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Renal function monitoring in heart failure - what is the optimal frequency? A narrative review.

ABSTRACT: The second most common cause of hospitalization due to adverse drug reactions in the UK is renal dysfunction due to diuretics, particularly in patients with heart failure, where diuretic therapy is a mainstay of treatment regimens. Therefore, the optimal frequency for monitoring renal function in these patients is an important consideration for preventing renal failure and hospitalization. This review looks at the current evidence for optimal monitoring practices of renal function in patients with heart failure according to national and international guidelines on the management of heart failure (AHA/NICE/ESC/SIGN). Current guidance of renal function monitoring is in large part based on expert opinion, with a lack of clinical studies that have specifically evaluated the optimal frequency of renal function monitoring in patients with heart failure. Furthermore, there is variability between guidelines, and recommendations are typically nonspecific. Safer prescribing of diuretics in combination with other antiheart failure treatments requires better evidence for frequency of renal function monitoring. We suggest developing more personalized monitoring rather than from the current medication-based guidance. Such flexible clinical guidelines could be implemented using intelligent clinical decision support systems. Personalized renal function monitoring would be more effective in preventing renal decline, rather than reacting to it.

SUBMITTER: Al-Naher A

PROVIDER: S-EPMC5736847 | biostudies-other | 2018 Jan

REPOSITORIES: biostudies-other

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Renal function monitoring in heart failure - what is the optimal frequency? A narrative review.

Al-Naher Ahmed A Wright David D Devonald Mark Alexander John MAJ Pirmohamed Munir M

British journal of clinical pharmacology 20171022 1

The second most common cause of hospitalization due to adverse drug reactions in the UK is renal dysfunction due to diuretics, particularly in patients with heart failure, where diuretic therapy is a mainstay of treatment regimens. Therefore, the optimal frequency for monitoring renal function in these patients is an important consideration for preventing renal failure and hospitalization. This review looks at the current evidence for optimal monitoring practices of renal function in patients wi ...[more]

PMID: 28901643

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Project description:Background and Objective Heart failure (HF) is a global public health problem with high morbidity, readmission, and mortality rates. The central mediators of cardiomyocyte survival and death are mitochondria. Mitochondria are a key therapeutic target for HF and are closely involved in the pathophysiological process of HF. A recent study proposes that cuproptosis, a novel cell death mechanism, is closely related to mitochondrial respiration. Therefore, this study aims to explore the link between cuproptosis and HF, and to find novel therapeutic targets and treatments for HF. Methods A literature search (up to April 2022) was conducted through PubMed database, and the search range was limited to publications in English. After further literature search and screening, we found that we are currently the first study to explore the association between HF and cuproptosis. Key Content and Findings Research has found that mitochondria are a key therapeutic target in HF and are involved in the pathophysiological processes of energy metabolism, oxidative stress, calcium regulation, and cell death in HF. The micronutrient copper is involved in regulating mitochondrial biological processes, and high serum copper levels are significantly associated with HF. Copper overload affects mitochondrial function and exacerbates the development of HF. And cuproptosis induced by copper overload targeting lipoylated tricarboxylic acid cycle proteins, is closely related to mitochondrial respiration. Copper chelators not only treat HF but also partially rescue copper-mediated cell death. Copper binding to lipoylated components may be the reason for the hyperacetylation of mitochondrial proteins in HF. Ferredoxin 1 (FDX1) may be an upstream regulator of protein lipoylation and is closely related to cuproptosis. Conclusions This study demonstrates the important roles of mitochondria and micronutrient copper in HF. Cuproptosis may be involved in the pathophysiological process of HF and is responsible for the hyperacetylation of mitochondrial proteins in HF. Cuproptosis has the potential to be a novel therapeutic mechanism for HF, and FDX1 may be a key target for cuproptosis-based treatment of HF. This study provides a new research direction for the treatment of HF and new ideas for the development of new drugs.

Project description:BackgroundExercise-based cardiac rehabilitation (CR) is considered an effective treatment for enhancing endothelial function in patients with heart failure (HF). However, recent studies have been published and the optimal "dose" of exercise required to increase the benefits of exercise-based CR programmes on endothelial function is still unknown.Objectives(a) To estimate the effect of exercise-based CR on endothelial function, assessed by flow-mediated dilation (FMD), in patients with HF; (b) to determine whether high-intensity interval training (HIIT) is better than moderate-intensity training (MIT) for improving FMD; and (c) to investigate the influence of exercise modality (i.e. resistance exercise vs. aerobic exercise and combined exercise vs. aerobic exercise) on the improvement of endothelial function.MethodsElectronic searches were carried out in PubMed, Embase, and Scopus up to February 2022. Random-effects models of between-group mean differences were estimated. Heterogeneity analyses were performed by means of the chi-square test and I2 index. Subgroup analyses and meta-regressions were used to test the influence of potential moderator variables on the effect of exercise.ResultsWe found a FMD increase of 3.09% (95% confidence interval [CI] = 2.01, 4.17) in favour of aerobic-based CR programmes compared with control groups in patients with HF and reduced ejection fraction (HFrEF). However, the results of included studies were inconsistent (p < .001; I2 = 95.2%). Higher FMD improvement was found in studies which were randomised, reported radial FMD, or performed higher number of training sessions a week. Moreover, HIIT enhanced FMD to a greater extent than MIT (2.35% [95% CI = 0.49, 4.22]) in patients with HFrEF. Insufficient data prevented pooled analyses for the effect of exercise in patients with HF and preserved ejection fraction and the influence of exercise modality on the improvement of endothelial function.ConclusionAerobic-based CR is a non-pharmacological treatment for enhancing endothelial function in patients with HFrEF. However, higher training frequency and HIIT induce greater adaptation of endothelial function in these patients, which should betaken into consideration when designing exercise-based CR programmes. Trial registration The protocol was prospectively registered on the PROSPERO database (CRD42022304687).

