Contrast nephropathy and its prevention

Contrast-induced nephropathy is one of the adverse events of diagnostic and therapeutic intravascular application of contrast agent. In general, the condition was defined as an increase in the serum creatinine concentration of more than 44 mmol/l or of more than 25% within 48 hours after the contrast agent administration. Other cause of creatinine increase should be excluded. Contrast-induced nephropathy has been reported to be the third leading cause of acute nephropathy in hospitalized patients, occurring at a rate of 1-6% in unselected population and of 30-50% in high-risk patients. One year mortality can be as high as 45% in high-risk patient population. The most important risk factors are chronic renal insufficiency, diabetes mellitus and high volume of contrast agent. Clinical presentation is mostly asymptomatic, but in some patients acute renal failure with necessity of hemodialysis can occur. Prevention is underlying tool in reducing of contrast-induced nephropathy incidence. It is based on the identification of risk patients, stop of medication which can increase risk of contrast-induced nephropathy and proper hydratation of patients before, during and after the contrast agent administration. In high-risk patients, non-ionic and low-osmolarity contrast agent should be used. Several clinical studies testing different drugs to prevent contrast-induced nephropathy were performed, but no convincing result has been found. Promising substancies are N-acetylcysteine and fenoldopam.     

Comparison of N-acetylcysteine and fenoldopam for preventing contrast-induced nephropathy (CAFCIN)

BACKGROUND: N-acetylcysteine and fenoldopam are commonly prescribed for prevention of contrast mediated nephropathy, however, comparative superiority of either agent is unknown. METHODS: In a prospective, randomized, parallel-group trial, adult cardiac catheterization patients at the university and veterans' hospitals with pre-existing stable renal insufficiency were randomized to N-acetylcysteine 600 mg orally twice daily for 4 doses or fenoldopam 0.1 mcg/kg/min intravenously for a minimum of 8 h. All patients received intravenous hydration with normal saline (5% dextrose in normal saline for diabetics on insulin). Randomization was stratified for diabetes. The primary endpoint was mean change in Scr at 72 h. Secondary endpoint was the incidence of contrast-induced nephropathy (25% increase above baseline Scr or absolute increase of 0.5 mg/dL). RESULTS: Study termination occurred after ninety-five patients (mean age 68+/-10 years, female 25%, diabetic 42%, mean baseline Scr 1.5+/-0.4 mg/dL) were randomized, with 84 completing follow-up (44 N-acetylcysteine, 40 fenoldopam). Overall, there were no significant differences in mean change in Scr at 72 h (N-acetylcysteine 0.20+/-0.72 vs. fenoldopam 0.08+/-0.48 mg/dL, p=0.4) or incidence of contrast-induced nephropathy (N-acetylcysteine 5 vs fenoldopam 8, p=0.4). No differences were detected in subgroup analyses for diabetes, baseline Scr >1.7 or 2.0 mg/dL, gender, age >70 years, or contrast volume >150 mL. Results were similar after multivariate adjustment for diabetes, contrast volume, heart failure and gender. CONCLUSIONS: Our randomized comparison failed to demonstrate a significant difference in the abilities of N-acetylcysteine and fenoldopam to prevent the decline in renal function or the incidence of contrast-induced nephropathy during cardiac catheterization.     

High-dose N-acetylcysteine for the Prevention of Contrast-induced Nephropathy

Background

Whether N-acetylcysteine is beneficial for the prevention of contrast-induced nephropathy is uncertain.

Methods

We conducted a meta-analysis to evaluate the efficacy of high-dose N-acetylcysteine for the prevention of contrast-induced nephropathy. Our prespecified inclusion criteria were as follows: adult subjects; English language literature; administration of high-dose N-acetylcysteine a priori defined as a daily dose greater than 1200 mg or a single periprocedural dose (within 4 hours of contrast exposure) greater than 600 mg; prospective trials of individuals randomized to N-acetylcysteine, administered orally or intravenously, versus a control group; and trials that included the end point of the incidence of contrast-induced nephropathy. Trials that compared N-acetylcysteine with another active treatment were excluded.

