The Experts below are selected from a list of 20100 Experts worldwide ranked by ideXlab platform
Omer Toprak - One of the best experts on this subject based on the ideXlab platform.
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What is the best definition of Contrast-Induced Nephropathy?
Renal Failure, 2009Co-Authors: Omer ToprakAbstract:Radiological procedures require the intravascular administration of iodinated contrast media, which are becoming a great source of an iatrogenic disease known as Contrast-Induced Nephropathy. The development of Contrast-Induced Nephropathy is associated with prolonged hospitalization, the potential need for renal replacement therapy, and increased mortality. Despite numerous clinical and experimental studies, several important issues regarding Contrast-Induced Nephropathy remain controversial. One of the controversial points is its very definition: a universally accepted definition of Contrast-Induced Nephropathy does not exist. This can be a major problem. Differing definitions of Contrast-Induced Nephropathy and the clinical importance of these definitions were discussed in this letter.
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Interactions between serum creatinine, volume status, N-acetylcysteine, and Contrast-Induced Nephropathy.
Renal Failure, 2009Co-Authors: Omer ToprakAbstract:Contrast-Induced Nephropathy is reported to be the third leading cause of acute renal failure. The development of Contrast-Induced Nephropathy is associated with prolonged hospitalization, the potential need for renal replacement therapy, and increased mortality. N-acetylcysteine is commonly used for the prevention of Contrast-Induced Nephropathy despite inconsistent results from numerous clinical trials and meta-analyses. The advantage of N-acetylcysteine in most studies was based on a decrease in the serum creatinine concentration and a decrease in oxidative stress. N-acetylcysteine itself can directly lower serum creatinine concentration without improving renal function, and hypovolemia can affect the oxidative stress. In most of the N‐acetylcysteine studies, there are a lack of volume status and secondary end points. The value of N-acetylcysteine for the prevention of Contrast-Induced Nephropathy seems questionable. The interactions between serum creatinine, N-Acetylcysteine, volume status, and the de...
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Conflicting and New Risk Factors for Contrast Induced Nephropathy
The Journal of Urology, 2007Co-Authors: Omer ToprakAbstract:Purpose: Iodinated contrast medium is commonly used in diagnostic or interventional procedures in uroradiology. Procedures requiring the intravascular administration of iodinated contrast medium are becoming a great source of an iatrogenic disease known as contrast induced Nephropathy. Identifying patients at high risk is the first step to minimize the overall risk of contrast induced Nephropathy. This review describes conflicting and new risk factors for contrast induced Nephropathy.Materials and Methods: A MEDLINE®/PubMed® search from 1966 to 2006 was performed. All articles related to the use of contrast medium and the risk factors for contrast induced Nephropathy were reviewed.Results: The classic risk factors for contrast induced Nephropathy are preexisting renal failure, diabetes mellitus, advanced age, nephrotoxic agent administration, hypovolemia, use of a large amount of contrast medium or an ionic hyperosmolar contrast medium and congestive heart failure. Metabolic syndrome, prediabetes and hype...
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Risk markers for Contrast-Induced Nephropathy.
The American Journal of the Medical Sciences, 2007Co-Authors: Omer ToprakAbstract:ABSTRACT Radiological procedures requiring intravascular administration of iodinated contrast media are becoming a common source of an iatrogenic disease known as Contrast-Induced Nephropathy (CIN). The treatment of established CIN is limited to supportive measures and dialysis. Therefore, identifying high-risk patients is the first step to minimize the overall risk of CIN. The purpose of this review is to describe classic and possible risk markers of CIN according to the ultimate clinical research and developments. Original publications, review articles, papers from our personal library, and guidelines on CIN were reviewed. Terms used for PubMed and Medline searches were as follows: “Contrast-Induced Nephropathy,” “radio-contrast Nephropathy,” “contrast Nephropathy,” “contrast medium-induced Nephropathy,” “contrast media,” and “risk factors.” No restriction was placed on date of publication. Preexisting renal failure, especially when secondary to diabetic Nephropathy, is the most important risk marker for CIN.
