scholarly journals TO019PROGNOSTIC VALUE OF ACUTE KIDNEY INJURY AND HEMOCONCENTRATION DURING ACUTE HEART FAILURE

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.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Lombardi ◽  
F Boccara ◽  
K Baldet ◽  
S Lang ◽  
S Ederhy ◽  
...  

Abstract Background Acute kidney injury (AKI) frequently occurs after diuretic treatment initiation during acute heart failure (AHF). Treatment-induced hemoconcentration seems associated with improved prognosis. Transient AKI, with or without hemoconcentration, is of unsettled prognosis. Purpose We aimed to determine the independent prognostic values of transient AKI, persistent AKI and hemoconcentration in the context of hospitalized AHF. Methods Data were obtained from our institution's Clinical Data Warehouse. Patients that visited our unit at least once were screened. All hospitalizations in our institution were examined (>30 hospitals). Inclusion criteria were: ≥1 hospitalization with ≥1 recorded furosemide administration and ≥1 AHF ICD-10 code. Only the first hospitalization fulfilling these criteria was considered. AKI during 1–13 days following first furosemide administration was defined based on Kidney Disease Improving Global Outcome guidelines. Hemoconcentration was defined as an increase in serum proteins ≥5 g/l during the same period. We performed multivariate logistic regression to determine which characteristics were predictive of AKI. We used Cox regression of 100-days all-cause mortality using several confounders to determine the prognostic values of transient AKI (lasting <14 days), persistent AKI (lasting ≥14 days) and hemoconcentration. To account for immortality bias, AKI and hemoconcentration were treated as time-dependent covariates. Results We included 579 patients in the study. Median follow-up was 114 days. AKI following furosemide initiation occurred in 234 patients (40.4%). Patients that experienced AKI more frequently suffered from chronic kidney disease (43.6% vs. 33%, p=0.01) or presented with right ventricular dilatation (12% vs. 6.7%, p=0.04). Independent predictors of AKI were arterial hypertension (adjusted OR: 1.86 [1.08–3.22]), elevated serum creatinine at baseline (adjusted OR: 1.07 [1.01–1.14] per 10 μmol/l increase) and initial intravenous 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 Cox regression, 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 In the context of hospitalized AHF, AKI that developed 1–13 days after furosemide initiation and that lasted ≥14 days was independently associated with decreased 100 days survival. Hemoconcentration, using a clinically relevant definition, was independently associated with improved survival. These findings show that serum creatinine and proteins, routinely used and with limited cost, accurately stratify mortality risk during AHF. Kaplan-Meier curves 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.


2019 ◽  
Vol 9 (1) ◽  
pp. 5-22 ◽  
Author(s):  
E. V. Reznik ◽  
I. G. Nikitin

The combination of heart failure and renal failure is called cardiorenal syndrome. It is a stage of the cardiorenal continuum and, possibly, a small link of the cardiorenal-cerebral-metabolic axis. Despite the fact that the phrase “cardiorenal syndrome” and its five types have become a part of the medical lexicon, many aspects of this problem are still not clear. Cardiorenal syndrome can be diagnosed in 32-90.3% of patients with heart failure. Cardiorenal syndrome type 1 or 2 develops in most cases of heart failure: cardiorenal syndrome presents with the development ofchronic kidney disease in patients with chronic heart failure and acute kidney injury in patients with acute heart failure. Impaired renal function has an unfavorable prognostic value. It leads to an increase in the mortality of patients with heart failure. It is necessary to timely diagnose the presence of cardiorenal syndrome and take into account its presence when managing patients with heart failure. Further researches are needed on ways toprevent the development and prevent the progression of kidney damage in patients with heart failure, to which the efforts of the multidisciplinary team should be directed. The first part of this review examines the currently definition, classification, pathogenesis, epidemiology and prognosis of cardiorenal syndrome in patients with heart failure.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Hao T Phan