Results

Sixteen comparisons of patients randomized to high-dose N-acetylcysteine versus controls met our prespecified inclusion criteria with a total sample size of 1677 subjects (842 assigned to high-dose N-acetylcysteine and 835 assigned to the control arm). The average population age was 68 years, 38.7% were diabetic, and the majority was male (67.8% of reported instances). The weighted mean baseline creatinine of the overall population was 1.58 mg/dL. No significant heterogeneity was detected (P = .09; I² = 34%). The overall effect size assuming a common odds ratio revealed an odds ratio of 0.46 (95% confidence interval [CI], 0.33-0.63) for the occurrence of contrast-induced nephropathy with the use of high-dose N-acetylcysteine. The results of the more conservative random effects approach were similar (odds ratio = 0.52; 95% CI, 0.34-0.78). There was no evidence of publication bias (P = .34).

Conclusion

Our results suggest that high-dose N-acetylcysteine decreases the incidence of contrast-induced nephropathy.     

Role of N-acetylcysteine in prevention of contrast-induced nephropathy after cardiovascular procedures: a meta-analysis

BACKGROUND: Contrast-induced nephropathy is one of the common causes of acute renal insufficiency after cardiovascular procedures. HYPOTHESIS: The objective of this paper was to analyze the published data on the usefulness of N-acetylcysteine in the prevention of contrast-induced nephropathy after these procedures. METHODS: Trials were selected if they were prospective, randomized, controlled, had selected patients with impaired renal function, used low-osmolality, nonionic contrast media intra-arterially, administered a total of four doses of N-acetylcysteine in addition to intravenous saline hydration, and had contrast-induced nephropathy as their primary outcome. Contrast-induced nephropathy was defined as an increase in serum creatinine concentration by >0.5 mg/dl or a 25% increase above baseline at or within 48 h post procedure. Meta-analysis was performed using the Fisher's Combined Test with a measure of effect size. The magnitude of the N-acetylcysteine effect was estimated using random-effects models. Homogeneity was evaluated using the chi-square test of homogeneity and standard Q statistic. Reporting bias was explored by the Rosenthal method. RESULTS: The Fisher's Combined Test was significant at p < 0.005 in favor of N-acetylcysteine. The size of the N-acetylcysteine effect was to reduce contrast-induced nephropathy by 20%. There was a 62% relative risk reduction in contrast-induced nephropathy with N-acetylcysteine using a fixed-effects model, and a 70% relative risk reduction using the random-effects model. In addition, we found that 27 unpublished trials showing no effects of N-acetylcysteine would exist to overturn the combined significance of p < 0.005 of the five trials in our meta-analysis. CONCLUSION: Oral administration of N-acetylcysteine in addition to intravenous saline hydration has a beneficial effect in the prevention of contrast-induced nephropathy after cardiovascular procedures in patients with impaired renal function.     

Acetylcysteine, coronary procedure and prevention of contrast-induced worsening of renal function: which benefit for which patient?

OBJECTIVES: This study was designed to determine whether acetylcysteine could provide a protective effect on renal function in a population of patients with normal renal function or mild to moderate chronic renal failure, usually referred for a coronary procedure. BACKGROUND: Contrast-induced nephropathy is a well-recognized complication of coronary angiography. Recent studies suggest that saline hydration and acetylcysteine reduce the incidence of contrast-induced worsening of renal function in patients with pre-existing chronic renal failure who are undergoing computed tomography examinations. METHODS: One hundred eight patients were blindly and randomly assigned to receive either acetylcysteine or placebo before and after administration of contrast agent in association with a moderate hydration protocol. Serum creatinine and urea nitrogen were measured before and 24 hours after coronary procedure. RESULTS: The mean serum creatinine concentration remained unchanged 24 hours after contrast agent administration in both groups: from 1.04 +/- 0.26 to 1.03 +/- 0.29 mg/dl in the acetylcysteine group and from 1.16 +/- 1.1 to 1.06 +/- 0.41 mg/dl in the control group (p = 0.29, for the comparison between two groups, NS). We divided the population into 3 subgroups according to their creatinine clearance: no significant change of serum creatinine concentration was observed in patients with normal renal function nor in patients with pre-existing mild to moderate chronic renal failure in both groups. There was no significant difference for the incidence of contrast-induced nephropathy between both groups (2 of the 53 patients in the acetylcysteine group and 3 of the 51 patients in the placebo group, p = 0.98, NS). CONCLUSIONS: Our data do not support the systematic use of acetylcysteine before a coronary procedure in patients with normal renal function or mild to moderate chronic renal failure, to prevent contrast-induced nephropathy.     

