Statins and Contrast-Induced Nephropathy: A Systematic Review and Meta-Analysis

2018 ◽  
Vol 23 (46) ◽  
pp. 7141-7148 ◽  
Author(s):  
Alexandros Briasoulis ◽  
Mohan Pala ◽  
Tesfaye Telila ◽  
Obsinet Merid ◽  
Emmanuel Akintoye ◽  
...  
Keyword(s):  
Systematic Review ◽  
Serum Creatinine ◽  
Enzyme Inhibitors ◽  
Meta Analysis ◽  
Kidney Injury ◽  
Contrast Induced Nephropathy ◽  
Vessel Occlusion ◽  
Iodinated Contrast ◽  
Noninvasive Coronary Angiography ◽  
Increased Risk

Contrast-induced nephropathy (CIN) is a type of acute kidney injury associated with intravascular administration of iodinated contrast, usually reversible. Contrast agents are an essential component of invasive and noninvasive coronary angiography. These agents have been modified over time to enhance patient safety and tolerability, but adverse reactions still occur. CIN has been variably defined, as a rise in serum creatinine of 0.5 mg/dl, or a 25% increase in serum creatinine above baseline within 24-72 hours after the procedure. The incidence of CIN varies based on the definition used and risk profile of the patients. CIN is rare among patients with normal renal function at baseline. In low-risk patients, CIN occurs in 1-5%, whereas in higher-risk populations, the incidence can be as high as 30%. CIN is also associated with a 5- to 20-fold increased risk of other early adverse events including in-hospital myocardial infarction, target vessel occlusion, and early mortality. The main prevention strategies are adequate intravenous hydration before, during and after the procedure as well as restriction of contrast load with maximum volume approximately no more than three times the serum creatinine clearance. Recent observational and small prospective randomized trials demonstrate the reduction of CIN incidence with HMG-CoA enzyme inhibitors. In this systematic review and meta-analysis we explore the effects of statin administration in prevention of CIN.

Strategies Preventing Contrast-Induced Nephropathy After Coronary Angiography: A Comprehensive Meta-Analysis and Systematic Review of 125 Randomized Controlled Trials

Angiology ◽  
2016 ◽  
Vol 68 (5) ◽  
pp. 389-413 ◽  
Author(s):  
Sadegh Ali-Hassan-Sayegh ◽  
Seyed Jalil Mirhosseini ◽  
Zahra Ghodratipour ◽  
Zahra Sarrafan-Chaharsoughi ◽  
Elham Rahimizadeh ◽  
...  
Keyword(s):  
Systematic Review ◽  
Coronary Angiography ◽  
Vitamin C ◽  
Enzyme Inhibitors ◽  
Meta Analysis ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Pooled Analysis ◽  
Loop Diuretics ◽  
Contrast Induced Nephropathy ◽  
Converting Enzyme Inhibitors

This systematic review with meta-analysis sought to determine the strength of evidence for the effects of hydration (sodium bicarbonate [SB] and normal saline [NS]), supplementations ( N-acetylcysteine [NAC] and vitamin C), and some common drugs (adenosine antagonists [AAs], statins, loop diuretics, and angiotensin-converting enzyme inhibitors [ACEIs]) on the incidence of contrast-induced nephropathy (CIN) and requirement for hemodialysis after coronary angiography. After screening, a total of 125 trials that reported outcomes were identified. Pooled analysis indicated beneficial effects of SB versus NS (odds ratio [OR] = 0.73; 95% confidence interval [CI]: 0.56-0.94; P = .01), NAC (OR = 0.79; 95% CI: 0.70-0.88; P = .001), vitamin C (OR = 0.64; 95% CI: 0.45-0.89; P = .01), statins (OR = 0.45; 95% CI: 0.35-0.57; P = .001), AA (OR = 0.28; 95% CI: 0.14-0.47; P = .001), loop diuretics (OR = 0.97; 95% CI: 0.33-2.85; P = .9), and ACEI (OR = 1.06; 95% CI: 0.69-1.61; P = .8). Overall, hydration with SB, use of supplements, such as NAC and vitamin C, and administration of statins and AA should always be considered for the prevention of CIN after coronary angiography.

