scholarly journals Predictors of acute kidney injury in patients admitted with ST-elevation myocardial infarction – results from the Bremen STEMI-Registry

2017 ◽  
Vol 7 (8) ◽  
pp. 710-722 ◽  
Author(s):  
Johannes Schmucker ◽  
Andreas Fach ◽  
Matthias Becker ◽  
Susanne Seide ◽  
Stefanie Bünger ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Kidney Injury ◽  
Creatine Kinase ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Contrast Media ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Mortality Rates ◽  
St Elevation

Background: Deterioration of renal function after exposition to contrast media is a common problem in patients with myocardial infarction undergoing percutaneous coronary interventions. The aim of the present study was to assess the incidence of acute kidney injury in patients admitted with ST-elevation-myocardial infarction (STEMI) and its association with infarction severity, comorbidities and treatment modalities, including amount of contrast media applied. Methods: All patients with STEMI from the metropolitan area of Bremen, Germany are treated at the Bremen Heart Centre and since 2006 documented in the Bremen STEMI-Registry. Acute kidney injury was graded from stage 0 to 3 following the Kidney-disease-improving-global outcomes criteria from 2012. Results: Data from 3810 patients admitted with STEMI were included in this study. No acute kidney injury was observed in 3120 (82%) patients while acute kidney injury was detected in 690 (18%) patients: Stage 1: n=497 (13%), 2: n=66 (2%), 3: n=127 (3%). Acute kidney injury was associated with elevated 30-day (0: 3%, 1: 20%, 2: 46%, 3: 58%) and one-year mortality rates (0: 6%, 1: 26%, 2: 49%, 3: 66%). Higher acute kidney injury stages were associated with higher peak creatine kinase (in U/l±SEM): stage 0: 1748±33, 1: 2588±127, 2: 3684±395, 3: 3330±399, p (<0.01), lower mean systolic blood pressure at admission (in mmHG±SD): 0: 133±28, 1: 129±31; 2: 121±31, 3: 115±33 ( p<0.01) and higher Thrombolysis in Myocardial Infarction risk score for STEMI (scale 0–14±SD): 0: 2.71±2, 1: 4.08±2, 2: 4.98±2, 3: 5.05±2, ( p<0.01). However, no such association could be found between acute kidney injury stage and amount of contrast media applied (in ml±SD) 0: 138±57, 1: 139±61; 2: 140±76; 3: 145±80 ( p=0.5). Reduced initial glomerular filtration rate was associated with higher incidences of acute kidney injury while again no relation to amount of contrast media could be observed in subgroups ranked by initial glomerular filtration rate. A multivariate analysis confirmed these results: while left-heart-failure/cardiogenic shock (odds ratio (OR) 4.2, 95% confidence interval (CI) 3.3–5.5) as well as larger infarctions (peak creatine kinase >3000 U/l (OR 2.2, 95% CI 1.7–2.8)) were independently associated with a greater risk for acute kidney injury, amount of contrast media applied during angiography was not (150–250 ml, OR 0.95, 95% CI 0.8–1.2 ( p=0.7), >250 ml, OR 1.3, 95% CI 0.8–2.0 ( p=0.5)). Conclusions: Acute kidney injury, which was associated with elevated short- and long-term mortality rates, could be observed in 18% of patients admitted with STEMI. The present data suggest that severity and haemodynamic impairment due to STEMI rather than contrast-media-induced nephropathy is the key contributor for acute kidney injury in STEMI patients. The deleterious effect of the myocardial infarction itself on renal function can be explained through renal hypoperfusion, neurohormonal activation or other pathomechanisms that might have been underestimated in the past.

Acute kidney injury

2018 ◽  
Author(s):  
Aron Chakera ◽  
William G. Herrington ◽  
Christopher A. O’Callaghan
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urine Volume ◽  
Kidney Injury ◽  
Rapid Decrease

Acute renal failure (also referred to as acute kidney injury) refers to a rapid decrease in renal function; it is reflected by an increase in blood urea and creatinine and is often associated with oliguria (a urine volume of less than 400 ml/24 hours). It usually develops over days to weeks. Acute kidney injury has been variously classified, but the current classifications are based on the glomerular filtration rate (or creatinine), looking at changes from baseline, and the presence of oliguria or anuria. The potential etiologies of acute kidney injury are usually considered anatomically under the headings prerenal, renal (intrinsic), and postrenal. This chapter looks at the etiology, symptoms, clinical features, demographics, complications, diagnosis, and treatment of acute kidney injury.

scholarly journals P06 Improving renal function monitoring during chemotherapy- a role for cystatin C?