Efficacy of N-acetylcysteine and hydration versus placebo and hydration in decreasing contrast-induced renal dysfunction in patients undergoing coronary angiography with or without concomitant percutaneous coronary intervention

OBJECTIVE: Contrast-induced renal dysfunction is an iatrogenic complication that occurs more frequently in patients with preexisting renal dysfunction. A prospective, double-blind, randomized, placebo, controlled trial was completed to assess the efficacy of N-acetylcysteine in decreasing the incidence of contrast-induced renal dysfunction in patients with an acute coronary syndrome and renal insufficiency who underwent coronary angiography with or without percutaneous coronary intervention. METHODS: With similar intravenous hydration protocols, 20 patients received N-acetylcysteine (treatment group) and 20 patients received placebo (control group) in a twice per day dosing regimen with one dose before and three doses after contrast media exposure. RESULTS: The two groups were similar at baseline on demographic and clinical characteristics, and preexisting renal insufficiency. Contrast-induced renal dysfunction, defined as an increase in serum creatinine greater than 44 micromol/L (.5 mg/dL) and/or 25% above baseline within 48 hours, occurred in 7.5% of the cohort, with 2.5% in the treatment group, and 5% in the control group, for an absolute difference of 2.5%. There was no difference in serum creatinine or creatinine clearance at 24 hours or at 48 hours between the treatment and control groups. CONCLUSION: These results suggest that this cohort gained no added protection to renal function with the use of N-acetylcysteine.     

Effectiveness of theophylline prophylaxis of renal impairment after coronary angiography in patients with chronic renal insufficiency

Contrast media can lead to renal impairment that results in longer hospitalization and increased mortality. Adenosine is a crucial mediator of contrast-induced nephropathy (CIN; an increase in serum creatinine of >or=0.5 mg/dl within 48 hours). Therefore, it was the purpose of our study to investigate whether the adenosine antagonist theophylline reduces the incidence of CIN after coronary angiography. We also characterized risk factors for CIN after coronary angiography. One hundred patients with serum creatinine concentrations of >or=1.3 mg/dl randomly received 200 mg IV theophylline or placebo 30 minutes before coronary angiography (amount of contrast medium >or=100 ml). Patients who received theophylline and the controls were comparable with regard to baseline creatinine levels (means +/- SD) (1.65 +/- 0.41 vs 1.72 +/- 0.69 mg/dl) and the amount of contrast medium received (235 +/- 89 vs 261 +/- 139 ml). Theophylline significantly reduced the incidence of CIN (4% vs 20%, p = 0.0138). With placebo, creatinine significantly increased at 12 (1.82 +/- 0.79 mg/dl, p = 0.0057), 24 (1.90 +/- 0.86 mg/dl, p = 0.0001), and 48 hours (1.90 +/- 0.89 mg/dl, p = 0.0007) after administration of contrast medium. With pretreatment with theophylline, mean creatinine only increased 24 hours after contrast medium administration (1.70 +/- 0.40 mg/dl, p = 0.029), but was stable 12 hours (1.65 +/- 0.43 mg/dl, p = 0.99) and 48 hours after contrast medium administration (1.65 +/- 0.41 mg/dl, p = 0.99). The following parameters were significantly associated with contrast-induced renal impairment: Cigarroa quotient >5 (contrast medium [milliters] x serum creatinine/body weight [kg]), elevated troponin T, >300 ml of contrast medium, and emergency angiography. In conclusion, theophylline reduces the incidence of CIN in patients with chronic renal insufficiency undergoing coronary angiography. It should be used especially in patients receiving large amounts of contrast medium, and in patients with a Cigarroa quotient of >5 and/or elevated troponin T levels.     