scholarly journals Comparative safety of the sodium glucose co-transporter 2 (SGLT2) inhibitors: a systematic review and meta-analysis

BMJ Open ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. e022577 ◽  
Author(s):  
Jennifer R Donnan ◽  
Catherine A Grandy ◽  
Eugene Chibrikov ◽  
Carlo A Marra ◽  
Kris Aubrey-Bassler ◽  
...  
Keyword(s):  
Systematic Review ◽  
Bone Fractures ◽  
Meta Analysis ◽  
Kidney Injury ◽  
Sglt2 Inhibitors ◽  
Current Evidence ◽  
Random Effects Models ◽  
Relative Risks ◽  
Increased Risk ◽  
Tract Infections

ObjectiveTo estimate the association between the use of sodium glucose co-transporter-2 (SGLT2) inhibitors and postmarket harms as identified by drug regulatory agencies.DesignWe conducted a systematic review and meta-analysis of randomised controlled trials (RCT). Six large databases were searched from inception to May 2018. Random effects models were used to estimate pooled relative risks (RRs).InterventionSGLT2 inhibitors, compared with placebo or active comparators.Primary outcomesAcute kidney injury (AKI), diabetic ketoacidosis (DKA), urinary tract infections (UTI), bone fractures and lower limb amputations.ResultsWe screened 2418 citations of which 109 were included. Most studies included one of four SGLT2 inhibitors, dapagliflozin, canagliflozin, empagliflozin and ipragliflozin. When compared with placebo, SGLT2 inhibitors were found to be significantly protective against AKI (RR=0.59; 95% CI 0.39 to 0.89; I2=0.0%), while no difference was found for DKA (RR 0.66; 95% CI 0.30 to 1.45, I2=0.0%), UTI (RR 1.02; 95% CI 0.95 to 1.09, I2=0.0%) or bone fracture (RR 0.87; 95% CI 0.69 to 1.09, I2=1.3%). Three studies reported on amputation, with one finding a significant increase risk. No increased risk for either outcome was found when compared with active controls. Subgroup analysis did show an increased risk of UTI with dapagliflozin only (RR 1.21; 95% CI 1.02 to 1.43, I2=0.0%), but no other analysis supported an increased risk of AKI, DKA, UTI or fracture.ConclusionsCurrent evidence from RCTs does not suggest an increased risk of harm with SGLT2 inhibitors as a class over placebo or active comparators with respect to AKI, DKA, UTI or fracture. However, wide CIs for many comparisons suggest limited precision, and therefore clinically important adverse events cannot be ruled out. Dapagliflozin, appears to independently increase the risk of UTI, although the mechanism for this intraclass variation in risk is unclear.PROSPERO registration numberCRD42016038715.

scholarly journals The Chronic Kidney Disease and Acute Kidney Injury Involvement in COVID-19 Pandemic: A Systematic Review and Meta-analysis

2020 ◽  
Author(s):  
Ya-Fei Liu ◽  
Zhe Zhang ◽  
Xiao-Li Pan ◽  
Guo-Lan Xing ◽  
Ying Zhang ◽  
...  
Keyword(s):  
Systematic Review ◽  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Serum Creatinine ◽  
Blood Urea Nitrogen ◽  
Meta Analysis ◽  
Kidney Injury ◽  
Urea Nitrogen ◽  
Severe Group

