scholarly journals Bisoprolol Caused Warm Shock and Acute Kidney Injury in a Severe Heart Failure Patient

2015 ◽  
Vol 21 (10) ◽  
pp. S191 ◽  
Author(s):  
Hiromi Tsuchiya ◽  
Hidetaka Kioka ◽  
Norifumi Nakamura ◽  
Kei Nakamoto ◽  
Yasumasa Tsukamoto ◽  
...  
2020 ◽  
Vol 7 (5) ◽  
pp. 3161-3164
Author(s):  
Jonathan Slawik ◽  
Juliane Dederer ◽  
Ingrid Kindermann ◽  
Michael Böhm

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
L Lei ◽  
Y He ◽  
Z Guo ◽  
B Liu ◽  
J Liu ◽  
...  

Abstract Background Patients with congestive heart failure (CHF) are vulnerable to contrast-induced acute kidney injury (CI-AKI), but few prediction models are currently available. Objectives We aimed to establish a simple nomogram for CI-AKI risk assessment for patients with CHF undergoing coronary angiography. Methods A total of 1876 consecutive patients with CHF (defined as New York Heart Association functional class II-IV or Killip class II-IV) were enrolled and randomly (2:1) assigned to a development cohort and a validation cohort. The endpoint was CI-AKI defined as serum creatinine elevation of ≥0.3 mg/dL or 50% from baseline within the first 48–72 hours following the procedure. Predictors for the nomogram were selected by multivariable logistic regression with a stepwise approach. The discriminative power was assessed using the area under the receiver operating characteristic (ROC) curve and was compared with the classic Mehran score in the validation cohort. Calibration was assessed using the Hosmer–Lemeshow test and 1000 bootstrap samples. Results The incidence of CI-AKI was 9.06% (n=170) in the total sample, 8.64% (n=109) in the development cohort and 9.92% (n=61) in the validation cohort (p=0.367). The simple nomogram including four predictors (age, intra-aortic balloon pump, acute myocardial infarction and chronic kidney disease) demonstrated a similar predictive power as the Mehran score (area under the curve: 0.80 vs 0.75, p=0.061), as well as a well-fitted calibration curve. Conclusions The present simple nomogram including four predictors is a simple and reliable tool to identify CHF patients at risk of CI-AKI, whereas further external validations are needed. Figure 1 Funding Acknowledgement Type of funding source: None


2021 ◽  
Author(s):  
Toby J L Humphrey ◽  
Glen James ◽  
Eric T Wittbrodt ◽  
Donna Zarzuela ◽  
Thomas F Hiemstra

Abstract Background Users of guideline-recommended renin–angiotensin–aldosterone system (RAAS) inhibitors may experience disruptions to their treatment, e.g. due to hyperkalaemia, hypotension or acute kidney injury. The risks associated with treatment disruption have not been comprehensively assessed; therefore, we evaluated the risk of adverse clinical outcomes in RAAS inhibitor users experiencing treatment disruptions in a large population-wide database. Methods This exploratory, retrospective analysis utilized data from the UK’s Clinical Practice Research Datalink, linked to Hospital Episodes Statistics and the Office for National Statistics databases. Adults (≥18 years) with first RAAS inhibitor use (defined as angiotensin-converting enzyme inhibitors or angiotensin receptor blockers) between 1 January 2009 and 31 December 2014 were eligible for inclusion. Time to the first occurrence of adverse clinical outcomes [all-cause mortality, all-cause hospitalization, cardiac arrhythmia, heart failure hospitalization, cardiac arrest, advancement in chronic kidney disease (CKD) stage and acute kidney injury] was compared between RAAS inhibitor users with and without interruptions or cessations to treatment during follow-up. Associations between baseline characteristics and adverse clinical outcomes were also assessed. Results Among 434 027 RAAS inhibitor users, the risk of the first occurrence of all clinical outcomes, except advancement in CKD stage, was 8–75% lower in patients without interruptions or cessations versus patients with interruptions/cessations. Baseline characteristics independently associated with increased risk of clinical outcomes included increasing age, smoking, CKD, diabetes and heart failure. Conclusions These findings highlight the need for effective management of factors associated with RAAS inhibitor interruptions or cessations in patients for whom guideline-recommended RAAS inhibitor treatment is indicated.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yannis Lombardi ◽  
Franck Boccara ◽  
Kadiatou Baldet ◽  
Stéphane Ederhy ◽  
Pascal Nhan ◽  
...  