Abbreviated dosing of N-acetylcysteine prevents contrast-induced nephropathy after elective and urgent coronary angiography and intervention

BACKGROUND AND HYPOTHESIS: Several studies have utilized low-dose regimens of N-acetylcysteine (NAC) for 48 hours to prevent contrast-induced nephropathy (CIN) after cardiac catheterization (cath) and percutaneous coronary intervention (PCI). A lengthy pretreatment period with NAC may not be feasible in urgent situations. The purpose of this study was to assess the efficacy of an abbreviated, higher dose regimen of NAC for the prevention of CIN after elective and urgent coronary angiography (cath) and/or percutaneous coronary intervention (PCI). METHODS: We prospectively evaluated 80 patients referred for elective or urgent cath and/or PCI with stable chronic renal insufficiency (creatinine clearance <50 cc/min). Patients were randomized to: NAC 1000 mg PO 1 hour before cath/PCI and 4 hours later, or placebo. All patients received hydration (0.9% saline) before and after cath/PCI (minimum total volume > or = 1500 mL). CIN was defined as an increase of Cr > or = 0.5 mg/dL or > or = 25% 48 hours after cath/PCI. RESULTS: CIN occurred in 3 of 36 (8%) patients of the NAC group vs. 11 of 44 (25%) in the placebo group (P = 0.051; OR 3.7, 95% CI 0.94-14.4). Serum creatinine (mean +/- SD) remained stable in the NAC group after cath/PCI (2.02 +/- 0.56 vs. 2.10 +/- 0.81 mg/dL; P = 0.34), but increased after cath/PCI in the placebo group (1.93 +/- 0.53 vs. 2.10 +/- 0.74 mg/dL; P < 0.01). CONCLUSIONS: An abbreviated, higher dose regimen of NAC prevents the rise of serum creatinine 48 hours after cath/PCI, and may prevent CIN after cath/PCI.     

Comparison of usefulness of sodium bicarbonate versus sodium chloride to prevent contrast-induced nephropathy in patients undergoing an emergent coronary procedure

In the case of an emergency coronary procedure where the risk of contrast-induced nephropathy is especially high, there are few reliable methods to attenuate renal injury. We examined the efficacy of sodium bicarbonate for the prevention of contrast-induced nephropathy in patients undergoing an emergency coronary procedure. We enrolled 59 patients who were scheduled to undergo an emergency coronary angiography or intervention. These patients were randomized to receive a 154-mEq/L infusion of sodium bicarbonate (n = 30) or sodium chloride (n = 29), as a bolus of 3 ml/kg/hour for 1 hour before the administration of contrast, followed by an infusion of 1 ml/kg/hour for 6 hours during and after the procedure. In the sodium bicarbonate group, serum creatinine concentration remained unchanged within 2 days of contrast administration (1.31 +/- 0.52 to 1.31 +/- 0.59 mg/dl), whereas it increased in the sodium chloride group (1.32 +/- 0.65 to 1.52 +/- 0.92 mg/dl, p = 0.01). The incidence of contrast-induced nephropathy (an increase >0.5 mg/dl or >25% in serum creatinine concentration within 2 days of contrast) was significantly lower in the sodium bicarbonate group than in the sodium chloride group (7% vs 35%, p = 0.01, risk ratio 0.19, 95% confidence interval 0.046 to 0.80). In conclusion, hydration with sodium bicarbonate is more effective than with sodium chloride for the prevention of contrast-induced nephropathy in patients undergoing an emergency coronary procedure.     

N-acetylcysteine prophylaxis significantly reduces the risk of radiocontrast-induced nephropathy: comprehensive meta-analysis.

