Prognosis of acute kidney injury during acute heart failure: the role of diuretics

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

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.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3463-3463
Author(s):  
Tatsunori Shimoi ◽  
Minoru Ando ◽  
Takeshi Kobayashi ◽  
Kazuhiko Kakihana ◽  
Takuya Yamashita ◽  
...  

Abstract Abstract 3463 Introduction: Chronic kidney disease (CKD) is common in survivors of hematopoietic stem cell transplantation (SCT). However, evolution over time of kidney dysfunction and its association with post-SCT acute kidney injury (AKI) are unclear. Methods: A retrospective cohort study was performed in 86 myeloablative allogenic SCT patients who received SCT between 1990 and 1999 and lived without relapse for 10 years or more. CKD was defined as a sustained decrease in estimated GFR less than 60 ml/min/1.73 m2 at least for a period more than 3 months. Post-SCT AKI was classified into three stages according to the acute kidney injury network (AKIN) criteria within 100 days after SCT. Incidence of new-onset CKD was studied by 1-year interval along the course of follow-up. Cumulative CKD incidence was evaluated by the Kaplan-Meier analysis. The factors associated with CKD at the time of 10 years after SCT were examined using Cox regression analysis. Results: The incident of new CKD was the highest (10.5%) at the first year after SCT and then remained almost constant (2.3 to 3.5%) (Figure 1). The prevalence of CKD increased along the follow-up time (Table 1). The cumulative incidence of CKD increased according to increasing AKI stages with significant difference between stages ≥1 and no AKI (Figure 2). Cox regression showed that each AKIN stage was a significant predictor of CKD: stage 3: hazard ratio (HR) 12.7, 95% confidence interval (CI) 2.42–97.6; stage 2: HR 7.75, 95% CI 1.83–53.6; and stage 1: HR 4.36, 95% CI 1.06–29.5. Other predictors included total body irradiation (TBI) (HR, 4.00; 95% CI, 1.63–10.5) and age on SCT (HR, 1.08; 95% CI, 1.03–1.13). Conclusions: CKD accumulated among long-term survivors receiving myeloablative allogenic SCT. Post-SCT AKI, regardless of the AKIN stages, is the most significant risk of CKD in such SCT population. Disclosures: No relevant conflicts of interest to declare.


2019 ◽  
Vol 13 (4) ◽  
pp. 564-570 ◽  
Author(s):  
P S Priyamvada ◽  
Challa Jaswanth ◽  
Bobby Zachariah ◽  
Satish Haridasan ◽  
Sreejith Parameswaran ◽  
...  

Abstract Background Snakebite is a common occupational hazard in tropical countries. To date, the literature on snakebite-related acute kidney injury (AKI) has been limited by retrospective study designs, lack of uniformity in case definitions of AKI and limited follow-up. This study aims to identify the in-hospital outcomes and long-term changes in kidney function that follow haemotoxic envenomation. Methods All adult patients admitted with AKI following haemotoxic envenomation from January 2016 to June 2017 were recruited and followed up until July 2018. Predictors of in-hospital mortality was assessed. Long-term follow-up data on kidney function were collected from survivors. Results In total, 184 patients with haemotoxic envenomation and AKI were recruited. The mean age of the subjects was 42.2 years [95% confidence interval (CI) 40.3–44.7]. The majority were male (71.2%). The mortality of patients with haemotoxic envenomation was 21.5%. The mortality was considerably higher in patients with Kidney Disease: Improving Global Outcomes (KDIGO) Stage 3 AKI [relative risk (RR) 4.45 (95% CI 1.14–17.42)] and those who met KDIGO urine output criteria [RR 20.45 (95% CI 2.84–147.23)]. A Cox regression model identified mechanical ventilation [odds ratio (OR) 5.59 (95% CI 2.90–10.81)], hypotension [OR 2.48 (95% CI 1.31–4.72)] and capillary leak syndrome [OR 2.02 (95% CI 1.05–3.88)] as independent predictors of mortality. Long-term follow-up data were available for 73 patients. A total of 21 patients (28.7%) developed adverse renal outcomes (glomerular filtration rate <60 mL/min/1.73 m2, urine albumin excretion >30 mg/g and new-onset hypertension or prehypertension). Conclusions AKI resulting from snake envenomation is associated with considerable risk of mortality. The greater the AKI stage the greater the likelihood of mortality. One-third of patients with AKI developed long-term complications like chronic kidney disease, prehypertension and hypertension over the follow-up period.


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.