2020 ◽  
Vol 105 (9) ◽  
pp. e8.2-e9
Author(s):  
Rachel Boys
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Cystatin C ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Estimating Equations ◽  
Transformation Factor ◽  
Over Time

AimRenal toxicity causes major morbidity following chemotherapy- abnormal iGFRs may be detected in up to 73.7% of patients.1 Creatinine is universally used as a biomarker to track fluctuating function and to calculate surrogate glomerular filtration rate (GFR) in the form of estimating equations.2 There is concern regarding the suitability of creatinine as a biomarker in this population, and it is proposed that cystatin C as a biomarker alone and also included in estimating equations may offer improved clinical suitability and accuracy.3MethodsIn this prospective, longitudinal study over a period of 18 months, 132 combined isotope GFR (iGFR), creatinine and cystatin C measurements were taken from 48 paediatric oncology patients at a Northern Children’s Hospital. Correlation and agreement analysis was performed for both individual biomarkers and estimating equations. Sensitivity data, along with ROC curve analysis was performed for all biomarkers and estimating equations. Data from three identified patients was isolated to examine individual patient variation over time.ResultsCreatinine identified only 1/32 patients with an abnormal iGFR (<90 ml/min/1.73 m2) compared to cystatin C which identified 12/32. Creatinine values and both estimating equations failed to change significantly over a period of declining iGFR though cystatin C did show a significant inverse increase (p<0.05). Bland Altman analysis for both the creatinine and combined equation showed poor agreement (mean difference -64 ml/min/1.3 m2 and -20 ml/min/1.73 m2 respectively). All biomarkers and equations showed poor sensitivity to detect an abnormal iGFR either below 70 ml/min/1.73 m2 or 90 ml/min/1.73 m2. A transformation factor applied to the equations significantly improved the sensitivity and clinical applicability of all equations. The data from three individual patients failed to reveal any significant intra-patient relationships.ConclusionData from this study cannot support the use of creatinine or cystatin C as a single biomarker to monitor renal function in children undergoing chemotherapy. Newer cystatin C and creatinine combined equations, whilst offering statistical superiority, do not offer the clinical superiority to replace iGFR or provide a tool for accurate dose calculations. A transformation factor can be applied to the results gained from the estimating equations to significantly improve the detection of abnormal iGFR, though work in other patient cohorts is needed to support this. Previous work also supported the use of a transformation factor, though application of their transformation factor to this current cohort failed to replicate the 100% sensitivity findings previously demonstrated4. Three patients were identified from the cohort and their paired iGFR and estimated GFR were monitored prospectively, over a period of approximately a year. Significant variation was observed between iGFR and eGFR at each time point for all three patients and therefore personalisation of GFR estimation from baseline iGFR and demographic data could not be proposed. This requires exploration in a larger cohort with the possible inclusion of additional baseline variables.ReferencesCRUK Survival trends over time in Children’s Cancers. 1.2015. https://www.cancerresearchuk.org/health-professional/cancer-statistics/childrens-cancers/survival#heading-Two Accessed 28th March 2019.NICE ( 2013) CG169 Acute kidney injury: Prevention, detection and management of acute kidney injury up to the point of renal replacement therapy.Barnfield, MC, Burniston, MT, Reid, U, et al. Cystatin C in assessment of glomerular filtration rate in children and young adults suffering from cancer. Nuclear Medicine Communications 2013;34:609–614.Dodgshun, AJ, Quinlan, C, Sullivan, MJ. Cystatin C based equation accurately estimates glomerular filtration rate in children with solid and central nervous system tumours: enough evidence to change practice? Pediatric Blood and Cancer 2016;63:1535–1538.