The objectives of this study was to assess the overall effect of N-acetylcysteine (NAC) in preventing radiocontrast-induced nephropathy (RCIN) using all available data in the literature. RCIN is associated with increased morbidity and mortality. Existing randomized trials of NAC are small and show inconsistent results. Prior meta-analyses do not include data from the most current studies. We used standard search protocols to identify all published articles and abstracts of prospective trials using NAC with fluid hydration compared to hydration alone in patients with chronic renal insufficiency undergoing contrast procedures. A rise in serum creatinine by 0.5 mg/dl or 25% above baseline at 48-72 hr after contrast exposure was used as the primary outcome. We identified 14 trials of NAC with 1,584 patients published as full-text articles. Using a random-effects model, the use of oral NAC resulted in a significant reduction in the risk for developing RCIN (RR = 0.57; 95% CI = 0.37-0.84; P = 0.01). This finding did not significantly change in a fixed-effect model (RR = 0.55; 95% CI = 0.42-0.73) or when the data were reanalyzed using only randomized trials in all forms (i.e., articles and abstracts; RR = 0.67; 95% CI = 0.47-0.95). We identified only one important difference between the positive and the negative studies: the cumulative exposure to contrast media (174 vs. 152 ml). Metaregression did not show a significant relationship between contrast volume and the RR of developing RCIN (P > 0.10). In the trials showing benefit for NAC, the treated patients' postprocedure creatinine unexpectedly decreased by 0.21 mg/dl (95% CI = 0.33-0.08). Prophylaxis with NAC significantly reduces the risk for RCIN. The reasons for improvement in serum creatinine in patients treated with NAC are unclear, but may include improved renal blood flow due to NAC and/or vigorous hydration.     

Early Creatinine Shifts Predict Contrast-induced Nephropathy and Persistent Renal Damage after Angiography

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 <.001). At multivariate analysis, percentage change of creatinine 12 hour-basal was the best predictor of nephropathy (P <.001). A 5% increase of its value yielded 75% sensitivity and 72% specificity (area under the curve 0.80; odds ratio 7.37; 95% confidence interval, 3.34-16.23) for early contrast-induced nephropathy detection. Furthermore, it strongly correlated with the development of renal impairment at 30 days (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.     

Gender as a risk factor for contrast nephropathy: effects of hydration and N-acetylcysteine

BACKGROUND: In a few studies, N-acetylcysteine has been shown to prevent contrast-induced nephropathy in patients with chronic, stable renal failure undergoing elective procedures. Other studies have shown variable outcomes. Furthermore, the majority of prior studies have mainly studied men, and gender as a risk factor has not been studied. HYPOTHESIS: The study sought to evaluate the effectiveness of N-acetylcysteine and hydration in unselected patients with both acute and stable renal insufficiency (RI) undergoing urgent or elective cardiac or peripheral angiography. METHODS: We evaluated records of 146 patients with RI undergoing angiography. We compared patients receiving periprocedure hydration and acetylcysteine with patients who were only hydrated or received no pretreatment. We evaluated the 48-h change in serum creatinine between groups and further analyzed the effect of hydration and gender on outcomes. RESULTS: Demographics and baseline creatinine were similar between groups. Post procedure, the creatinine increased significantly in both groups, but less so in the acetylcysteine group (control: 0.35 +/- 0.08 mg/dl; acetylcysteine: 0.14 +/- 0.04 mg/dl, p < 0.05). When the control group was further stratified by hydration, the increase in creatinine for the hydrated patients was only 0.17 +/- 0.10 mg/dl compared with 0.54 +/- 0.12 mg/dl in patients with inadequate hydration. In the control group, women were more likely to receive no preprocedural hydration (59 vs. 40%), had a bigger rise in creatinine, received less protection from hydration alone, but were equally well protected by hydration plus acetylcysteine. In the acetylcysteine group, change in creatinine for women was minimal (+ 0.14 +/- 0.07 mg/dl) and not different from men (+ 0.15 +/- 0.05). CONCLUSION: Unselected patients with acute and chronic RI had no benefit from acetylcysteine beyond that seen with hydration alone. Gender may be a risk factor for contrast-induced nephropathy, with hydration offering less protection in women. Acetylcysteine (with hydration) seems to minimize the gender difference.     

Comparison of two hemofiltration protocols for prevention of contrast-induced nephropathy in high-risk patients

Purpose

Contrast-induced nephropathy is a complication of contrast medium administration during diagnostic and interventional procedures, with important prognostic relevance. Patients with chronic kidney disease have a higher risk for contrast-induced nephropathy and poorer outcome. In patients with chronic kidney disease, hemofiltration reduces contrast-induced nephropathy incidence and improves long-term survival. We assessed the mechanisms involved in the prophylactic effect of hemofiltration and of the most effective hemofiltration protocol to prevent contrast-induced nephropathy in patients with chronic kidney disease.

