Hypervolemia (volume overload) and hypovolemia (volume deficit) are sub-optimal blood volume conditions that influence overall circulation and organ function, with substantial shifts posing serious risk of death. In both conditions, the body's response mechanisms can compensate for sub-optimal volume up to a point at which the cardiovascular system decompensates. Most current methods for assessing blood volume status are either limited to clinical settings or are inaccurate, posing a particular challenge for triaging or monitoring in austere environments. Recent work has aimed at developing novel wearable sensing and machine learning technologies to yield early and accurate signs of sub-optimal volume status prior to decompensation. Seismocardiogram (SCG) signals, representing vibrations of the chest wall due to heartbeat, have been leveraged as a non-invasive and convenient means of extracting cardiac timing representative of sub-optimal volume status. In this work, we aimed to elucidate the changes in morphological variability in the SCG signal in both hypervolemic and hypovolemic conditions. We hypothesized that the variability in the SCG signal would be heightened in decompensated versus compensated states, since the decompensated state would represent hemodynamic conditions that were less stable and thus more variable on a beat-by-beat basis.

submission trends to the ERA Congress provide a valuable lens through which to observe the evolution of nephrology research and education. Analysing submissions from 2020 to 2026, we document a marked recovery following the COVID-19 disruption, culminating in a record number of abstracts for the 2026 Congress in Glasgow. Beyond volume, notable shifts have occurred in subject mix, geographic participation and reviewer scoring patterns. Chronic kidney disease and glomerular disorders now dominate submissions, reflecting major scientific advances and changing clinical priorities, while international engagement has broadened substantially. These trends suggest that the ERA Congress has entered a new phase characterised by sustained high activity rather than transient post-pandemic rebound. We discuss the implications for congress programme design, peer review, inclusiveness and future strategic planning, highlighting how abstract data can inform the direction of large scientific meetings and the nephrology community at large.

Pulmonary hypertension (PH) is a progressive and multifactorial disease marked by elevated pulmonary arterial pressure and right ventricular (RV) dysfunction. Among its subtypes, pulmonary arterial hypertension (PAH) is characterised by profound vascular remodelling, inflammation and fibrosis. Despite therapeutic advances targeting the endothelin, nitric oxide, prostacyclin, and, more recently, the activin signalling pathway via sotatercept, outcomes in PAH remain suboptimal, particularly in patients with cardiovascular comorbidities. This has prompted growing interest in novel metabolic-based interventions, such as glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1RAs). GLP-1RAs, initially developed for type 2 diabetes and obesity, exhibit pleiotropic properties including vasodilation, anti-inflammatory, antifibrotic and endothelial-protective effects. In experimental models of PAH GLP-1RAs administration attenuates the severity of PH. Additional studies highlight their ability to protect against lung fibrosis and preserve endothelial function. Indirect enhancement of GLP-1 signalling through dipeptidyl peptidase-4 (DPP-4) inhibition similarly improves pulmonary haemodynamics and mitigates fibrosis and inflammation, underscoring the relevance of this pathway. Although no clinical trials have specifically evaluated GLP-1RAs in PH, observational studies in patients with heart failure with preserved ejection fraction suggest potential cardiopulmonary benefits. GLP-1RAs emerge as promising candidates bridging metabolic, vascular and cardiac domains in PH, warranting rigorous clinical validation. These findings support further translational research and randomised clinical trials to evaluate GLP-1RAs as a disease-modifying therapy in PAH.

Diabetic cardiomyopathy (DCM) is a distinct myocardial disease in diabetic patients, independent of coronary artery disease or hypertension, and a leading cause of heart failure. Its pathogenesis has evolved from a linear "glucolipotoxicity" model to a complex, dynamic network involving metabolic disturbances, mitochondrial dysfunction, oxidative stress, chronic inflammation, diverse programmed cell death pathways, cellular senescence, and cardiac autonomic neuropathy. These interconnected events are amplified through positive feedback loops, driving progressive myocardial damage. This review provides a systems-level synthesis of the networked pathogenesis of DCM, integrating evidence across core mechanistic components and their dynamic interactions. We discuss how metabolic disturbances initiate and propagate injury signals through mitochondrial dysfunction, inflammatory activation, and alterations in cardiomyocyte fate-including apoptosis, necroptosis, ferroptosis, and senescence. Distinct from prior reviews, this article explores two emerging integrative concepts: "metabolic-structural coupling"-abnormal physical interactions between metabolic molecules and myocardial structural proteins-and "metabolic memory"-epigenetically mediated persistence of injury despite glycemic control. We further provide a horizontal comparison and stage-specific assessment of emerging therapeutic strategies, including the pleiotropic network effects of SGLT2 inhibitors, the cardiovascular benefits of GLP-1 receptor agonists, targeting ferroptosis (e.g. irisin, alpha-lipoic acid), senolytics (e.g. dasatinib + quercetin), and the modulation of lipid droplet dynamics and the farnesoid X receptor (FXR). Finally, we critically evaluate the current evidence levels and translational barriers for these emerging therapies-from preclinical targets to completed randomized controlled trials-and propose a forward-looking roadmap to advance precision medicine in DCM. This roadmap emphasizes the multi-omics dissection of clinical heterogeneity, the development of mechanism-based biomarkers, and the validation of targeted combination therapies in well-designed clinical trials, with metabolic-structural coupling and metabolic memory serving as integrative links between classical pathways and disease persistence.