scholarly journals Continued monitoring of acute kidney injury survivors might not be necessary in those regaining an estimated glomerular filtration rate >60 mL/min at 1 year

2017 ◽  
Vol 32 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Sokratis Stoumpos ◽  
Patrick B. Mark ◽  
Emily P. McQuarrie ◽  
Jamie P. Traynor ◽  
Colin C. Geddes
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Normal Renal Function ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Kidney Injury ◽  
Risk Of Progression

Background. Severe acute kidney injury (AKI) among hospitalized patients often necessitates initiation of short-term dialysis. Little is known about the long-term outcome of those who recover to normal renal function. The aim of this study was to determine the long-term renal outcome of patients experiencing AKI requiring dialysis secondary to hypoperfusion injury and/or sepsis who recovered to apparently normal renal function. Methods. All adult patients with AKI requiring dialysis in our centre between 1 January 1980 and 31 December 2010 were identified. We included patients who had estimated glomerular filtration rate (eGFR) >60 mL/min/1.73 m2 12 months or later after the episode of AKI. Patients were followed up until 3 March 2015. The primary outcome was time to chronic kidney disease (CKD) (defined as eGFR persistently <60 mL/min/1.73 m2) from first dialysis for AKI. Results. Among 2922 patients with a single episode of dialysis-requiring AKI, 396 patients met the study inclusion criteria. The mean age was 49.8 (standard deviation 16.5) years and median follow-up was 7.9 [interquartile range (IQR) 4.8–12.7] years. Thirty-five (8.8%) of the patients ultimately developed CKD after a median of 5.3 (IQR 2.8–8.0) years from first dialysis for AKI giving an incidence rate of 1 per 100 person-years. Increasing age, diabetes and vascular disease were associated with higher risk of progression to CKD [adjusted hazard ratios (95% confidence interval): 1.06 (1.03, 1.09), 3.05 (1.41, 6.57) and 3.56 (1.80, 7.03), respectively]. Conclusions. Recovery from AKI necessitating in-hospital dialysis was associated with a very low risk of progression to CKD. Most of the patients who progressed to CKD had concurrent medical conditions meriting monitoring of renal function. Therefore, it seems unlikely that regular follow-up of renal function is beneficial in patients who recover to eGFR >60 mL/min/1.73 m2 by 12 months after an episode of AKI.

scholarly journals Edaravone in contrast-induced acute kidney injury prophelaxis

2020 ◽  
Vol 27 (1) ◽  
pp. 39-44
Author(s):  
D. D. Ivanov ◽  
M. D. Ivanova ◽  
I. I. Burlachenko
Keyword(s):  
Acute Kidney Injury ◽  
Glomerular Filtration Rate ◽  
Contrast Media ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Controlled Study ◽  
Ckd Stage ◽  
Group A ◽  
Group B

The aim – to evaluate the effectiveness of edaravon in preventing the development of contrast-induced acute kidney injury. Materials and methods. We have conducted a multicenter open prospective randomized controlled study to evaluate the efficacy of edaravone in preventing contrast-induced acute kidney injury in patients with chronic kidney disease (CKD) 3b–4 stages. The study included 2 groups of patients aged 46 to 68 (55±3): group A (n=16) with CKD stage 3b or 4 (еstimated glomerular filtration rate (formula СКD-EPI) 32±4 ml/min) that received intravenous edaravone 30 mg bid on 0, 1, 2 day of contrast media infusion and control group B (n=20) with CKD stage 3b or 4 (еstimated glomerular filtration rate 33±3 ml/min) with no edaravone intervention during CT coronarography. Patients of both groups received intravenous hydration with 0.9 % sodium before CT. Primary endpoint: contrast-induced acute kidney injury onset in 48 hours after contrast media infusion and need for RRT. Secondary endpoint: serum potassium level above 5.5 mmol/l. Results. Contrast-induced acute kidney injury onset was obtained in 4 patients of group A and 12 patients of group B (p≤0.05, RR 0.417, RRR 0.583, RD 0.350, NNT 2.857). The results shows statistical significance both of endpoints which demonstrates the promising possibilities for contrast-induced acute kidney injury prophylaxis with edaravone in CKD 3b–4. Individual data analyses shows that edaravone was more effective in CKD 3b (3 cases of contrast-induced acute kidney injury of 10) instead of CKD 4 (1 of 2). Conclusions. Edaravone is promising solution for contrast-induced acute kidney injury prevention in patients with CKD 3b–4 who urgently undergo CT coronarography