Subjects and methods

We randomized 92 patients with chronic kidney disease (creatinine clearance ≤30 mL/min) to three different prophylactic treatments: intravenous hydration with isotonic saline (1 mL · kg · h for 12 hours before and after contrast exposure, control group; n = 30); intravenous hydration for 12 hours before contrast exposure, followed by hemofiltration for 18 to 24 hours after contrast exposure (post-hemofiltration group; n = 31), and hemofiltration performed for 6 hours before and for 18 to 24 hours after contrast exposure (pre/post-hemofiltration group; n = 31). The incidence of contrast-induced nephropathy (>25% increase in creatinine) and the in-hospital clinical course were compared in the three groups.

Results

Twelve patients (40%) in the control group, 8 patients (26%) in the post-hemofiltration group, and 1 patient (3%) in the pre/post-hemofiltration group experienced contrast-induced nephropathy (P = .0013); hemodialysis was required in 9 (30%), three (10%), and zero (0%) patients, respectively (P = .002). In-hospital mortality was 20%, 10%, and 0%, respectively (P = .03).

Conclusions

Hemofiltration is an effective strategy for contrast-induced nephropathy prevention in patients with chronic kidney disease who are undergoing cardiovascular procedures. Pre-hemofiltration is required to obtain the full clinical benefit, suggesting that, among different mechanisms possibly involved, high-volume controlled hydration before contrast media exposure plays a major role.     

Cardiovascular and renal toxicity of a nonionic radiographic contrast agent after cardiac catheterization. A prospective trial

STUDY OBJECTIVE: To determine the incidence of cardiovascular and renal toxicity of a nonionic contrast agent when used for cardiac catheterization, and to assess the value of electrolytes and urinalysis results as predictors of nephropathy induced by a contrast agent. STUDY DESIGN: Nonrandomized trial using a criterion standard and a cohort analytic study with a 48-hour follow-up. SETTING: Referral-based university hospital. PATIENTS: Convenience sample of patients having diagnostic cardiac catheterization. Renal function and clinical status were evaluated at baseline in 1,144 patients; at 24 hours in 1,077 (94%); and at 48 hours in 663 (57%). INTERVENTIONS: After patients received saline for hydration, coronary angiography and left ventriculography were done with iopamidol (average dose, 203 +/- 56 cc). MEASUREMENTS AND MAIN RESULTS: The definite and possible incidence of major acute cardiovascular complications from nonionic contrast media was 0.2% and 0.7%, respectively. The mean serum creatinine level increased 11.5 mumol/L from baseline at 24 hours (P less than 0.0001) and 16.8 mumol/L from baseline at 48 hours (P less than 0.0001). Results in a randomly selected training sample were studied to determine predictors of a rise in serum creatinine of 44.2 mumol/L or more. The baseline serum creatinine level and age were significant predictors of renal injury, but hypertension, diabetes mellitus, congestive heart failure, vascular disease, the volume of contrast agent injected or baseline values of urinary variables did not predict nephrotoxicity. In an independent validation sample, only the baseline serum creatinine level was confirmed as a predictor of nephrotoxicity, whereas age was not. A model that predicted contrast-induced nephropathy by the serum creatinine level showed an exponential increase in the risk for nephrotoxicity if the baseline level was 106.1 mumol/L or higher. CONCLUSIONS: Patients have a small but significant rise in serum creatinine after cardiac catheterization with a nonionic contrast agent. Baseline renal insufficiency is the only confirmed predictor of nonionic contrast-induced nephrotoxicity.     

