Contrast media-associated nephrotoxicity

Rudnick, Michael R.; Berns, Jeffrey S.; Cohen, Raphael M.; Goldfarb, Stanley

doi:10.1097/00041552-199603000-00005

Cited by 88 publications

(96 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1 It is commonly defined as an acute deterioration of the renal function characterized by a significant increase in serum creatinine levels, usually more than 0.5 mg/dl (44 mmol/L) or 25% of baseline levels, within 24e48 h after exposure to a contrast agent compared to baseline serum creatinine values, when alternative explanations for renal impairment have been excluded. 2 The CIN is associated with increased mortality and morbidity and costs, 3e5 in fact, although usually transient, its resolution needs 1e3 weeks on average, the impairment of renal function may be permanent in some cases with the risk of progression towards chronic renal failure and the necessity of a temporary or permanent dialysis. 6 Prevention is the key to reduce the incidence of CIN and it begins with identification of the high risk patient coupled with appropriate peri-procedural management.…”

Section: Introductionmentioning

confidence: 99%

Risk factors for contrast induced nephropathy: A study among Italian patients

Evola

Lunetta

Macaione

et al. 2012

Indian Heart Journal

View full text Add to dashboard Cite

Atherosclerosis Percutaneous coronary intervention Coronary angiography a b s t r a c tThis study aimed to make a profile of patients at highest risk of developing contrast induced nephropathy (CIN) in order to take appropriate prevention measures. 591 patients undergoing coronary procedures were divided into two groups: patients with (CIN-group) and without (no-CIN) an increase in creatinine level equal or more than 25% from baseline values within 24e48 h after the coronary procedure. All patients underwent an accurate anamnesis, objective exam, hematochemical measurements, and diagnostic exams. The results of this study while confirming that, average age ( p ¼ 0.01), diabetes mellitus IntroductionContrast-induced nephropathy (CIN) is the third leading cause of hospital-acquired acute renal failure, accounting for 10% of all cases of hospital-acquired renal failure. 1 It is commonly defined as an acute deterioration of the renal function characterized by a significant increase in serum creatinine levels, usually more than 0.5 mg/dl (44 mmol/L) or 25% of baseline levels, within 24e48 h after exposure to a contrast agent compared to baseline serum creatinine values, when alternative explanations for renal impairment have been excluded. 2 The CIN is associated with increased mortality and morbidity and costs, 3e5 in fact, although usually transient, its resolution needs 1e3 weeks on average, the impairment of renal function may be permanent in some cases with the risk of progression towards chronic renal failure and the necessity of a temporary or permanent dialysis. 6 Prevention is the key to reduce the incidence of CIN and it begins with identification of the high risk patient coupled with appropriate peri-procedural management. Many studies have been conducted to identify the main risk factors for CIN, in fact many score systems have been proposed 7e12 and increasing number of guidelines have been suggested in literature 13,14 to help lessen the complication of CIN. Available online at www.sciencedirect.com journal homepage: w ww.el sevier.com/locate /ihj i n d i a n h e a r t j o u r n a l 6 4 ( 2 0 1 2 ) 4 8 4 e4 9 1

show abstract

Section: Introductionmentioning

confidence: 99%

Risk factors for contrast induced nephropathy: A study among Italian patients

Evola

Lunetta

Macaione

et al. 2012

Indian Heart Journal

View full text Add to dashboard Cite

show abstract

“…A lthough the clinical features of contrast-induced nephropathy (CIN) have been well described for some time (1,2), during the past 15 yr, interest among physicians on the subject of CIN has dramatically increased. A PubMed search of the phrase "contrast-induced nephropathy" between 1990 and 2007 produced 347 citations.…”

mentioning

confidence: 99%

Contrast-Induced Nephropathy

Rudnick

Goldfarb

Tumlin

2008

Clinical Journal of the American Society of Nephrology

Self Cite

View full text Add to dashboard Cite

A lthough the clinical features of contrast-induced nephropathy (CIN) have been well described for some time (1,2), during the past 15 yr, interest among physicians on the subject of CIN has dramatically increased. A PubMed search of the phrase "contrast-induced nephropathy" between 1990 and 2007 produced 347 citations. During the past 5 yr alone, there were 290 citations, 159 of which appeared since 2006 (3).Intravascular administration of contrast is widely known to be a common cause of hospital-acquired acute kidney injury (AKI). In 1983, Hou et al. (4) prospectively evaluated 2216 patients with hospital-acquired AKI and found decreased renal perfusion and major surgery to be the leading causes of AKI. Contrast medium (CM) was the next most common cause, accounting for 12% of cases of AKI, and was associated with an in-hospital mortality of 6%. In 1987, Shusterman et al. (5) demonstrated that CM was one of four major factors contributing to hospital acquired AKI (the others being volume depletion, congestive heart failure, and aminoglycosides).The exact risk for CIN is difficult to determine. It is widely known that in patients with normal renal function, even in the presence of diabetes, the risk for CIN is Յ1 to 2% (1). In patients with chronic kidney disease (CKD), it is also well accepted that the risk for CIN is significantly increased and rises in proportion to the severity of underlying renal impairment (1,6,7). Another established observation is that the coupling of CKD and diabetes dramatically increases the risk for CIN compared with that observed for CKD alone (6). Recent studies on CIN in "high-risk" patients have demonstrated a wide range of incidences from 1 to 45% (8,9). Reasons for this wide variation in CIN risk include study differences in the number and severity of underlying risk factors, definition of CIN used, prospective or retrospective collection of data, exclusion or nonexclusion of patients with other AKI etiologies, timing of the baseline serum creatinine (SCr) relative to hydration administration, type and amount of CM used, type and amount of hydration, and presence or absence of other prophylactic measures. Unfortunately, the consequence of these multiple factors makes it difficult to state with reasonable accuracy the clinical risk for CIN in a "high-risk" patient. Additional problems caused by the apparently observed wide range of CIN incidences are methodologically inadequate comparisons of studies for the value of procedural or prophylactic strategies to minimize CIN risk and prospective, randomized, controlled trials that are underpowered to answer the question for which they were designed.Despite the uncertainty of the incidence of CIN in "high-risk" patients, there are a number of reasons to believe that CIN will be an increasing cause of hospital-and outpatient-acquired AKI. Use of intravascular contrast is widespread and continues to expand. In 2003, 80 million doses of CM were administered worldwide (10,11). As of 2004, 3.3 million coronary angiograms, 25.7 million c...

show abstract

“…15 The direct renal tubular cytotoxicity is suggested by histological changes such as cell injury and the presence of enzymuria following contrast administration. 16 An increased production of oxygen free radicals was documented in an experimental model of CIN. 17 According to this finding, oxidant-mediated injury has been suggested as a mechanism of cytotoxic effect in the pathogenesis of CIN.…”

Section: A) Direct Cytotoxic Effectmentioning

confidence: 99%