Non-ST elevation myocardial infarction; admission to angiogram time at a busy district general hospital

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
A Harris ◽  
M Prabhakar ◽  
W Mattar
Keyword(s):  
Myocardial Infarction ◽  
Acute Kidney Injury ◽  
General Hospital ◽  
Kidney Injury ◽  
Mortality Rates ◽  
St Elevation Myocardial Infarction ◽  
Junior Doctors ◽  
Medical Problems ◽  
Esc Guidelines ◽  
St Elevation

Abstract Funding Acknowledgements Type of funding sources: None. Background Cardiovascular disease is the leading cause of morbidity and mortality worldwide. Timely management of acute coronary syndromes, including patients presenting with non-ST elevation myocardial infarction (NSTEMI), is crucial in improving outcomes and reducing mortality. Clinical Guideline 94 (CG94) by National Institute of Health and Care Excellence (NICE) states that patients presenting with a NSTEMI with an intermediate or higher risk score should be offered coronary angiography within 96 hours of admission to hospital. Purpose The purpose of this audit is to assess how well our General Hospital adhered to the recommended NSTEMI intervention set by the NICE guidelines. Methods Data was collected between September and December 2019 for patients admitted with an NSTEMI to the cardiology department at our General Hospital. Data was analysed using in-patient paper notes and Microsoft Excel. Results Of the 54 patients admitted with NSTEMI, 67% met the NICE guideline for angiogram within 96 hours of admission. The most common reason for delay was infection or raised inflammatory markers (28%). Other medical reasons include pulmonary oedema (11.1%), acute kidney injury (11.1%) and stroke (11.1%). Another notable reason for delay to angiogram was weekend admissions and wait for cardiology bed (22.2%). Six-month mortality rates showed that, 75% of deceased patients did not undergo an angiogram within 96 hours of admission. Conclusion We have an elderly population with multiple co-morbidities. Therefore, whilst patients are being managed for other acute medical problems they are deemed unfit for an immediate angiogram ultimately causing a delay. Furthermore, some patients were not referred to cardiology immediately after the NSTEMI event which causes delay in organising the angiogram. Finally, some patients were awaiting a cardiology bed in the Acute Admissions Unit. This causes delay as patients cannot undergo angiogram without a cardiology bed available for recovery. These delays are causing significant differences in the mortality rates of NSTEMI patients. In order to address these issues, a hospital guideline for junior doctors regarding the management of NSTEMIs has been designed and distributed. The guideline emphasises the importance of early cardiology referral, the management of acute medical problems in NSTEMIs such pre-hydration to prevent acute kidney injury, and the medical management of NSTEMIs in line with the 2020 ESC guidelines. Finally, it would be useful to re-audit these findings to assess if mortality rates and adherence to the NICE and ESC guidelines improve following these interventions.

scholarly journals Estimated Glomerular Filtration Rate Correlates Poorly with Four-Hour Creatinine Clearance in Critically Ill Patients with Acute Kidney Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Christopher J. Kirwan ◽  
Barbara J. Philips ◽  
Iain A. M. MacPhee
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Critically Ill ◽  
Cystatin C ◽  
Critically Ill Patients ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Serum Cystatin C ◽  
Serum Cystatin

