Acute kidney injury and risk of cardiovascular outcomes: A nationwide cohort study

Schytz, Philip Andreas; Blanche, Paul; Nissen, Anders Bonde; Torp‐Pedersen, Christian; Gislason, Gunnar; Nelveg-Kristensen, Karl Emil; Hommel, Kristine; Carlson, Nicholas

doi:10.1016/j.nefroe.2022.06.003

Cited by 6 publications

(5 citation statements)

References 46 publications

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“…their use in clinical practice is not without controversy [40,41]. Likewise, WRF has been classically defined on several occasions using an arbitrary ∂-creatinine cutoff value of 0.3 mg/dl [42].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, a change in renal function is readily recognizable on ED arrival and can be used in the decision-making process. We consider this new evidence to be of great interest because definitions imported from nephrology, such as the AKI criteria, although they have demonstrated their value in predicting adverse events in hospitalized patients [39], their use in routine clinical practice is not without controversy [40,41]. Likewise, WRF has been classically defined on several occasions using an arbitrary ∂-creatinine cutoff value of 0.3 mg/dl [42].…”

Section: Discussionmentioning

confidence: 99%

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Impact of worsening renal function detected at emergency department arrival on acute heart failure short-term outcomes

Llauger

Espinosa

Rafique

et al. 2023

European Journal of Emergency Medicine

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Background and importance Deterioration of renal function with respect to baseline during an acute heart failure (AHF) episode is frequent, but impact on outcomes is still a matter of debate. Objective To investigate the association of creatinine deterioration detected at emergency department (ED) arrival and short-term outcomes in patients with AHF. Design Secondary analysis of a large multipurpose registry. Settings and participants Patients with AHF were diagnosed in 10 Spanish ED for whom a previous baseline creatinine was available. Exposure Difference between creatinine at ED arrival and at baseline was calculated (∂-creatinine). Outcome measures and analysis Primary outcome was 30-day all-cause death, and secondary outcomes were inhospital all-cause death, prolonged hospitalization (>7 days) and 7-day postdischarge adverse events. Associations between ∂-creatinine and outcomes were explored using logistic regression by restricted cubic spline (RCS) curves and expressed as odds ratio (OR) with 95% confidence interval (CI), taking ∂-creatinine = 0 mg/dl as reference. Curves were adjusted by age, sex, comorbidities, patient baseline status, chronic treatments, and vitals and laboratory results at ED arrival. Interactions for the primary outcome also were investigated. Main results We analyzed 3036 patients (median age = 82 years; IQR = 75–87; women = 55%), with ∂-creatinine ranged from −0.3 to 3 mg/dl. The 30-day mortality was 11.6%. Increments of ∂-creatinine were associated with progressive increase in risk of 30-day death, although adjustment attenuated this association: ∂-creatinine of 0.3/1/2/3 mg/dl were, respectively, associated with adjusted OR of 1.41 (1.02–1.95), 1.69 (1.02–2.80), 1.46 (0.56–3.80) and 1.27 (0.27–5.83). Distinctively significant higher risk was found for patients over 80 years old, female, nondiabetic, functionally disabled and on digoxin therapy. With respect to secondary outcomes, inhospital mortality was 8.1%, prolonged hospitalization was 33.6% and 7-day postdischarge adverse event was 9.7%. Inhospital death steadily increased with increments in ∂-creatinine [from 1.50 (1.04–2.17) with ∂-creatinine = 0.3 to 3.78 (0.78–18.3) with ∂-creatinine = 3], as well as prolonged hospitalization did [from 1.41 (1.11–1.77) to 2.24 (1.51–3.33), respectively]. Postdischarge adverse events were not associated with ∂-creatinine. Conclusion WRF detected at ED arrival has prognostic value in AHF, being associated with increased risk of death and prolonged hospitalization. These associations showed different patterns of risk but, remarkably, risk started with increments as low as 0.3 mg/dl.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Impact of worsening renal function detected at emergency department arrival on acute heart failure short-term outcomes

Llauger

Espinosa

Rafique

et al. 2023

European Journal of Emergency Medicine

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“…A better understanding of the cellular and molecular mechanisms underlying the pathogenesis of CRS3 is needed, particularly from the perspective of cardiac dysfunction. Several studies have highlighted the association between AKI and elevated rates of cardiovascular events in the short-term and even during the first year after hospital discharge [22], including an 86% increased risk of cardiovascular mortality, a 38% increased risk of major cardiovascular events [23], a 58% increased risk of congestive HF, a 40% increased risk of acute myocardial infarction, and a 15% increased risk of stroke [9]. Accordingly, the development of more effective therapies, in addition to better clinical management of AKI, is fundamental to targeting the high risk of cardiovascular events in patients with AKI.…”

Section: Discussionmentioning

confidence: 99%

Targeting the TWEAK–Fn14 pathway prevents dysfunction in cardiac calcium handling after acute kidney injury