Project description:BackgroundChronic heart failure (CHF) is the leading cause of all hospitalisations and readmissions in older people, accounting for a large proportion of developed countries' national health care expenditure. CHF can severely affect people's quality of life by reducing their independence and ability to undertake certain activities of daily living, as well as affecting their psychosocial and economic capacity. This paper reports the findings of a systematic narrative review of qualitative studies concerning people's experience of living with CHF, aiming to develop a wide-ranging understanding of what is known about the patient experience.MethodsWe searched eight relevant electronic databases using the terms based on the diagnosis of 'chronic heart failure', 'heart failure' and 'congestive heart failure' and qualitative methods, with restrictions to the years 1990-May 2008. We also used snowballing, hand searching and the expert knowledge of the research team to ensure all relevant papers were included in the review. Of 65 papers collected less than half (n = 30) were found relevant for this review. These papers were subsequently summarised and entered into QSR NVivo7 for data management and analysis.ResultsThe review has identified the most prominent impacts of CHF on a person's everyday life including social isolation, living in fear and losing a sense of control. It has also identified common strategies through which patients with CHF manage their illness such as sharing experiences and burdens with others and being flexible to changing circumstances. Finally, there are multiple factors that commonly impact on patients' self care and self-management in the disease trajectory including knowledge, understanding and health service encounters. These health service encounters encompass access, continuity and quality of care, co-morbid conditions, and personal relationships.ConclusionsThe core and sub-concepts identified within this study provide health professionals, service providers, policy makers and educators with broad insights into common elements of people's experiences of CHF and potential options for improving their health and wellbeing. Future studies should focus on building a comprehensive picture of CHF through examination of differences between genders, and differences within age groups, socioeconomic groups and cultural groups.

Project description:Background and objectiveHeart failure is the end-stage of various cardiovascular diseases. Recent progress in molecular biology has facilitated the understanding of the mechanisms of heart failure development at the molecular level. N6-adenosine methylation (m6A) is a post-transcriptional modification of RNA. Recent research work reported that m6A regulates gene expression and subsequently affects the activation of cell signaling pathways related to heart failure. Moreover, m6A regulators like methyltransferase-like 3 (METTL3) were reported to participate in myocardium hypertrophy. However, the current research work related to the role of m6A participating in the occurrence of heart failure is rare in some aspects like immune cell infiltration and diabetic heart diseases. Thus, it is reasonable to review the current achievements and provide further study orientation.MethodsWe searched related literature using the keywords: m6A AND heart failure in PubMed, Web of Science and Medline. The language was confined to English. The published year of searched literature ranged from 2012 to 2022. The searched results were put into Endnote software for management. Two authors investigated the searching terms and reviewed the full text of selected terms.Key content and findingsm6A and its regulators are involved in the metabolism of various types of RNAs. m6A modification can regulate various types of cell signaling pathways related to the heart failure via interaction with m6A regulators. m6A and its regulators broadly participate in the myocardium fibrosis, myocardium hypertrophy, myocardial cell apoptosis, and ischemic reperfusion injury. Specifically, m6A participates in the cell apoptosis via regulation of autophagy flux. However, the current research work does not have enough evidence to prove that m6A regulator played its specific effect on the target transcript via regulating the m6A level.Conclusionsm6A and its regulators participates in the progression of heart failure via modifying the RNA level. Future investigation of m6A should focus on the interaction between the m6A regulators and targeted transcript. Besides, the regulation role of m6A in immune cell infiltration and diabetic heart diseases should also be focused.

Project description:Background The relationship between intensive volume removal in acute decompensated heart failure patients with preexisting worsening renal function (WRF) and renal tubular injury, postdischarge renal function, and clinical outcomes is unknown. Methods and Results We used data from the multicenter CARRESS-HF trial (Cardiorenal Rescue Study in Acute Decompensated Heart Failure) that randomized patients with acute decompensated heart failure and preexisting WRF to intensive volume removal with stepped pharmacological therapy or fixed rate ultrafiltration. Patients in the urinary renal tubular injury biomarker substudy (NAG [N-acetyl-b-D-glucosaminidase], KIM-1 [kidney injury molecule-1], and NGAL [neutrophil gelatinase-associated lipocalin]) were evaluated (N=105). The severity of prerandomization WRF was unrelated to baseline renal tubular injury biomarkers ( r=0.14; P=0.17). During randomized intensive volume removal, creatinine further worsened in 53% of patients. Despite a small to moderate magnitude increase in creatinine in most of these patients, postrandomization WRF was strongly associated with worsening in renal tubular injury biomarkers (odds ratio, 12.6; P=0.004). This observation did not differ by mode of volume removal (stepped pharmacological therapy versus ultrafiltration, Pinteraction=0.46). Increase in renal tubular injury biomarkers was associated with a higher incidence of hemoconcentration (odds ratio, 3.1; P=0.015), and paradoxically, better recovery of creatinine at 60 days ( P=0.01). Conclusions In acute decompensated heart failure patients with preexisting WRF, intensive volume removal resulted in a further worsening of creatinine approximately half of the time, a finding associated with a rise in tubular injury biomarkers. However, decongestion and renal function recovery at 60 days were superior in patients with increased tubular injury markers. These data suggest that the benefits of decongestion may outweigh any modest or transient increases in serum creatinine or tubular injury markers that occur during intensive volume removal. Clinical Trial Registration URL: https://www.clinicaltrials.gov . Unique identifier: NCT00608491.

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Renal function monitoring in heart failure - what is the optimal frequency? A narrative review.

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Renal function monitoring in heart failure - what is the optimal frequency? A narrative review.

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