Effects of contrast medium exposure on urine albumin/creatinine ratio (original) (raw)
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Incidence of contrast-induced nephropathy a prospective study
Journal of Renal Injury Prevention
Introduction: Contrast-induced acute kidney injury (AKI) is one of the most common causes of hospital-acquired AKI. Objectives: To determine the incidence of contrast induced nephropathy (CIN), to identify significant risk factors associated with CIN and to compare the variations in serum creatinine levels with and without contrast exposure. Patients and Methods: A total of 222 patients (124 males and 98 females with mean age of 48.96 ± 16.74 years) who received iodinated contrast agents during different procedures over a period of 18 months were included in the study. CIN was defined as a relative increase of >25% or an absolute increase of > 0.5 mg/dL in serum creatinine levels 4 days post-procedure. 148 patients (82 males and 66 females with mean age of 47.48 ± 17.21 years) who did not receive any contrast agent were included as controls to determine the frequency with which the variations in serum creatinine levels fulfilled the definition of CIN. Results: The overall incidence of CIN was 12.6%. Incidence of CIN was 32.6% after percutaneous coronary intervention (PCI) and 7.38% after IV contrast exposure (P < 0.0001). Multivariate logistic regression analysis of risk factors revealed heart failure (P = 0.001), pre-procedure serum creatinine level ≥ 1.5 mg/dL (P = 0.005) and nature of contrast agent (P = 0.001), as independent risk factors of CIN. 2.02% patients in control group showed variations in serum creatinine levels within the range corresponding to the definition of CIN. Conclusion: Heart failure, pre-procedural serum creatinine of ≥ 1.5 mg/dL and the nature of contrast agent are independent predictors of CIN.
American Journal of Roentgenology, 2008
OBJECTIVE. Most studies of contrast-induced nephropathy lack controls to distinguish it from nephropathy from other causes. We assessed the frequency and magnitude of serum creatinine changes in patients not receiving iodinated contrast material to compare with creatinine changes in publications regarding contrast nephropathy. MATERIALS AND METHODS. From the electronic medical records of an academic medical center, adults with creatinine determinations on five consecutive days who had not received contrast material during the previous 10 days were identified. The first creatinine level was compared with those on subsequent days. We calculated the frequency with which these levels exceeded thresholds used to identify contrast nephropathy in previous publications. RESULTS. Among 32,161 patients, more than half showed a change of at least 25% and more than two fifths, a change of at least 0.4 mg/dL. Among patients with baseline creatinine levels of 0.6-1.2 mg/dL, increases of at least 25%, 33%, and 50% occurred in 27%, 19%, and 11% of patients, respectively. Increases of 0.4, 0.6, and 1.0 mg/dL occurred in 13%, 7%, and 3% of patients. Among patients with baseline creatinine levels greater than 2.0 mg/dL, increases of at least 25%, 33%, and 50% occurred in 16%, 12%, and 7%. Increases of 0.4, 0.6, and 1.0 mg/ dL occurred in 33%, 26%, and 18%. These increases were not different from the incidences of contrast nephropathy previously published. CONCLUSION. The creatinine level increases in patients who are not receiving contrast material as often as it does in published series of patients who are receiving contrast material. The role of contrast material in nephropathy may have been overestimated.
Clinical Journal of the American Society of Nephrology, 2009
Background and objectives: No prospective study has reported the incidence of contrast-induced nephropathy (CIN) or the associated morbidity and mortality after contrast-enhanced computed tomography (CECT) in the outpatient setting. Design, setting, participants, & measurements: We enrolled and followed a prospective, consecutive cohort (June 2007 through January 2009) of patients who received intravenous contrast for CECT in the emergency department of a large, academic, tertiary care center. Outcomes measured were as follows (1) CIN: An increase in serum creatinine ≥0.5 mg/dl or ≥25% 2 to 7 d after contrast administration; (2) severe renal failure: An increase in serum creatinine to ≥3.0 mg/dl or the need for dialysis at 45 d; and (3) renal failure as a contributing cause of death (consensus of three independent physicians) at 45 d. Results: The incidence of CIN was 11% (70 of 633) among the 633 patients enrolled. Fifteen (2%) patients died within 45 d, including six deaths after study-defined CIN. Seven (1%) patients developed severe renal failure, six of whom had study-defined CIN. Of the six patients with CIN and severe renal failure, four died, and adjudicators determined that renal failure significantly contributed to all four deaths. Thus, CIN was associated with an increased risk for severe renal failure and death from renal failure. Conclusions: CIN occurs in >10% of patients who undergo CECT in the outpatient setting and is associated with a significant risk for severe renal failure and death.
