The PREDICT Study: A Randomized Double-Blind Comparison of Contrast-Induced Nephropathy After Low- or Isoosmolar Contrast Agent Exposure (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.
Contrast-induced Nephropathy in a High-risk Patient Population
Interventional Cardiology Review, 2008
Contrast-induced nephropathy (CIN) is one of the most common causes of hospital-acquired acute renal failure. 1,2 The development of CIN after diagnostic coronary angiography and/or percutaneous coronary intervention (PCI) is associated with prolonged hospitalisation and a remarkable increase in morbidity, early and late mortality and costs. 3-6 CIN is an absolute (≥0.5mg/dl) or relative (≥25%) increase in serum creatinine compared with baseline after exposure to a contrast agent when alternative explanations for renal impairment have been excluded. The Contrast-induced Nephropathy Consensus Panel recommended using a relative increase in serum creatinine to define CIN given that this definition is independent of baseline renal function. 7 CIN typically develops within 24-72 hours post-exposure to contrast medium, with renal function returning to baseline level in two weeks. 8-10 The overall incidence of CIN in the general population is <2%. 1,11 In high-risk patients, including the elderly population and patients with chronic renal impairment, diabetes, congestive heart failure and anaemia, the incidence of CIN is much higher (≥20%). 8-10,12,13 Several risk factors have been described for CIN. 6,14 To reliably assess the risk of CIN, a simple risk score (see Figure 1) that can be quickly calculated based on readily available information is strongly recommended. 15 Pathogenesis of Contrast-induced Nephropathy The pathogenesis of CIN is not entirely understood. Several pathways of CIN development have been proposed, including altered rheological properties of blood, medullary hypoxia, impaired immunological mechanisms and direct toxic effects of contrast medium on renal epithelial cells and oxidative stress. 16-20 Iodinated contrast is known to provoke acute vasoconstriction due to a release of adenosine, endothelin and other renal vasoconstrictor agents. Apoptosis has also been implicated as a contributing factor. 21,22 Prevention of Radiocontrast Nephropathy The unfavourable prognostic implications of CIN in high-risk populations make preventing this condition of paramount importance. 20 Hydration Volume supplementation results in plasma volume expansion followed by suppression of the renin-angiotensin-aldosterone system and downregulation of tubuloglomerular feedback, leading to the attenuation of renal cortical vasoconstriction and tubular obstruction triggered by contrast agents. 23,24 The positive effect of adequate hydration in reducing CIN rates was first established in the randomised study by Solomon et al. 25 In patients with mild to moderate renal insufficiency, 0.45% saline administration at a rate of 1ml/kg/hour for 12 hours pre-and post-procedure was more effective in the prevention
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 (X0.5 mg/dl) or relative increase (X25%) 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]
Acta medica portuguesa, 2011
Contrast-induced nephropathy (CIN) is an iatrogenic disorder, resulting from procedures requiring the intravascular administration of iodinated contrast media. It has an association with increased morbidity and mortality, increased costs and it remains the third most common cause of hospital-acquired kidney failure. CIN is usually defined as an increase in serum creatinine by either at least 0.5 mg/dl or by 25% from baseline within the first 48 hours after contrast administration, in the absence of other causes of renal function impairment. In its pathogenesis have been implicated 2 main mechanisms: renal vasoconstriction resulting in medullary hypoxia and direct cytotoxic effects of the contrast agents. There are several risk factors for radiocontrast nephrotoxicity but patients with underlying renal insufficiency or diabetic nephropathy with renal insufficiency have the greatest risk. Other classic risk factors include: advanced age, peri-procedural intravascular depletion, conges...
Contrast Agents and Contrast-Induced Nephropathy
International Journal of Clinical Medicine, 2015
Recent advances in medical sciences, especially in imaging, have dramatically increased the use of contrast agents. The constantly changing nature of medicine and the availability of new information, such as new pharmaceutical formulations, have necessitated periodic revisions and drafting of new guidelines for the safe use of intravenous contrast agents in radiology. This study examined the majority of guidelines, articles, and authoritative references available on the use of intravenous contrast agents in adults to reduce the risk of contrast-induced nephropathy. The search engines of PubMed, Web of Science, Scopus, and Google Scholar were used, and relevant English articles cited at least twice between 1979 and 2014 were studied. Review of the collected papers showed no consensus among them for guidelines on the incidence of contrast-induced nephropathy in patients at risk. Different formulas were used to calculate estimated glomerular filtration rate, which could be problematic in some cases. Further studies are needed for unification of existing guidelines.
Preventing Nephropathy Induced by Contrast Medium
New England Journal of Medicine, 2006
A 71-year-old man with type 2 diabetes and hypertension is referred for coronary angiography. His medications include metformin and a thiazide. Before the angiogram, his serum creatinine level is 1.8 mg per deciliter (160 μmol per liter), yielding an estimated glomerular filtration rate of 40 ml per minute per 1.73 m 2 of body-surface area. What can be done to reduce the risk that an angiographic contrast medium will worsen his kidney function?
Renal Failure, 2021
Intravenous contrast media (CM) is often used in clinical practice to enhance CT scan imaging. For many years, contrast-induced nephropathy (CIN) was thought to be a common occurrence and to result in dire consequences. When treating patients with abnormal renal function, it is not unusual that clinicians postpone, cancel, or replace contrast-enhanced imaging with other, perhaps less informative tests. New studies however have challenged this paradigm and the true risk attributable to intravenous CM for the occurrence of CIN has become debatable. In this article, we review the latest relevant medical literature and aim to provide an evidence-based answer to questions surrounding the risk, outcomes, and potential mitigation strategies of CIN after intravenous CM administration.