ABSTRACTAimThe aim of this study was to uncover whether kidney diseases were involved in COVID-19 pandemic from a systematic review.MethodsThe studies reported the kidney outcomes in different severity of COVID-19 were included in this study. Standardized mean differences or odds ratios were calculated by employing Review Manager meta-analysis software.ResultsThirty-six trials were included in this systematic review with a total of 6395 COVID-19 patients. The overall effects indicated that the comorbidity of chronic kidney disease (CKD) (OR = 3.28), complication of acute kidney injury (AKI) (OR = 11.02), serum creatinine (SMD = 0.68), abnormal serum creatinine (OR = 4.86), blood urea nitrogen (SMD = 1.95), abnormal blood urea nitrogen (OR = 6.53), received continuous renal replacement therapy (CRRT) (OR = 23.63) was significantly increased in severe group than that in nonsevere group. Additionally, the complication of AKI (OR = 13.92) and blood urea nitrogen (SMD = 1.18) were remarkably elevated in critical group than that in severe group.ConclusionCKD and AKI are susceptible to occur in patients with severe COVID-19. CRRT is applied frequently in severe COVID-19 patients than that in nonsevere COVID-19 patients. The risk of AKI is higher in critical group than that in severe group.

Iodine contrast prior to or during pregnancy and neonatal thyroid function: a systematic review

2021 ◽  
Vol 184 (1) ◽  
pp. 189-198 ◽  
Author(s):  
Nienke van Welie ◽  
Maite Portela ◽  
Kim Dreyer ◽  
Linda J Schoonmade ◽  
Madelon van Wely ◽  
...  
Keyword(s):  
Systematic Review ◽  
Contrast Media ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Meta Analysis ◽  
Cochrane Library ◽  
Iodinated Contrast Media ◽  
Iodinated Contrast ◽  
Increased Risk ◽  
Neonatal Thyroid Function

Objective Thyroid dysfunction is a known side effect of iodinated contrast media. There is some evidence to suggest that iodinated contrast media administered to pregnant women may cause thyroid dysfunction not only in themselves but also in their offspring. Here, we systematically evaluated literature on the use of iodinated contrast media prior to or during pregnancy on the offspring’s thyroid function. Design Systematic review of published literature. Materials and methods Relevant studies were identified by PubMed, EMBASE and The Cochrane Library up to June 5, 2020. All study designs, reporting on the foetal or neonatal thyroid function after exposure to iodinated contrast media prior to or during pregnancy, were included. We undertook random effects meta-analysis and pooled the estimates as proportions with 95% CIs. Results We identified 402 articles, of which 26 were included. Six studies reported (n = 369) on exposure to iodinated contrast media prior to pregnancy by hysterosalpingography and 20 studies (n = 670) on exposure to these media during pregnancy by amniofetography, urography or CT. There was low to high risk of bias. The proportion of (transient) neonatal thyroid dysfunction was 0.0% (95% CI: 0.0–2.9% based on 3 studies) for hysterosalpingography, 2.25% (95% CI: 0.03–6.55% based on 2 studies) for amniofetography and 0.0% (95% CI: 0.0–0.02% based on 5 studies) for CT. There was a tendency towards an increased risk of thyroid dysfunction with higher amounts of contrast used. Conclusions Exposure to iodinated contrast media prior to or during pregnancy may increase the risk of thyroid dysfunction in offspring. We recommend keeping the amount of contrast used as low as possible.

Can sodium fluorescein cause contrast-induced nephropathy?

2019 ◽  
Author(s):  
Donghwan Yun ◽  
Dong Ki Kim ◽  
Jung Pyo Lee ◽  
Yon Su Kim ◽  
Sohee Oh ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Cox Regression ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Incidence Rates ◽  
Sodium Fluorescein ◽  
Contrast Imaging ◽  
Contrast Induced Nephropathy ◽  
Iodinated Contrast