Abstract Background and Aims Acute kidney injury (AKI) occurring after diuretic treatment initiation for acute heart failure (AHF) is a common phenomenon, with an incidence estimated between 20 and 50% of AHF hospitalizations. Previous studies found that persistent AKI is associated with poor prognosis. Treatment-induced hemoconcentration is associated with improved prognosis, but several definitions previously used are not suited for clinical practice. Transient AKI, with or without hemoconcentration, is of unsettled prognosis. We aim to determine the independent prognostic value of transient AKI, persistent AKI and hemoconcentration in the context of AHF hospitalization, using practical definitions. Method Data were obtained from the Greater Paris University Hospitals (GPUH) Clinical Data Warehouse. Patients hospitalized for AHF in various GPUH units were included. AHF hospitalization was defined as hospitalization with at least one AHF ICD-10 code and at least one recorded furosemide administration. Bumetanide is rarely used in GPUH hospitals hence it was not considered. AKI in a period of 14 days following first furosemide administration was defined based on KDIGO guidelines. Hemoconcentration was defined as an increase in serum proteins ≥ 5 g/l during the same period. Multivariate logistic regression was performed to determine which characteristics were predictive of AKI. Cox regression of 100 days all-cause mortality using multiple confounders was performed to determine the prognostic value of transient AKI (< 14 days), persistent AKI (≥ 14 days) and hemoconcentration. Patients with AKI upon hospital entry were excluded from regression analyses. AKI and hemoconcentration were treated as time-dependent covariates to adjust for immortality bias. Results Five hundred seventy nine patients were included. Among them, 529 had no AKI upon hospital entry and 513 had at least one recorded serum proteins and creatinine value following furosemide initiation. Median follow-up was 114 days. AKI in a period of 14 days following furosemide initiation occurred in 234 patients (40.4%). At baseline, patients in the AKI group more frequently suffered from chronic kidney disease or presented with clinical and echocardiographic signs of right heart failure. Independent predictors of AKI were arterial hypertension upon furosemide initiation (adjusted OR 1.86 [1.08 – 3.22]), elevated serum creatinine upon furosemide initiation (adjusted OR 1.07 [1.01 – 1.14] per 10 µmol/l increase) and initial intravenous administration of furosemide (adjusted OR 2.42 [1.39 – 4.29]). Death during follow-up occurred in 35% of patients in the AKI group compared to 21% in the non-AKI group (p < 0.001). In multivariate analysis, persistent AKI was independently associated with increased mortality in a period of 100 days following furosemide initiation (adjusted HR 2.31 [1.07 – 4.99]). Transient AKI was not significantly associated with mortality (adjusted HR 0.64 [0.34 – 1.19]). Hemoconcentration was independently associated with decreased mortality (adjusted HR 0.46 [0.27 – 0.79]). Conclusion After furosemide initiation during hospitalization for AHF, persistent AKI (≥ 14 days) was independently associated with increased 100 days mortality. Hemoconcentration, using a definition suited for clinical practice (≥ 5 g/l increase in serum proteins), was independently associated with decreased 100 days mortality. No significant association was found between mortality and transient AKI (< 14 days). Those findings show that laboratory tests at a limited cost – serum proteins and creatinine – are helpful to evaluate treatment response and mortality risk during AHF. Prospective randomized controlled trials are needed to establish diuretic strategies based on both AKI and hemoconcentration.


2015 ◽  
Vol 25 (10) ◽  
pp. 26-27
Author(s):  
Susan Patricia Romain

2022 ◽  
pp. ASN.2021060757
Author(s):  
Sherry Mansour ◽  
Pavan Bhatraju ◽  
Steven Coca ◽  
Wassim Obeid ◽  
Francis Wilson ◽  
...  