Introduction: The presence of acute kidney injury in the setting of acute heart failure (AHF) or acute decompensated heart failure (ADHF) is very common occurrence and was termed cardiorenal syndrome 1 (CRS1). Renal dysfunction is common in patients with AHF or ADHF and is associated with significant early and late morbidity and mortality. Neutrophil gelatinase-associated lipocalin (NGAL) is an early predictor of acute kidney injury and adverse events in various diseases; however, in AHF or ADHF patients, its significance remains poorly understood. This study was aimed to evaluate the 12 month prognostic value of plasma NGAL in AHF or ADHF patients Hypothesis: plasma NGAL has value in prognosis of 12-month all-cause mortality of Acute Heart Failure or Acute Decompensated Heart Failure Methods: This was a prospective cohort study Results: there were 46 all-cause mortality cases (rate 33.1%) 12 months follow up after discharge. There were 11 cases (rate 7.9%) lost to follow-up; mean age 66.12 ± 15.77, men accounted for 50.4%. The optimal cut-off of NGAL for 12-month all-cause mortality prognosis was > 383.74 ng/ml, AUC 0.632 (95% CI 0.53-0.74, p = 0.011), sensitivity 58.7 %, specificity 68.29 %, positive predictive value 50.9%, negative predictive value 74.7%. Kaplan-Meier analysis revealed that the high plasma NGAL (≥ 400 ng/ml) group exhibited a worse prognosis than the low plasma NGAL (< 400 ng/ml) group in 12-month all-cause death (Hazard Ratio 2.56; 95%CI 1.35-4.84, P=0.0039. Independent predictors of 12-month all-cause-mortality were identified using multivarable Cox proportional-hazards regression models with backward-stepwise selection method consisted of two variables: level of NGAL, mechanical ventialtion at admission. Conclusions: Plasma NGAL and mechanical ventilation at admission were independent predictors of 12-month all-cause mortality in patients with AHF or ADHF. The survival probability 12-month follow-up of high level NGAL (≥ 400 ng/ml) groups were lower than that of low level NGAL (<400 ng/ml,), difference was statistically significant χ2 = 8.31; p = 0.0047 by Kaplan-Meier curves.


2015 ◽  
Vol 21 (5) ◽  
pp. 382-390 ◽  
Author(s):  
Gregory Berra ◽  
Nicolas Garin ◽  
Jérôme Stirnemann ◽  
Anne-Sophie Jannot ◽  
Pierre-Yves Martin ◽  
...  

Kardiologiia ◽  
2019 ◽  
Vol 59 (2S) ◽  
pp. 25-30
Author(s):  
E. V. Efremova ◽  
A. M. Shutov ◽  
E. R. Makeeva ◽  
M. V. Menzorov ◽  
E. R. Sakaeva ◽  
...  

Actuality.Impaired kidney function adversely influences both immediate and remote prognosis for patients with chronic heart failure (CHF). However, early detection and prediction of acute kidney injury (AKI) are understudied.The aimof study was to investigate hypoxia-inducible factor 1 (HIF-1) as a biomarker for early diagnosis of AKI and determining prognosis in patients with acute decompensated CHF (ADCHF).Materials and methods:84 patients admitted for ADCHF (18 women; mean age, 61.4±7.1) were evaluated. ADCHF was diagnosed in accordance with SEHF guidelines for diagnosis and treatment of chronic heart failure (RCS, 2016). AKI was diagnosed according to KDIGO criteria (2012). HIF-1, N-terminal pro B-type natriuretic peptide (NТ-proBNP), and erythropoietin were measured in blood serum. The follow-up period lasted for 12 months.Results:AKI was diagnosed in 27 (32.1 %) patients. Level of HIF-1 was 1.27±0.63 ng / ml; NТ-proBNP – 2469.6 (interquartile range (IQR), 1312.2; 3300.0) pg / ml; eryhthropoietin – 56.0 mIU / ml (IQR, 13.2; 68.1). No correlation was found between HIF-1 and glomerular filtration rate, NТ-proBNP, or erythropoietin. Differences in biomarker levels were not observed between patients with and without AKI; however, HIF-1 was higher in the group of deceased patients than in the group of survived patients (1.64±0.9 vs. 1.17±0.44 ng / ml, р=0.004), which was not observed for NТ-proBNP and erythropoietin.Conclusion.AKI was observed in every third patient with ADCHF. In ADCHF, HIF-1 was not correlated with the kidney function; however, a relationship was found between the HIF-1 level and prediction for patients with CHF.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Natalie Ebert ◽  
Alice Schneider ◽  
Yanina Balabanova ◽  
Gunnar Brobert ◽  
Dörte Huscher ◽  
...  