Abstract Background Contrast-induced nephropathy (CIN) is a common cause of acute kidney injury (AKI), and can be diagnosed when the etiology of AKI is unclear other than via a contrast agent. Fluorescent angiography (FAG) with fluorescein sodium dye is generally considered to be safe for patients with kidney diseases. However, it remains unresolved whether or not FAG can induce CIN. Methods Patients from two tertiary hospitals who underwent FAG and had serum creatinine results within 4 weeks before FAG and 3 days after FAG between 2001 and 2017 were retrieved. Cases with concurrent iodinated contrast imaging or undergoing dialysis were excluded from the analysis. CIN was defined by two criteria: CIN criteria as >0.5 mg/dL or >25% increase in serum creatinine (sCr) level within 3 days after FAG, and contrast-induced acute kidney injury (CIAKI) criteria as ≥0.3 mg/dL increase within 2 days or ≥50% increase within 7 days after FAG. Results A total of 979 patients were screened, and we found 124 patients with AKI after FAG. After excluding 32 patients with clear causes of AKI other than FAG, the incidence rates of CIN were 7.3% by CIN criteria and 6.4% by CIAKI criteria. CIN incidence had a U-shaped distribution according to chronic kidney disease (CKD) stages in CIN criteria, while linear association between CIN incidence and CKD stages were found in CIAKI criteria. Kaplan–Meier curves showed the CIN group was significantly associated with end-stage renal disease (ESRD) progression (log-rank P < 0.001, in both CIN criteria and CIAKI criteria), and adjusted hazard ratios by multivariable Cox regression were 2.23 [95% confidence interval (CI) 1.468–3.378] in CIN criteria and 2.17 (95% CI 1.462–3.232) in CIAKI criteria. Conclusions According to CIN and CIAKI criteria, FAG may cause CIN and appeared to be a possible risk factor for ESRD progression. However, CIN or CIAKI criteria themselves may overestimate AKI and require meticulous attention to the interpretation of results.

scholarly journals Systematic Review and Meta-analysis of the Association of Acute Kidney Injury with the Concomitant Use of Vancomycin and Piperacillin-Tazobactam in Children

2019 ◽  
Vol 63 (12) ◽  
Author(s):  
Markos Kalligeros ◽  
Spyridon A. Karageorgos ◽  
Fadi Shehadeh ◽  
Ioannis M. Zacharioudakis ◽  
Eleftherios Mylonakis
Keyword(s):  
Systematic Review ◽  
Acute Kidney Injury ◽  
Publication Bias ◽  
Pediatric Population ◽  
Meta Analysis ◽  
Kidney Injury ◽  
Beta Lactam ◽  
Beta Lactam Antibiotic ◽  
Increased Risk ◽  
Lactam Antibiotic

ABSTRACT Concomitant use of vancomycin plus piperacillin-tazobactam (TZP) has been associated with increased risk of acute kidney injury (AKI) in hospitalized adults. In this systematic review and meta-analysis, we searched PubMed and EMBASE for pediatric studies examining this hypothesis, with reference to vancomycin monotherapy or in combination with another beta-lactam antibiotic. Of 1,381 nonduplicate studies, 10 met our inclusion criteria. We performed a random-effects meta-analysis, based on crude odds ratios (ORs), and we accounted for both quality of included studies and publication bias. In primary analysis, concomitant vancomycin and TZP use yielded a statistically significant association with the development of AKI. More specifically, children with AKI had higher odds of having been exposed to vancomycin plus TZP than to vancomycin monotherapy (OR, 8.15; 95% confidence interval [CI], 3.49 to 18.99) or to vancomycin plus any other beta-lactam antibiotic (OR, 3.48; 95% CI, 2.71 to 4.46). On the basis of the results of the Newcastle-Ottawa scale quality assessment, a secondary analysis that included only higher-quality studies (6 of 10 studies) again yielded higher odds of exposure to vancomycin plus TZP than to vancomycin plus another beta-lactam antibiotic (OR, 3.76; 95% CI, 2.56 to 5.51). Notably, even after controlling for possible publication bias, our results remained statistically significant (OR, 3.09; 95% CI, 2.30 to 4.14). In conclusion, the concomitant use of vancomycin and TZP could be associated with AKI development and the clinical significance of this potential association needs to be studied further in the pediatric population.

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