Contrast media-induced nephropathy: clinical burden and current attempts for prevention]

Contrast media-induced nephropathy is the third most common cause of hospital acquired acute renal failure. With the increasing use of contrast media in diagnostic and interventional procedures it has become one of the major challenges encountered during routine cardiology practice. Despite clinical importance it is an under-recognized event with major morbidity and mortality. Risk of developing contrast media-induced nephropathy depends mainly on patients preexisting characteristics and physicochemical properties of the contrast agent. Primary attempts for the prevention of contrast media-induced nephropathy should include systematic review of patient's characteristics and risk stratification. Patients at the greatest risk for contrast media-induced nephropathy can be defined as those having preexisting impaired renal function, diabetes mellitus, and congestive heart failure. Other risk factors include; age above seventy years, female gender, dehydration and use of high volume contrast media. The more expeditious use of iso-osmolar non-ionic contrast media reduced the incidence of contrast media related renal dysfunction. Currently, the only widely proven method of reducing the risk of contrast-induced nephropathy is adequate pre and postprocedural hydration. In addition, prophylactic use of free radical scavenger N-acetylcysteine has been shown to prevent contrast media-induced nephropathy in some moderate-scale clinical trials and a meta-analysis. Despite the attempts to reduce the risk of contrast nephropathy, this clinical event affects over 25% of high risk patients and mortality remains to be high.     

Comparing Trimetazidine with Allopurinol in Prevention of Contrast Induced Nephropathy After Coronary Angiography

ObjectivesContrast-induced nephropathy is considered a serious complication following coronary angiography increasing morbidity and mortality. Various drugs have been assessed to reduce the incidence of contrast-induced nephropathy. In this study, we compared trimetazidine and allopurinol as a pharmacological measure to reduce the incidence of contrast-induced nephropathy.MethodsOne hundred and twenty patients undergoing coronary angiography with baseline creatinine clearance more than 30 ml/minute were divided into three groups, 40 patients each. Group 1 received standard parenteral intravenous hydration in the form of isotonic saline at a rate of 1 ml/kg body weight per hour started 12 hours before angiography and up to 12 hours after the procedure. Group 2 received trimetazidine 35 mg twice per day for 72 hours starting 48 hours before the procedure in addition to intravenous hydration. Group 3 received allopurinol 300 mg once daily for 72 hours starting 48 hours before the procedure in addition to intravenous hydration. Serum creatinine and creatinine clearance were measured before and 72 hours after the procedure in addition to the volume of contrast media used.ResultsTrimetazidine and allopurinol failed to reduce contrast-induced nephropathy significantly. Among patients with contrast-induced nephropathy volume of contrast media was significantly higher.ConclusionAdding trimetazidine or allopurinol in addition to regular intravenous hydration with isotonic saline without targeting selectively high-risk patients did not reduce contrast-induced nephropathy following coronary angiography     

Preventive strategies of renal insufficiency in patients with diabetes undergoing intervention or arteriography (the PREVENT Trial)

Few studies have compared the ability of sodium bicarbonate plus N-acetylcysteine (NAC) and sodium chloride plus NAC to prevent contrast-induced nephropathy (CIN) in diabetic patients with impaired renal function undergoing coronary or endovascular angiography or intervention. Diabetic patients (n = 382) with renal disease (serum creatinine ≥1.1 mg/dl and estimated glomerular filtration rate <60 ml/min/1.73 m(2)) were randomly assigned to receive prophylactic sodium chloride (saline group, n = 189) or sodium bicarbonate (bicarbonate group, n = 193) before elective coronary or endovascular angiography or intervention. All patients received oral NAC 1,200 mg 2 times/day for 2 days. The primary end point was CIN, defined as an increase in serum creatinine >25% or an absolute increase in serum creatinine ≥0.5 mg/dl within 48 hours after contrast exposure. There were no significant between-group differences in baseline characteristics. The primary end point was met in 10 patients (5.3%) in the saline group and 17 (9.0%) in the bicarbonate group (p = 0.17), with 2 (1.1%) and 4 (2.1%), respectively, requiring hemodialysis (p = 0.69). Rates of death, myocardial infarction, and stroke did not differ significantly at 1 month and 6 months after contrast exposure. In conclusion, hydration with sodium bicarbonate is not superior to hydration with sodium chloride in preventing CIN in patients with diabetic nephropathy undergoing coronary or endovascular angiography or intervention.     