2021 ◽  
Author(s):  
Steven G. Coca ◽  
George Vasquez-Rios ◽  
Sherry Mansour ◽  
Dennis G. Moledina ◽  
Heather Thiessen-Philbrook ◽  
...  

Background: The role of plasma soluble tumor necrosis factor receptor (sTNFR)1 and sTNFR2 in the prognosis of clinical events after hospitalization with or without acute kidney injury (AKI) is unknown. Methods: We measured sTNFR1 and sTNFR2 obtained 3 months post-discharge using samples from Assessment, Serial Evaluation, and Subsequent Sequelae of Acute Kidney Injury (ASSESS-AKI) and AKI Risk in Derby (ARID) that enrolled patients with and without AKI. The associations between biomarkers with longitudinal kidney disease incidence and progression, heart failure, and death were evaluated. Analyses were adjusted for demographics and key covariates at the 3-month visit. Results: Among 1474 participants with plasma biomarker measurements, 19% developed kidney disease progression, 14% had later heart failure, and 21% died over a median follow-up of 4.4 years. For the kidney outcome, the adjusted HRs per doubling in concentration were 2.9 (2.2-3.9) for sTNFR1 and 1.9 (1.5-2.5) for sTNFR2. AKI during the index hospitalization did not modify the association between biomarkers and kidney events. For heart failure, the adjusted HRs per doubling in concentration were 1.9 (1.4-2.5) for sTNFR1 and 1.5 (1.2-2.0) for sTNFR2. For mortality, the adjusted HRs were 3.3 (2.5-4.3) for sTNFR1 and 2.5 (2.0-3.1) for sTNFR2. The findings in ARID were qualitatively similar for the magnitude of association between biomarkers and outcomes. Conclusion: Plasma sTNFR1 and sTNFR2 measured 3 months after discharge were independently associated with clinical events, regardless of AKI status during the index admission. sTNFR1 and sTNFR2 may assist with the risk stratification of patients during follow-up.


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.


Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. 686-686
Author(s):  
Santosh L. Saraf ◽  
Maya Viner ◽  
Ariel Rischall ◽  
Binal Shah ◽  
Xu Zhang ◽  
...  

Abstract Acute kidney injury (AKI) is associated with tubulointerstitial fibrosis and nephron loss and may lead to an increased risk for subsequently developing chronic kidney disease (CKD). In adults with sickle cell anemia (SCA), high rates of CKD have been consistently observed, although the incidence and risk factors for AKI are less clear. We evaluated the incidence of AKI, defined according to Kidney Disease Improving Global Outcomes (KDIGO) guidelines as a rise in serum creatinine by ≥0.3mg/dL within 48 hours or ≥1.5 times baseline within seven days, in 158 of 299 adult SCA patients enrolled in a longitudinal cohort from the University of Illinois at Chicago. These patients were selected based on the availability of genotyping for α-thalassemia, BCL11A rs1427407, APOL1 G1/G2, and the HMOX1 rs743811 and GT-repeat variants. Median values and interquartile range (IQR) are provided. With a median follow up time of 66 months (IQR, 51-74 months), 137 AKI events were observed in 63 (40%) SCA patients. AKI was most commonly observed in the following settings: acute chest syndrome (25%), an uncomplicated vaso-occlusive crisis (VOC)(24%), a VOC with pre-renal azotemia determined by a fractional excretion of sodium <1% or BUN-to-creatinine ratio >20:1 (14%), or a VOC with increased hemolysis, defined as an increase in serum LDH or indirect bilirubin level >1.5 times over the baseline value at the time of enrollment (12%). Compared to individuals who did not develop AKI, SCA adults who developed an AKI event were older (AKI: median and IQR age of 35 (26-46) years, no AKI: 28 (23 - 26) years; P=0.01) and had a lower estimated glomerular filtration rate (eGFR) (AKI: median and IQR eGFR of 123 (88-150) mL/min/1.73m2, no AKI: 141 (118-154) mL/min/1.73m2; P=0.02) by the Kruskal-Wallis test at the time of enrollment. We evaluated the association of a panel of candidate gene variants with the risk of developing an AKI event. These included loci related to the degree of hemolysis (α-thalassemia, BCL11A rs1427407), to chronic kidney disease (APOL1 G1/G2 risk variants), and to heme metabolism (HMOX1) . Using a logistic regression model that adjusted for age and eGFR at the time of enrollment, the risk of an AKI event was associated with older age (10-year OR 2.6, 95%CI 1.4-4.8, P=0.002), HMOX1 rs743811 (OR 3.1, 95%CI 1.1-8.7, P=0.03), and long HMOX1 GT-repeats, defined as >25 repeats (OR 2.5, 95%CI 1.01-6.1, P=0.04). Next, we assessed whether AKI is associated with a more rapid decline in eGFR and with CKD progression, defined as a 50% reduction in eGFR, on longitudinal follow up. Using a mixed effects model that adjusted for age and eGFR at the time of enrollment, the rate of eGFR decline was significantly greater in those with an AKI event (β = -0.51) vs. no AKI event (β = -0.16) (P=0.03). With a median follow up time of 66 months (IQR, 51-74 months), CKD progression was observed in 21% (13/61) of SCA patients with an AKI event versus 9% (8/88) without an AKI event. After adjusting for age and eGFR at the time of enrollment, the severity of an AKI event according to KDIGO guidelines (stage 1 if serum creatinine rises 1.5-1.9 times baseline, stage 2 if the rise is 2.0-2.9 times baseline, and stage 3 if the rise is ≥3 times baseline or ≥4.0 mg/dL or requires renal replacement therapy) was a risk factor for CKD progression (unadjusted HR 1.6, 95%CI 1.1-2.3, P=0.02; age- and eGFR-adjusted HR 1.6, 95%CI 1.1-2.5, P=0.03). In conclusion, AKI is commonly observed in adults with sickle cell anemia and is associated with increasing age and the HMOX1 GT-repeat and rs743811 polymorphisms. Furthermore, AKI may be associated with a steeper decline in kidney function and more severe AKI events may be a risk factor for subsequent CKD progression in SCA. Future studies understanding the mechanisms, consequences of AKI on long-term kidney function, and therapies to prevent AKI in SCA are warranted. Disclosures Gordeuk: Emmaus Life Sciences: Consultancy.


