Effect of SGLT-2 inhibitors on acute kidney injury in patients with heart failure: a systematic review and meta-analysis
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ABSTRACT:
SUBMITTER: Wang X
PROVIDER: S-EPMC11348759 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:A quarter of patients with acute decompensated heart failure (ADHF) experience acute kidney injury (AKI), an abrupt loss of kidney function that doubles the risk of death at one-year. There is a critical need to identify early markers for AKI in ADHF, however, no protein candidates have been validated as diagnostic or prognostic biomarkers in this setting. We aimed to identify novel candidate protein biomarkers by quantifying changes in protein expression in the kidney that occur during ADHF development and recovery in an ovine model. Relative quantitative protein profiling was performed using Sequential Window Acquisition of All Theoretical Mass Spectrometry (SWATH-MS) in kidney cortex from healthy control sheep (n=5), sheep with established rapid pacing-induced ADHF (n=8) and sheep after ~4 weeks recovery from ADHF (n=7). Of 790 proteins quantified, we identified 17 candidate kidney injury markers, one potential marker of kidney recovery and two markers of long-term renal impairment that were differentially expressed between groups (1.2-2.6 fold-change, p<0.05). Differentially expressed proteins were enriched in pro-inflammatory signaling pathways: Glycoprotein VI (activated during ADHF development, adjusted p<0.01) and acute phase response (repressed during recovery from ADHF, p<0.01). This research identified 20 candidate protein markers of kidney injury, including 6 promising candidates supported by existing evidence and 14 novel candidates never implicated in AKI. Early awareness of AKI in ADHF through the use of biomarkers has the potential to reduce mortality and improve outcomes for these at-risk patients.
2022-01-19 | PXD028983 | Pride
Project description:Acute kidney injury (AKI) is common in patients with heart failure (HF), but studies have been inconsistent about the incidence of AKI in patients with HF. We conducted a meta-analysis to examine the incidence of AKI and its impact on mortality in patients with HF. We also looked at inpatient variables that could predict the development of AKI to identify potential risk factors, so that these can be used as a starting point for intervention and prevention in this group. The Embase, Medline, PubMed, Cochrane libraries, and Web of Science databases were used for searching articles from the inception of the database to October 2022. The EndNote software was used for screening. Meta-analysis was performed using Stata 16.0 software to combine effect sizes. A total of 37 studies were included. Of all the 3 533 583 patients with HF, 774 887 had AKI, with a pooled incidence of 33% [95% confidence interval (CI): 32-35%]. The incidence rate of AKI in acute HF and chronic HF was 36% (95% CI: 31-40%) and 30% (95% CI: 24-35%), respectively. Eleven studies found that AKI patients had higher in-hospital mortality than non-AKI patients [risk ratio (RR): 3.65; 95% CI: 3.04-4.39, P < 0.001]. Mortality was assessed in five studies, and it was found that mortality remained high at 1-year follow-up after onset of AKI (RR: 1.85, 95% CI: 1.54-2.22, P < 0.001). Fifteen admission variables were included and analysed in 13 studies. The combined results showed that diabetes, hypertension, history of chronic kidney disease, chronic HF systolic, age, N-terminal pro-B-type natriuretic peptide, creatinine > 1.0 mg/dL, index estimated glomerular filtration rate < 60 mL/min/1.73 m2 , blood urea nitrogen > 24 mg/dL, intravenous dobutamine, and serum albumin were predictor factors for HF patients with AKI (P < 0.05). In this meta-analysis, AKI occurred in approximately 33% of HF patients during hospitalization and the risk of dying in the hospital was tripled. Even during 1-year long-term follow-up, the risk of death remained high, and multiple inpatient variables showed that HF patients tended to have AKI. Early intervention and treatment are important to reduce the incidence of AKI and improve the prognosis.
| S-EPMC10682870 | biostudies-literature
Project description:One-quarter of patients with acute decompensated heart failure (ADHF) experience acute kidney injury (AKI)-an abrupt reduction or loss of kidney function associated with increased long-term mortality. There is a critical need to identify early and real-time markers of AKI in ADHF; however, to date, no protein biomarkers have exhibited sufficient diagnostic or prognostic performance for widespread clinical uptake. We aimed to identify novel protein biomarkers of AKI associated with ADHF by quantifying changes in protein abundance in the kidneys that occur during ADHF development and recovery in an ovine model. Relative quantitative protein profiling was performed using sequential window acquisition of all theoretical fragment ion spectra-mass spectrometry (SWATH-MS) in kidney cortices from control sheep (n = 5), sheep with established rapid-pacing-induced ADHF (n = 8), and sheep after ~4 weeks recovery from ADHF (n = 7). Of the 790 proteins quantified, we identified 17 candidate kidney injury markers in ADHF, 1 potential kidney marker of ADHF recovery, and 2 potential markers of long-term renal impairment (differential abundance between groups of 1.2-2.6-fold, adjusted p < 0.05). Among these 20 candidate protein markers of kidney injury were 6 candidates supported by existing evidence and 14 novel candidates not previously implicated in AKI. Proteins of differential abundance were enriched in pro-inflammatory signalling pathways: glycoprotein VI (activated during ADHF development; adjusted p < 0.01) and acute phase response (repressed during recovery from ADHF; adjusted p < 0.01). New biomarkers for the early detection of AKI in ADHF may help us to evaluate effective treatment strategies to prevent mortality and improve outcomes for patients.