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Angiotensin converting enzyme inhibitors and Contrast-Induced Nephropathy.
Renal Failure, 2006Co-Authors: Omer ToprakAbstract:The available data on the use of angiotensin-converting enzyme inhibitors, and the associated risks for Contrast-Induced Nephropathy are sparse and conflicting. Nevertheless, it is a common practice to hold angiotensin-converting enzyme inhibitors before contrast media administration. The reduction of renal blood flow that occurs following the administration of contrast media may be due to the renin-angiotensin–aldosterone system causing constriction of the afferent arterioles. The influence of angiotensin–converting enzyme inhibitor administration on the development of Contrast-Induced Nephropathy was discussed in this letter.
Alexandra J Lansky - One of the best experts on this subject based on the ideXlab platform.
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low hematocrit predicts contrast induced Nephropathy after percutaneous coronary interventions
Kidney International, 2005Co-Authors: Zoran Lasic, Gary S Mintz, Eugenia Nikolsky, Roxana Mehran, Alexandra J LanskyAbstract:Low hematocrit predicts Contrast-Induced Nephropathy after percutaneous coronary interventions. Background The relationship between low hematocrit and Contrast-Induced Nephropathy has not been investigated. Methods Of 6,773 consecutive patients treated with percutaneous coronary intervention, Contrast-Induced Nephropathy (an increase of ≥25% or ≥0.5mg/dL in preprocedure serum creatinine, at 48 hours postprocedure) occurred in 942 (13.9%) patients. Results Rates of Contrast-Induced Nephropathy steadily increased as baseline hematocrit quintile decreased (from 10.3% in the highest quintile to 23.3% in the lowest quintile) (χ 2 for trend, P P 5.9% had almost doubled rates of Contrast-Induced Nephropathy compared with patients with hematocrit change P Conclusion Lower hematocrit is an important risk factor for Contrast-Induced Nephropathy. Whether correcting the hematocrit prepercutaneous coronary intervention might decrease the rates of Contrast-Induced Nephropathy should be addressed in a prospectively designed trial.
Christopher I. Doty - One of the best experts on this subject based on the ideXlab platform.
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Update: Prevention of Contrast-Induced Nephropathy in the emergency department.
Annals of emergency medicine, 2008Co-Authors: Richard Sinert, Christopher I. DotyAbstract:Some studies have suggested that there exist therapies that can prevent Contrast-Induced Nephropathy, which are practical in an emergency setting. This evidence-based emergency medicine (EBEM) critical appraisal reviews the literature, including additional studies appearing since the publication of an earlier EBEM review in 2007. The updated search for randomized controlled trials from 2006 to 2008 complemented the previous search from 1966 to 2005. The methodological quality of the studies was assessed. Qualitative methods were used to summarize the study results. The search identified 2 studies not included in the previously published review of prophylactic therapies against Contrast-Induced Nephropathy, yielding a total of 4 blinded, randomized, placebo-controlled trials involving bicarbonate and ascorbic acid. The present study of bicarbonate found a similar benefit as the previously reviewed bicarbonate trial. The early termination of both bicarbonate studies presents significant analytical concerns. The present study of ascorbic acid failed to reproduce the prophylactic effect of ascorbic acid observed in the previously reviewed trial. This difference in outcomes of the 2 ascorbic acid trials is related to variations in the volume of contrast and procedural hydration between the studies. Although bicarbonate should still be considered a low-risk prophylactic agent, it appears that other factors (type of contrast agent, volume of contrast, and procedural hydration protocol) have an important influence on the risk of Contrast-Induced Nephropathy. For the emergency physician, limiting exposure to contrast agents and adequate precontrast hydration are still the first line of defense against Contrast-Induced Nephropathy.