2019 ◽  
Vol 41 (4) ◽  
pp. 462-471 ◽  
Author(s):  
Kellen Hyde Elias Pinheiro ◽  
Franciana Aguiar Azêdo ◽  
Kelsy Catherina Nema Areco ◽  
Sandra Maria Rodrigues Laranja

Abstract Acute kidney injury (AKI) has an incidence rate of 5-6% among intensive care unit (ICU) patients and sepsis is the most frequent etiology. Aims: To assess patients in the ICU that developed AKI, AKI on chronic kidney disease (CKD), and/or sepsis, and identify the risk factors and outcomes of these diseases. Methods: A prospective observational cohort quantitative study that included patients who stayed in the ICU > 48 hours and had not been on dialysis previously was carried out. Results: 302 patients were included and divided into: no sepsis and no AKI (nsnAKI), sepsis alone (S), septic AKI (sAKI), non-septic AKI (nsAKI), septic AKI on CKD (sAKI/CKD), and non-septic AKI on CKD (nsAKI/CKD). It was observed that 94% of the patients developed some degree of AKI. Kidney Disease Improving Global Outcomes (KDIGO) stage 3 was predominant in the septic groups (p = 0.018). Nephrologist follow-up in the non-septic patients was only 23% vs. 54% in the septic groups (p < 0.001). Dialysis was performed in 8% of the non-septic and 37% of the septic groups (p < 0.001). Mechanical ventilation (MV) requirement was higher in the septic groups (p < 0.001). Mortality was 38 and 39% in the sAKI and sAKI/CKD groups vs 16% and 0% in the nsAKI and nsAKI/CKD groups, respectively (p < 0.001). Conclusions: Patients with sAKI and sAKI/CKD had worse prognosis than those with nsAKI and nsAKI/CKD. The nephrologist was not contacted in a large number of AKI cases, except for KDIGO stage 3, which directly influenced mortality rates. The urine output was considerably impaired, ICU stay was longer, use of MV and mortality were higher when kidney injury was combined with sepsis.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Jonghanne Park ◽  
Jin Joo Park ◽  
Young-Jin Cho ◽  
Yeon-Yee Yoon ◽  
Il-Young Oh ◽  
...  

Objectives: We investigated the risk factors for contrast-induced acute kidney injury (CIAKI) after coronary angiography (CAG) in patients with acute heart failure (AHF), especially with regard to the volume status. Background: Heart failure is a well-known risk factor for CIAKI after CAG. In HF patients, renal perfusion decreases with systemic congestion. Thus, the standard prevention strategy with isotonic solution infusion may be inappropriate while decongestion may be beneficiary in AHF patients undergoing CAG. Deviation from dry body weight suggests imbalanced volume status. Methods: A total of 199 AHF patients who underwent CAG were eligible for the analysis. Absolute deviation of body weight (


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