| S-EPMC8778509 | biostudies-literature
Project description: Not available
| S-EPMC11023357 | biostudies-literature
Project description:Objective: The study aimed to evaluate the effect of sodium-glucose transporter 2 (SGLT-2) inhibitors on various parameters of exercise capacity and provide an evidence-based basis for type 2 diabetes mellitus (T2DM) combined with heart failure (HF) patients or HF patients without T2DM who use SGLT-2 inhibitors to improve cardiorespiratory fitness (CRF). Methods: According to the participant, intervention, comparison, and outcome (PICO) elements, the effects of SGLT-2 inhibitor administration on VO2 or VO2peak were researched in this study. Weighted mean difference (WMD) and 95% confidence intervals (CIs) were calculated (random-effects model). Heterogeneity was assessed by the I2 test. Results: Six studies were included according to the eligibility criteria: four were RCTs, and two were non-RCTs. Compared with the control group, the merge results of RCTs showed that SGLT-2 inhibitors could significantly increase the VO2peak (WMD, 2.02 ml kg-1 min-1, 95% CI: 0.68-3.37, and p = 0.03; I2 = 0% and p = 0.40) and VAT (WMD, 1.57 ml kg-1 min-1, 95% CI: 0.06-3.07, and p = 0.04; I2 = 0% and p = 0.52) of the obese population, patients with T2DM, and chronic HF patients with or without T2DM. Subgroup analysis showed that SGLT-2 inhibitors improved the VO2peak in non-HF patients (WMD, 3.57 ml kg-1 min-1, 95% CI: 0.87-6.26, and p = 0.009; I2 = 4% and p = 0.31) more than in HF patients (WMD, 1.46 ml kg-1 min-1, 95% CI: -0.13-3.04, and p = 0.07; I2 = 0% and p = 0.81). Moreover, the merge of single-arm studies also indicated that empagliflozin could improve VO2peak (MD, 1.11 ml kg-1 min-1, 95% CI: 0.93-1.30, and p = 0.827, Δ p = 0.000 and I2 = 0%) of T2DM patients with chronic HF. Conclusion: Despite the limited number of studies and samples involved, the meta-analysis preliminarily demonstrated that SGLT-2 inhibitors could improve some parameters of exercise capacity (VO2peak, VAT) in chronic HF patients with or without T2DM and obese individuals, which had a positive effect on promoting cardiopulmonary fitness to help these populations improve their prognosis. Systematic Review Registration: [https://www.crd.york.ac.uk/prospero/#recordDetails], identifier [CRD42020202788].
| S-EPMC9871354 | biostudies-literature
Project description:BackgroundGalectin-3, a biomarker of inflammation and fibrosis, can be associated with renal and myocardial damage and dysfunction in patients with acute heart failure (AHF).Methods and resultsWe retrospectively analyzed 790 patients with AHF who were enrolled in the AKINESIS study. During hospitalization, patients with galectin-3 elevation (> 25.9 ng/mL) on admission more commonly had acute kidney injury (assessed by KDIGO criteria), renal tubular damage (peak urine neutrophil gelatinase-associated lipocalin [uNGAL] > 150 ng/dL) and myocardial injury (≥ 20% increase in the peak high-sensitivity cardiac troponin I [hs-cTnI] values compared to admission). They less commonly had ≥ 30% reduction in B-type natriuretic peptide from admission to last measured value. In multivariable linear regression analysis, galectin-3 was negatively associated with estimated glomerular filtration rate and positively associated with uNGAL and hs-cTnI. Higher galectin-3 was associated with renal replacement therapy, inotrope use and mortality during hospitalization. In univariable Cox regression analysis, higher galectin-3 was associated with increased risk for the composite of death or rehospitalization due to HF and death alone at 1 year. After multivariable adjustment, higher galectin-3 levels were associated only with death.ConclusionsIn patients with AHF, higher galectin-3 values were associated with renal dysfunction, renal tubular damage and myocardial injury, and they predicted worse outcomes.