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Update: Prevention of Contrast-Induced Nephropathy in the Emergency Department
Annals of Emergency Medicine, 2007Co-Authors: Richard Sinert, Christopher I. DotyAbstract:Study objective Contrast-Induced Nephropathy is the third leading cause of hospital-acquired acute renal failure. Expanded use of contrast-enhanced imaging exposes an ever-widening number of patients to this renal toxin. We perform an evidence-based emergency medicine review comparing different therapies to prevent Contrast-Induced Nephropathy. We limit our review to prophylactic therapies that are practical for an emergency department setting. Methods We searched MEDLINE, EMBASE, and the Cochrane Library for randomized trials comparing a wide range of medications to prevent Contrast-Induced Nephropathy. We defined Contrast-Induced Nephropathy by a commonly used surrogate measure of renal failure: a 25% or 0.5 mg/dL absolute increase in serum creatinine level from baseline 48 to 72 hours postcontrast. We limited our review to only trials for patients with baseline renal insufficiency, who are most at risk for Contrast-Induced Nephropathy. We excluded prophylactic protocols requiring more than 2 hours precontrast to initiate and any trials of experimental medications or those that required invasive monitoring. We used standard criteria to appraise the quality of published trials. Results We found 7 randomized trials; 3 using N -acetylcysteine, 2 using theophylline, and 1 each using bicarbonate and ascorbic acid. Although many of these trials showed statistically significant reductions in the risk for Contrast-Induced Nephropathy, none were sufficiently powered to detect reductions in mortality rate or the need for dialytic therapy. Conclusion Evidence from randomized trials shows that these interventions (theophylline, bicarbonate, and ascorbic acid) under review were appropriate to an ED setting and decreased the risk of Contrast-Induced Nephropathy. The case for the effectiveness ( N -acetylcysteine) was less certain.
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Evidence-based emergency medicine review. Prevention of Contrast-Induced Nephropathy in the emergency department.
Annals of Emergency Medicine, 2007Co-Authors: Richard Sinert, Christopher I. DotyAbstract:STUDY OBJECTIVE: Contrast-Induced Nephropathy is the third leading cause of hospital-acquired acute renal failure. Expanded use of contrast-enhanced imaging exposes an ever-widening number of patients to this renal toxin. We perform an evidence-based emergency medicine review comparing different therapies to prevent Contrast-Induced Nephropathy. We limit our review to prophylactic therapies that are practical for an emergency department setting. METHODS: We searched MEDLINE, EMBASE, and the Cochrane Library for randomized trials comparing a wide range of medications to prevent Contrast-Induced Nephropathy. We defined Contrast-Induced Nephropathy by a commonly used surrogate measure of renal failure: a 25% or 0.5 mg/dL absolute increase in serum creatinine level from baseline 48 to 72 hours postcontrast. We limited our review to only trials for patients with baseline renal insufficiency, who are most at risk for Contrast-Induced Nephropathy. We excluded prophylactic protocols requiring more than 2 hours precontrast to initiate and any trials of experimental medications or those that required invasive monitoring. We used standard criteria to appraise the quality of published trials. RESULTS: We found 7 randomized trials; 3 using N-acetylcysteine, 2 using theophylline, and 1 each using bicarbonate and ascorbic acid. Although many of these trials showed statistically significant reductions in the risk for Contrast-Induced Nephropathy, none were sufficiently powered to detect reductions in mortality rate or the need for dialytic therapy. CONCLUSION: Evidence from randomized trials shows that these interventions (theophylline, bicarbonate, and ascorbic acid) under review were appropriate to an ED setting and decreased the risk of Contrast-Induced Nephropathy. The case for the effectiveness (N-acetylcysteine) was less certain.
Paolo Rizzotti - One of the best experts on this subject based on the ideXlab platform.
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Early creatinine shifts predict Contrast-Induced Nephropathy and persistent renal damage after angiography.