Acta Radiologica, 2010
Contrast Induced Nephropathy (CIN) is a feared complication of numerous radiological procedures that expose patients to contrast media. The most notorious of these procedures is percutaneous coronary intervention (PCI). Not only is this a leading cause of morbidity and mortality, but it also adds to increased costs in high risk patients undergoing PCI. It is thought to result from direct cytotoxicity and hemodynamic challenge to renal tissue. CIN is defined as an increase in serum creatinine by either ≥0.5 mg/dL or by ≥25% from baseline within the first 2-3 days after contrast administration, after other causes of renal impairment have been excluded. The incidence is considerably higher in diabetics, elderly and patients with pre-existing renal disease when compared to the general population. The nephrotoxic potential of various contrast agents must be evaluated completely, with prevention as the mainstay of focus as no effective treatment exists. The purpose of this article is to examine the pathophysiology, risk factors, and clinical course of CIN, as well as the most recent studies dealing with its prevention and potential therapeutic interventions, especially during PCI. The role of gadolinium as an alternative to iodinated contrast is also discussed. Cardiology Research and Practice 2 definitions ([Cr] ≥0.5 mg/dL, ≥25%) consistently predicted adverse events after PCI . Therefore, a complete definition for CIN encompasses absolute (≥0.5 mg/dL) and relative increase (≥25%) in serum creatinine at 48-72 hours after exposure to a contrast agent compared to baseline serum creatinine values, when alternative explanations for renal impairment have been excluded .
Renal Risk of Contrast-Enhanced Imaging – Is It a Myth? The Latest Opinions of the Guidelines
Medicina Moderna - Modern Medicine
Over the last decade, several divergent views have been expressed regarding the effect that iodinated contrast agents may have on renal function. Evidence-based medicine often requires the recommendation of high-performance contrast-enhanced imaging exams for precise positive diagnosis. The fear of intravenous contrast use in patients with elevated serum creatinine seems to become an old dogma, outdated by the benefi ts of the procedures. Patients with glomerular fi ltration rate below 30 mL/min/1.73 m 2 can be protected by peri-procedural hydration and withdrawal of other nephrotoxics. Whatever the degree of risk, current guidelines recommend contrast-enhanced investigations in any situations where the advantages for the diagnosis are certain.
American Journal of Roentgenology, 2008
C ontrastinduced nephropathy (CIN) is usually defined as a sudden, rapid deterioration in renal status after administration of iodinated contrast medium with no alternative clinical explanation [1, 2]. The incidence of CIN in patients with normal renal function is less than 3% but can be much higher in individuals with one or more risk factors for CIN (12-50%) [3-7]. Most studies define CIN as an increase in the serum creatinine value (≥ 0.5 mg/dL, ≥ 25%, or both) or a diminution of renal function identified by a decrease in creatinine clear ance or the estimated glomerular filtration rate (GFR) 2-3 days after contrast medium exposure [8, 9]. Recently, investigators have
Canadian Association of Radiologists Journal, 2014
The development of acute renal failure significantly complicates intravascular contrast medium (CM) use and is linked with high morbidity and mortality. The increasing use of CM, an aging population, and an increase in chronic kidney disease (CKD) will result in an increased incidence of contrast-induced nephropathy (CIN)-unless preventive measures are used. The Canadian Association of Radiologists has developed these guidelines as a practical approach to risk stratification and prevention of CIN. The major risk factor predicting CIN is preexisting CKD, which can be predicted from the glomerular filtration rate (GFR). In terms of being an absolute measure, serum creatinine (SCr) is an unreliable measure of renal function.