| S-EPMC11427130 | biostudies-literature
Project description: Not available
| S-EPMC8978138 | biostudies-literature
Project description:BackgroundHeart failure with preserved ejection fraction (HFpEF) is becoming the main subtype of heart failure, but lacks proven effective therapies. Sodium-glucose cotransporter-2 (SGLT-2) inhibitor, a new kind of oral glucose-lowering agent, shows a great effect on improving cardiovascular outcomes. Based on the results of current RCTs, we perform this meta-analysis to illustrate the therapeutic impact of SGLT2i in HFpEF patients.MethodsWe systematically searched the online database and 10 RCTs were involved. The primary outcome was the prognosis outcome of HFpEF patients, including a composite outcome of cardiovascular (CV) death and hospitalization for heart failure (HHF), CV mortality, HHF, and all-cause mortality. Main secondary outcomes included improvement of KCCQ-TSS (Kansas City Cardiomyopathy Questionnaire and total symptom score) and 6-Minute Walk Test (6MWT). All pooled results were calculated by the random-effects model. Statistical heterogeneity was assessed using the chi-squared test and was quantified using the I-squared statistic.ResultsTen RCTs comprising 10,334 patients were involved in. Incidence of composite outcome was reduced in SGLT-2 inhibitor group compared with placebo (HR: 0.78, 95% CI: 0.69-0.88, p = 0.00). Improvement of KCCQ-TSS was also more pronounced in the SGLT-2 inhibitor group (MD: 2.74, 95% CI: 1.30-4.18, p = 0.00). No statistical difference was observed in 6MWT.ConclusionTreating HFpEF patients with SGLT-2 inhibitors is associated with reducing the composite outcome of CV death and HHF and improving health-related quality of life. Further studies with more evidence are in need to confirm this conclusion.
| S-EPMC9492916 | biostudies-literature
Project description:BackgroundAcute kidney injury (AKI) is a common complication of acute heart failure (HF) that can prolong hospitalization time and worsen the prognosis. The objectives of this research were to ascertain independent risk factors of AKI in hospitalized HF patients and validate a nomogram risk prediction model established using those factors.MethodsFinally, 967 patients hospitalized for HF were included. Patients were randomly assigned to the training set (n = 677) or test set (n = 290). Least absolute shrinkage and selection operator (LASSO) regression was performed for variable selection, and multivariate logistic regression analysis was used to search for independent predictors of AKI in hospitalized HF patients. A nomogram prediction model was then developed based on the final identified predictors. The performance of the nomogram was assessed in terms of discriminability, as determined by the area under the receiver operating characteristic (ROC) curve (AUC), and predictive accuracy, as determined by calibration plots.ResultsThe incidence of AKI in our cohort was 19%. After initial LASSO variable selection, multivariate logistic regression revealed that age, pneumonia, D-dimer, and albumin were independently associated with AKI in hospitalized HF patients. The nomogram prediction model based on these independent predictors had AUCs of 0.760 and 0.744 in the training and test sets, respectively. The calibration plots indicate a strong concordance between the estimated AKI probabilities and the observed probabilities.ConclusionsA nomogram prediction model based on pneumonia, age, D-dimer, and albumin can help clinicians predict the risk of AKI in HF patients with moderate discriminability.
| S-EPMC11367008 | biostudies-literature
Project description:ObjectiveTo quantify the risk of hyperkalemia and acute kidney injury (AKI) when spironolactone use is added on to loop diuretic use among patients with heart failure, and to evaluate whether the risk is modified by level of kidney function.MethodsWe identified 17,110 patients with heart failure treated with loop diuretics between January 1, 2004, and December 31, 2016 within the Geisinger Health System. We estimated the incidence of hyperkalemia and AKI associated with spironolactone initiation, and used target trial emulation methods to minimize confounding by indication.ResultsDuring a mean follow-up of 134 mo, 3229 of 17,110 patients (18.9%) initiated spironolactone. Incidence rates of hyperkalemia and AKI in patients using spironolactone with a loop diuretic were 2.9 and 10.1 events per 1000 person-months, respectively. In propensity score-matched analyses, spironolactone initiation was associated with higher hyperkalemia and AKI risk compared with loop alone (hazard ratio, 1.69; 95% CI, 1.35 to 2.10; P<.001, and hazard ratio, 1.12; 95% CI, 1.00 to 1.26; P=.04, respectively). There were no differences in the relative risk of either outcome associated with spironolactone by level of kidney function.ConclusionThe addition of spironolactone to loop diuretics in patients with heart failure was associated with higher risk of hyperkalemia and AKI; these risks must be weighed against the potential benefits of spironolactone.
| S-EPMC8005315 | biostudies-literature