The American Journal of Medicine, 2010Co-Authors: Flavio Ribichini, Maria Stella Graziani, Paolo Pasoli, Michele Pighi, Gabriele Pesarini, Tewoldemedhn Yabarek, Sandra Brunelleschi, Giovanni Gambaro, Cataldo Abaterusso, Paolo RizzottiAbstract:Abstract Purpose The purpose of this study was to evaluate incidence and predictors of Contrast-Induced Nephropathy after coronary angiography and interventions, and to assess renal function at 30 days. The prognostic value of any early shift of serum creatinine compared with baseline was investigated; such measurement, being a delta, is largely independent of creatinine variations. Methods There were 216 patients at risk for Contrast-Induced Nephropathy prospectively evaluated at baseline and at 12, 24, and 48 hours after exposure to contrast media, and 190 (88%) evaluated 1 month after discharge. Results Contrast-Induced Nephropathy occurred in 39 patients (18%), and 30-day renal damage was detected in 15 (7%). Contrast media/kg volume predicted Contrast-Induced Nephropathy ( P =.002), and percentage change of creatinine 12 hours from baseline was significantly higher in patients with Nephropathy ( P P P =.002; sensitivity 87%, specificity 70%; area under the curve 0.85; odds ratio 13.29; 95% confidence interval, 2.91-60.64). Conclusion Minimal elevations of serum creatinine at 12 hours are highly predictive of Contrast-Induced Nephropathy and 30-day renal damage after exposure to contrast media.
Roxana Mehran - One of the best experts on this subject based on the ideXlab platform.
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contrast induced Nephropathy
Catheterization and Cardiovascular Interventions, 2008Co-Authors: Tereza Pucelikova, George Dangas, Roxana MehranAbstract:Contrast induced Nephropathy (CIN) is an iatrogenic disorder, resulting from exposure to contrast media. Contrast-Induced hemodynamic and direct cytotoxic effects on renal structures are highly evident in its pathogenesis, whereas other mechanisms are still poorly understood. CIN is typically 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. Although rare in the general population, CIN has a high incidence in patients with an underlying renal disorder, in diabetics, and the elderly. The risk factors are synergistic in their ability to produce CIN. The best way to prevent CIN is to identify the patients at risk and to provide adequate peri-procedural hydration. The role of various drugs in prevention of CIN is still controversial and warrants future studies. Despite remaining uncertainty regarding the degree of nephrotoxicity produced by various contrast agents, in current practice non-ionic low-osmolar contrast media are preferred over the high-osmolar contrast media in patients with renal impairment. © 2007 Wiley-Liss, Inc.
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low hematocrit predicts contrast induced Nephropathy after percutaneous coronary interventions
Kidney International, 2005Co-Authors: Zoran Lasic, Gary S Mintz, Eugenia Nikolsky, Roxana Mehran, Alexandra J LanskyAbstract:Low hematocrit predicts Contrast-Induced Nephropathy after percutaneous coronary interventions. Background The relationship between low hematocrit and Contrast-Induced Nephropathy has not been investigated. Methods Of 6,773 consecutive patients treated with percutaneous coronary intervention, Contrast-Induced Nephropathy (an increase of ≥25% or ≥0.5mg/dL in preprocedure serum creatinine, at 48 hours postprocedure) occurred in 942 (13.9%) patients. Results Rates of Contrast-Induced Nephropathy steadily increased as baseline hematocrit quintile decreased (from 10.3% in the highest quintile to 23.3% in the lowest quintile) (χ 2 for trend, P P 5.9% had almost doubled rates of Contrast-Induced Nephropathy compared with patients with hematocrit change P Conclusion Lower hematocrit is an important risk factor for Contrast-Induced Nephropathy. Whether correcting the hematocrit prepercutaneous coronary intervention might decrease the rates of Contrast-Induced Nephropathy should be addressed in a prospectively designed trial.