophylaxis for CIN. Dialysis was not required in any patient. Three patients also had a > 25% decrease in baseline serum creatinine after ICS, and all of them had allograft angiography with angioplasty for renal artery stenosis. CONCLUSION: In our retrospective study, the incidence of CIN in renal allograft recipients applying a broader classification of > or = 25% increase in baseline serum creatinine was 21.2% (7 of 33 patients). The incidence of CIN was lower 15.3% (4 of 26) in patients who received intravenous hydration compared to 42.8% (3 of 7) in patients who received no prophylaxis prior to ICS.     

Contrast-induced acute kidney injury: short- and long-term implications

The intravascular administration of iodine-based contrast media remains a common cause of acute kidney injury and a leading cause of iatrogenic renal disease. Past research has elucidated the principal risk factors for contrast-induced acute kidney injury (CIAKI) and helped to establish the efficacy of various interventions for the prevention of this condition. The importance of preventing CIAKI has been underscored by a growing number of studies showing strong associations of CIAKI with serious adverse short- and long-term outcomes. However, it remains unclear whether these associations are causal. This is important because considerable health care resources are used to prevent CIAKI. If CIAKI is a marker, but not a mediator, of serious adverse downstream outcomes, more judicious and selective use of preventive care may be appropriate. Moreover, with an increasing number of studies reporting the underuse of coronary angiography in patients with acute coronary syndrome and underlying chronic kidney disease, presumably in part because of a fear of CIAKI, a clear understanding of whether this condition directly results in adverse downstream outcomes is essential. Careful inspection of past studies that investigated the association of CIAKI with adverse short- and long-term events sheds light on their strengths and weaknesses and provides insight into how future research may be better able to characterize the short- and long-term implications of this iatrogenic condition.     

Contrast-induced nephropathy: current practices among cardiologists

Objective: Contrast-induced nephropathy (CIN) is a serious complication of diagnostic and therapeutic coronary angiography. There are an increasing number of guidelines in the literature to help lessen this complication. Practice patterns in the cardiology community remain relatively unknown. This survey is an effort to better understand such practices. Methods: Questions were written based on the American College of Cardiology (ACC), the American Heart Association (AHA), and the Society of Cardiovascular Angiography and Intervention (SCAI) guidelines to identify cardiologist background and experience. The survey was emailed to 5000 randomly chosen cardiologists in December 2009. Results: A total of 291 responses were received. Among these, 97% reported checking renal function in all patients prior to angiography, 45% checked both estimated glomerular filtration rate (eGFR) and serum creatinine (SCr), 31% checked SCr alone, 19% checked eGFR alone, and 2% checked albumin-to-creatinine (A–C) ratio. Among responding cardiologists, 70% considered eGFR level less than 60 mL/min/1.73 m² a high risk for CIN whereas 25% considered a level less than 30 mL/min/1.73 m² a high risk. Thirty percent used only isosmolar media in high-risk patients, 33% used only low osmolar media, and 37% used either one. Conclusions: There is significant diversity in the measures taken by cardiologists to prevent CIN. More studies and clearer guidelines are needed to unify the practices.     

Bone remodeling markers: Assessment of fracture risk and fracture risk reduction

There is an increasing repertoire of laboratory tests available for assessing the bone remodeling process. Biochemical markers of bone remodeling can be measured in serum or urine, and have a number of potential roles in the management of fracture risk. Differences in remodeling between individuals might be related to fracture risk and could be used to target therapy. Change in remodeling with therapy could be related to fracture risk reduction and the choice of therapy could be influenced by knowledge of bone remodeling. Biochemical therapeutic monitoring may improve patient understanding and therapeutic adherence. The rate of bone remodeling is weakly predictive of fracture risk in individuals who are not receiving therapy; however, it is not clear whether this is independent of other risk factors. There is increasing evidence that change in bone mineral density does not explain fracture risk reduction with antiresorptive therapies, and that therapeutic benefit might be explained by change in bone turnover. Additional studies and information are required to allow these scientific advances to be translated into cost-effective and validated clinical protocols. Optimizing the precision and accuracy of bone turnover assessment remains an important priority.