Introduction.RIFLE and AKIN provide a standardised classification of acute kidney injury (AKI), but their categorical rather than continuous nature restricts their use to a research tool. A more accurate real-time description of renal function in AKI is needed, and some published data suggest that equations based on serum creatinine that estimate glomerular filtration rate (eGFR) can provide this. In addition, incorporating serum cystatin C concentration into estimates of GFR may improve their accuracy, but no eGFR equations are validated in critically ill patients with AKI.Aim.This study tests whether creatinine or cystatin-C-based eGFR equations, used in patients with CKD, offer an accurate representation of 4-hour creatinine clearance (4CrCl) in critically ill patients with AKI.Methods.Fifty-one critically ill patients with AKI were recruited. Thirty-seven met inclusion criteria, and the performance of eGFR equations was compared to 4CrCl.Results.eGFR equations were better than creatinine alone at predicting 4CrCl. Adding cystatin C to estimates did not improve the bias or add accuracy. The MDRD 7 eGFR had the best combination of correlation, bias, percentage error and accuracy. None were near acceptable standards quoted in patients with chronic kidney disease (CKD).Conclusions.eGFR equations are not sufficiently accurate for use in critically ill patients with AKI. Incorporating serum cystatin C does not improve estimates. eGFR should not be used to describe renal function in patients with AKI. Standards of accuracy for validating eGFR need to be set.

P2660Definition of clinically relevant thresholds of acute kidney injury in patients with ST-elevation myocardial infarctions undergoing primary percutaneous coronary interventions

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J Schmucker ◽  
A Fach ◽  
R Osteresch ◽  
T Retzlaff ◽  
S Michel ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Contrast Media ◽  
Kidney Injury ◽  
Fold Increase ◽  
Left Ventricular ◽  
Myocardial Infarctions ◽  
Left Ventricular Ejection ◽  
St Elevation ◽  
The Impact

Abstract Background Although the clinical importance of deteriorating kidney function in patients with ST-elevation-myocardial infarctions (STEMI) on overall prognosis is generally accepted, there is conflicting evidence on the importance of small changes in renal function. Aim of the present study was to calculate clincially relevant thresholds for deterioration of renal function after STEMI. Methods From a large registry of patients with STEMI renal function was estimated calculating the glomerular filtration rate (GFR in ml/min/1.73 m2) with the CKD-EPI-equation. To assess acute kidney injury the ratio GFR (at peak creatinine))/ GFR (at admission) was calculated for each patient (with 1 representing no change). Patients were graded by GFR-reduction and assigned to 11 groups (G1 to G11) each representing 5% intervals. Results Of 6583 patients admitted with STEMI between 2006–2017 3518 (53%) had no change or a change <5% during hospital stay (G1) while 161 (3%) showed a decrease in GFR of ≥50% (G11). The rest of the patients could be attributed to G2- G10 (table). There was a pronounced correlation between extent of GFR-reduction and peak creatine kinase (indicating size of STEMI, r2=0.785; G1: 1521±1684 U/l vs. G11: 2885±2943 U/l, p<0.01) as well as left-ventricular ejection fraction (LVEF) (r2=0.79; G1: 50.9±9% vs. G11: 41.4±10%, p<0.01). However, no such correlation could be detected between GFR-reduction and amount of contrast media (CM) applied (r2=0.05, G1: 141±60 ml vs. G11: 139±61 ml, p=0.5). Analysis of outcome-data (1-year-mortality and major adverse cardiovascular and cerebrovascular events (MACCE: death, stroke, re-infarction)) revealed, that beneath a threshold of 25% deterioration of renal function did not significantly impact prognosis, while higher degrees of deterioration led to a 7-fold increase in mortality and a 5-fold increase in MACCE-rates (table). Impact of GFR-reduction on outcome Group G1 G2 G3 G4 G5 G6 G7 G8 G9 G10 G11 GFR-reduction (in %) 0–4 5 to 9 10 to 14 15 to 19 20 to 24 25 to 29 30 to 34 35 to 39 40 to 44 45 to 49 ≥50 Patients, n (%) 3518 (53) 881 (13) 717 (11) 492 (7) 327 (5) 196 (3) 119 (2) 88 (1) 48 (1) 36 (1) 161 (3) 1 year mortality (%) 7 4 5 8 7 15 20 22 39 43 50 1-year-MACCE (%) 12 8 8 12 10 19 27 27 49 49 52 Conclusions These data from a large STEMI-registry show that small changes (less than 25%) in GFR did not significantly impact long-term outcome, while the impact was pronounced for all patients beyond that threshold. The degree of renal deterioration furthermore correlated with size of STEMI as well as reduction of LV-function after STEMI while no correlation to amount of contrast media could be found.

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