Prehydration alone is sufficient to prevent contrast-induced nephropathy after day-only angiography procedures--a randomised controlled trial

BACKGROUND: Contrast agents used in angiography procedures for patients with cardiovascular disease are known to cause contrast-induced nephropathy (CIN), which may be partially due to the production of nephrotoxic oxygen-free radicals. It is uncertain whether administration of intravenous (IV) anti-oxidant, N-acetylcysteine (NAC), can prevent reduction in renal function and whether this is a cost-effective approach. METHODS: Sixty-five day-only patients with renal impairment (mean serum creatinine concentration 0.16+/-0.03 mmol/l) due to undergo coronary or peripheral angiography and/or stenting were randomly assigned to IV NAC 300 or 600 mg immediately before and after the procedure or IV fluid alone. RESULTS: Of the 60 patients with complete data, none had acute CIN (increase in serum creatinine concentration > or = 0.044 mmol/l, 48 h after administration of contrast agent). Eight patients (13%) have demonstrated an increase in their serum creatinine concentration > or = 0.044 mmol/l 30 days after administration of contrast agent: 2/19 (11%) in the control group, 2/21 (10%) in the 600 mg NAC group and 4/20 (20%) the 300 mg NAC group (p = 0.66). The mean volumes of contrast agent used and prehydration given for each of the three groups did not differ significantly (p > 0.83). There was significant improvement in creatinine clearance within each group from baseline to 30 days (p < or = 0.03), but no significant difference between the groups at 48 h and 30 days (p > or = 0.43). Considering the cost of NAC and its administration, we estimate that this would translate to a saving of dollar 26,637 per annum. CONCLUSION: For day-stay patients with mild-to-moderate chronic renal impairment undergoing angiography and/or intervention, prehydration alone is less complicated and more cost-effective than a combination of IV NAC (at doses used) and hydration.     

水化和他汀类药物预防对比剂肾病的临床观察

目的探讨他汀类药物在预防对比剂肾病(contras-t induced nephropathy,CIN)中的作用。方法选择行经皮冠状动脉造影病人115例,采用随机数字表法将病人分为他汀组(n=40)、水化组(n=34)以及对照组(n=41)。他汀组于冠状动脉造影术前3d开始每晚顿服阿托伐他汀20mg,水化组予0.9%氯化钠注射液静脉滴注,速度为1ml/(kg.h),一般于术前4h开始至术后12h结束,对照组未服用阿托伐他汀及其他调脂类药物亦未应用水化处理。观察患者术前1d、术后36～48h血清肌酐(Scr)、内生肌酐清除率(Ccr)、尿白蛋白肌酐比(UACR)以及超敏C反应蛋白(hsCRP)的改变情况。结果他汀组及对照组两组患者术后血hsCRP、Scr,UACR较术前均升高(均P<0.05),而血Ccr较术前降低(P<0.05)。对照组患者术后血hsCRP、UACR较他汀组术后明显升高(P<0.05),对照组对比剂肾病发生率(9.76%)高于他汀组(5.00%)。水化组术后血hsCRP、Scr、UACR及血Ccr与术前相比差异无统计学意义,对比剂肾病发生率明显小于他汀组及对照组。结论造影剂可造成轻微的肾功能损害;术前3d使用他汀药物,可能具有减轻炎症反应、预防造影剂肾病发生的作用,但相比之下水化处理更能明显减少对比剂肾病的发生。     

Effect of statins on contrast-induced nephropathy in patients with acute myocardial infarction treated with primary angioplasty

We investigated whether pretreatment with statin may prevent contrast-induced nephropathy in patients who underwent primary coronary intervention for acute myocardial infarction (AMI). A total of 279 consecutive patients who underwent successful primary angioplasty for a first AMI were studied. Contrast-induced nephropathy was defined as an increase in serum creatinine of > or =5 mg/dL after the primary PCI. 56 patients receiving statin treatment before admission had lower incidence of the contrast-induced nephropathy than those without it (7.1% and 20.6%, P<0.01). Multivariable logistic regression analysis revealed that absence of statin pre-treatment was a significant predictor of the reperfusion arrhythmia along with anterior AMI, baseline creatinine value, time-to-reperfusion, higher volume of the contrast agent. Pre-treatment with statin could reduce the contrast-induced nephropathy after primary coronary intervention in patients with AMI.