Poveda,

González‐Lafuente,

Vázquez‐Sánchez

et al. 2023

The Journal of Pathology

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Heart and kidney have a closely interrelated pathophysiology. Acute kidney injury (AKI) is associated with significantly increased rates of cardiovascular events, a relationship defined as cardiorenal syndrome type 3 (CRS3). The underlying mechanisms that trigger heart disease remain, however, unknown, particularly concerning the clinical impact of AKI on cardiac outcomes and overall mortality. Tumour necrosis factor‐like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor‐inducible 14 (Fn14) are independently involved in the pathogenesis of both heart and kidney failure, and recent studies have proposed TWEAK as a possible therapeutic target; however, its specific role in cardiac damage associated with CRS3 remains to be clarified. Firstly, we demonstrated in a retrospective longitudinal clinical study that soluble TWEAK plasma levels were a predictive biomarker of mortality in patients with AKI. Furthermore, the exogenous application of TWEAK to native ventricular cardiomyocytes induced relevant calcium (Ca2+) handling alterations. Next, we investigated the role of the TWEAK–Fn14 axis in cardiomyocyte function following renal ischaemia–reperfusion (I/R) injury in mice. We observed that TWEAK–Fn14 signalling was activated in the hearts of AKI mice. Mice also showed significantly altered intra‐cardiomyocyte Ca2+ handling and arrhythmogenic Ca2+ events through an impairment in sarcoplasmic reticulum Ca2+‐adenosine triphosphatase 2a pump (SERCA2a) and ryanodine receptor (RyR2) function. Administration of anti‐TWEAK antibody after reperfusion significantly improved alterations in Ca2+ cycling and arrhythmogenic events and prevented SERCA2a and RyR2 modifications. In conclusion, this study establishes the relevance of the TWEAK–Fn14 pathway in cardiac dysfunction linked to CRS3, both as a predictor of mortality in patients with AKI and as a Ca2+ mishandling inducer in cardiomyocytes, and highlights the cardioprotective benefits of TWEAK targeting in CRS3. © 2023 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

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“…PAH is a reported prevalence of 5.0–7.5% of hospitalized patients and in 50–60% of critically ill patients [3]. There are substantial causative factors of AKI, like cardiovascular events [4], older adults [5], mechanical ventilator [6], nephrotoxic agents [7], vasopressors [8], hypertension [9], hypercholesterolemia [10], liver disease [11], hypoalbuminemia [12], sepsis [13], renal ischemia [14], diabetes mellitus [15], obesity [16], anemia [17] and chronic kidney disease [18]. Studies have revealed that the progression of AKI is related to genetic factors [19].…”

Section: Introductionmentioning

confidence: 99%

Identification of novel prognostic targets in acute kidney injury using bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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Acute kidney injury (AKI) is a type of renal disease occurs frequently in hospitalized patients, which may cause abnormal renal function and structure with increase in serum creatinine level with or without reduced urine output. With the incidence of AKI is increasing. However, the molecular mechanisms of AKI have not been elucidated. It is significant to further explore the molecular mechanisms of AKI. We downloaded the GSE139061 next generation sequencing (NGS) dataset from the Gene Expression Omnibus (GEO) database. Limma R bioconductor package was used to screen the differentially expressed genes (DEGs). Then, the enrichment analysis of DEGs in Gene Ontology (GO) function and REACTOME pathways was analyzed by g:Profiler. Next, the protein-protein interaction (PPI) network and modules was constructed and analyzed, and the hub genes were identified. Next, the miRNA-hub gene regulatory network and TF-hub gene regulatory network were built. We also validated the identified hub genes via receiver operating characteristic (ROC) curve analysis. Overall, 956 DEGs were identified, including 478 up regulated and 478 down regulated genes. The enrichment functions and pathways of DEGs involve primary metabolic process, small molecule metabolic process, striated muscle contraction and metabolism. Topological analysis of the PPI network and module revealed that hub genes, including PPP1CC, RPS2, MDFI, BMI1, RPL23A, VCAM1, ALB, SNCA, DPP4 and RPL26L1, might be involved in the development of AKI. miRNA-hub gene and TF-hub gene regulatory networks revealed that miRNAs and TFs including hsa-mir-510-3p, hsa-mir-6086 and mir-146a-5p, MAX and PAX2, might be involved in the development of AKI. Various known and newtherapeutic targets were obtained via network analysis. The results of the current investigation might be beneficial for the diagnosis and treatment of AKI.

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Acute kidney injury and risk of cardiovascular outcomes: A nationwide cohort study

Cited by 6 publications

References 46 publications

Impact of worsening renal function detected at emergency department arrival on acute heart failure short-term outcomes

Impact of worsening renal function detected at emergency department arrival on acute heart failure short-term outcomes

Targeting the TWEAK–Fn14 pathway prevents dysfunction in cardiac calcium handling after acute kidney injury

Identification of novel prognostic targets in acute kidney injury using bioinformatics and next generation sequencing data analysis

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