Abstract Background and Aims Acute kidney injury (AKI) is amongst the most common in-hospital complications especially in old age. Epidemiological data on incidence rates (IR) of nosocomial AKI in individuals aged 70+ years, stratified by age, gender and pre-existing diseases are scarce because older adults are usually underrepresented in clinical research. Method We used data from the Berlin Initiative Study (BIS), a longitudinal, population-based cohort of adults aged ≥70 with biennial follow-up visits (including blood and urine tests) in combination with claims data from the AOK Nordost insurance fund to complement information on diagnoses and in-hospital procedures (based on ICD-10 and OPS coding). Nosocomial AKI was defined as documented in-hospital diagnosis (ICD-10: N17.xx) excluding cases with AKI as admission diagnosis. Incidence rates (IR) and 95% confidence intervals (CI) of the first nosocomial AKI were calculated with the number of incident cases during observation divided by the total person-years of follow-up, for AKI cases truncated at the first incidence of nosocomial AKI. IR are reported by age strata, sex and preexisting diseases (diabetes, arterial hypertension, atrial fibrillation, heart failure, angina pectoris, peripheral artery disease and impaired kidney function). Results In 2020 individuals (mean age 80.5 years; 52.6% women), 383 developed nosocomial AKI over the median [IQR] follow up time of 8.8 [5.9-9.3] years (Fig.1). The IR of nosocomial AKI was 26.8 (95%CI 24.1-29.6) per 1000 person years among all patients, with higher IR in men compared to women, and - when stratified by age - lowest IR in age category 70-75 versus the highest IR in age category of ≥ 90 years (Fig.1). IR per 1000 person years were higher in patients with diabetes mellitus (IR: 39.3 vs 22.7), arterial hypertension (IR: 31.1 vs 12.2), chronic heart failure (IR: 41.9 vs 22.3), angina pectoris (IR: 37.6 vs 25.7), peripheral artery disease (IR: 55.0 vs 25.1) and impaired kidney function (IR: 43.3 vs 12.4), respectively (Fig.2). Conclusion Nosocomial AKI is an in-hospital complication common in older adults with IRs rising continuously with age above the age of 70 years. IR of AKI are considerably higher in patients with cardiovascular comorbidities. A better understanding of the patient population at risk is of great clinical relevance when aiming to improve prevention strategies.


2020 ◽  
Vol 21 (4) ◽  
pp. 147032032097979
Author(s):  
Li Lei ◽  
Yulu Huang ◽  
Zhaodong Guo ◽  
Feier Song ◽  
Yibo He ◽  
...  

Introduction: Renin-angiotensin system inhibitors (RASi) reduce mortality among heart failure (HF) patients, but their effect among those complicating contrast-induced acute kidney injury (CI-AKI) remains unexplored. We aimed to investigate whether the relationship between RASi prescription at discharge and mortality differs between HF patients with or without CI-AKI following coronary angiography (CAG). Methods: About 596 HF patients from an observational cohort were divided into a CI-AKI group ( n = 104) and a non-CI-AKI group ( n = 492) based on whether they had CI-AKI following CAG. The endpoint was all-cause mortality. Multivariable Cox regression was performed in each group to explore the associations between RASi at discharge and mortality. Results: During the median follow-up time of 2.26 (1.70; 3.24) years, higher mortality rate was observed in the CI-AKI group compared to the non-CI-AKI group (18.3% vs 8.9%, p = 0.002). Among HF patients with CI-AKI, after adjusting for confounding factors, the association was not significant between RASi prescription at discharge and mortality (HR: 0.39, 95%CI: 0.12–1.31, p = 0.128), while it was among those without CI-AKI (HR: 0.39, 95%CI: 0.18–0.84, p = 0.016). Conclusion: RASi prescription at discharge for HF patients complicating CI-AKI tended to be ineffective, while it benefited those without CI-AKI. Further randomized evidence is needed to confirm this trend.


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