Background The mechanisms underlying long-term sequelae following acute kidney injury (AKI) remain unclear. Vessel instability, an early response to endothelial injury, may reflect a shared mechanism and early trigger for chronic kidney disease (CKD) and heart failure. Methods To investigate whether plasma angiopoietins, markers of vessel homeostasis, are associated with CKD progression and heart failure admissions after hospitalization in patients with and without AKI, we conducted a prospective cohort study to analyze the balance between angiopoietin-1 (Angpt-1), which maintains vessel stability, and angiopoietin-2 (Angpt-2), which increases vessel destabilization. Three months after discharge, we evaluated the associations between angiopoietins and development of the primary outcomes of CKD progression and heart failure, as well as the secondary outcome of all-cause mortality 3 months after discharge or later. Results Median age for the 1503 participants was 65.8 years; 746 (50%) had AKI. Compared with the lowest quartile, the highest quartile of the Angpt-1:Angpt-2 ratio was associated with 72% lower risk of CKD progression (adjusted hazard ratio [aHR], 0.28; 95% confidence interval [95% CI], 0.15 to 0.51), 94% lower risk of heart failure (aHR, 0.06; 95% CI, 0.02 to 0.15), and 82% lower risk of mortality (aHR, 0.18; 95% CI, 0.09 to 0.35) for those with AKI. Among those without AKI, the highest quartile of Angpt-1:Angpt-2 ratio was associated with 71% lower risk of heart failure (aHR, 0.29; 95% CI, 0.12 to 0.69) and 68% less mortality (aHR, 0.32; 95% CI, 0.15 to 0.68). There were no associations with CKD progression. Conclusions A higher Angpt-1:Angpt-2 ratio was strongly associated with less CKD progression, heart failure, and mortality in the setting of AKI.


2011 ◽  
Vol 17 (9) ◽  
pp. S163
Author(s):  
Shigeru Matsui ◽  
Junnichi Ishii ◽  
Kousuke Hattori ◽  
Tousei Hashimoto ◽  
Hiroyuki Naruse ◽  
...  

2019 ◽  
Author(s):  
Suzanne J Faber ◽  
Nynke Scherpbier ◽  
Hans Peters ◽  
Annemarie Uijen

Abstract Background Elderly, patients with chronic kidney disease (CKD) and patients with heart failure who continue using renin-angiotensin-aldosterone-system (RAAS) inhibitors, diuretics, or non-steroidal-anti-inflammatory drugs (NSAIDs) during times of fluid loss have a high risk of developing complications like acute kidney injury (AKI). The aim of this study was to assess how often advice to discontinue high-risk medication was offered to high-risk patients consulting the general practitioner (GP) with increased fluid loss. Furthermore, we assessed the number and nature of the complications that occurred after GP consultation. Methods We performed a cross-sectional study with patients from seven Dutch general practices participating in the Family Medicine Network between 1-6-2013 and 1-7-2018. We included patients who used RAAS-inhibitors, diuretics, or NSAIDs, and had at least one of the following risk factors: age ≥70 years, CKD, or heart failure. From this population, we selected patients with a ‘dehydration-risk’ episode (vomiting, diarrhoea, fever, chills, or gastrointestinal infection). We manually checked their electronic patient files and assessed the percentage of episodes in which advice to discontinue the high-risk medication was offered and whether a complication occurred in three months after the ‘dehydration-risk’ episode. Results We included 3607 high-risk patients from a total of 44.675 patients (8.1%). We found that patients were advised to discontinue the high-risk medication in 38 (4.6%) of 816 ‘dehydration-risk’ episodes. In 59 of 816 episodes (7.1%) complications (mainly AKI) occurred. Conclusions Dutch GPs do not frequently advise high-risk patients to discontinue high-risk medication during ‘dehydration-risk’ episodes. Complications occur frequently. Timely discontinuation of high-risk medication needs attention.


2018 ◽  
Vol 71 (2) ◽  
pp. 236-245 ◽  
Author(s):  
Nisha Bansal ◽  
Michael E. Matheny ◽  
Robert A. Greevy ◽  
Svetlana K. Eden ◽  
Amy M. Perkins ◽  
...  

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