Congenital Heart Disease (CHD) encompasses a range of structural abnormalities of the heart and great vessels present at birth and is associated with significant lifelong morbidity, including heart failure and arrhythmias. Early diagnosis is critical for optimizing perinatal management and improving outcomes. This review focuses on early fetal echocardiography, a specialized ultrasound technique that enables detection of cardiac abnormalities in utero, as early as 11-14 weeks of gestation, compared to traditional imaging performed at approximately 20 weeks. Advancements in early imaging have improved the identification of high-risk fetuses, particularly those with genetic predispositions or family history of CHD, allowing for earlier clinical decision-making and intervention planning. In select cases, prenatal detection facilitates in utero management of conditions such as aortic stenosis and hypoplastic left heart syndrome. Additionally, emerging applications of artificial intelligence (AI) have enhanced image analysis and diagnostic accuracy, supporting clinicians in the early recognition of CHD. Despite these advances, challenges remain, including variability in diagnostic accuracy in early gestation, risk of false positives, and limited access to specialized imaging technologies. Continued integration of AI-driven tools and the development of standardized screening protocols hold promise for improving diagnostic consistency and long-term outcomes in patients with CHD.

Cardiac aging reflects a convergence of intrinsic molecular damage and maladaptive stress responses that progressively erode myocardial resilience. Accumulating genomic instability, telomere dysfunction, chromatin remodeling, and metabolic dysregulation activate innate immune signaling and cellular senescence across cardiomyocytes, endothelial cells, fibroblasts, and immune cells. At the tissue level, these processes manifest as microvascular rarefaction, fibrosis, hypertrophy, neurovascular uncoupling, and impaired adaptive capacity, creating a substrate that overlaps extensively with cardiomyopathy, heart failure, and atrial fibrillation (AF). Importantly, senescence in the heart is not monolithic. Emerging multi-omics and spatial analyses reveal context-dependent senescence programs, including transient, injury-associated states that support angiogenesis and repair, alongside chronic senescent phenotypes that propagate inflammation and remodeling through the senescence-associated secretory phenotype (SASP). These observations indicate that senescence is not uniformly deleterious but rather comprises functionally heterogeneous responses within the aging myocardium. Non-cell autonomous interactions-spanning cardiomyocyte-fibroblast crosstalk, immune niche signaling, endothelial cell-neuronal axis, and systemic organ-to-heart communication-further amplify or constrain these trajectories. Advances in biomarker discovery, imaging, and circulating epigenetic signatures now enable biological aging of the heart to be quantified beyond chronological aging, although many circulating biomarkers are not cardiac-specific and may also reflect systemic inflammation, fibrosis, frailty, or generalized biological aging. In parallel, preclinical studies demonstrate that senolytic, senomorphic, metabolic, and nutrient-sensing-targeted interventions can partially restore cardiac homeostasis. Together, these insights suggest that cellular senescence may represent a key mechanism and a potentially targetable process in cardiac aging, with important implications for the prevention and treatment of age-related cardiovascular disease.

Infantile hepatic hemangiomatosis (IHH) is a rare benign vascular tumor of infancy, defined by multiple angiomatous lesions diffusely replacing the hepatic parenchyma. Its clinical course can be severe due to systemic complications, particularly consumptive hypothyroidism and high-output heart failure. We report the case of a four-month-old female infant admitted for abdominal distension evolving over two weeks. Physical examination revealed massive hepatomegaly (hepatic span of 14 cm) with abdominal-thoracic collateral venous circulation and no cutaneous hemangiomas. Laboratory workup showed normochromic normocytic non-regenerative anemia (hemoglobin = 6.7 g/dL), hepatic cytolysis (aspartate aminotransferase = 3× normal), cholestasis (alkaline phosphatase = 188 IU/L, gamma-glutamyl transferase = 335 IU/L), and a prothrombin time reduced to 54%. Alpha-fetoprotein was 470 ng/L. Abdominal MRI revealed multiple rounded hepatic lesions, T1 hypointense and T2 hyperintense with diffusion restriction and progressive centripetal contrast enhancement, consistent with diffuse IHH. Cardiac (echocardiography) and cerebral (transfontanellar ultrasound) assessments were normal. Systematic thyroid function tests revealed severe consumptive hypothyroidism, with thyroid-stimulating hormone level of 500 µIU/mL and free T4 of 6 pmol/L, without antithyroid antibodies. Management included progressive propranolol (Hemangiol®) up to 3 mg/kg/day, levothyroxine at 20 µg/kg/day, and red blood cell transfusion. At the six-month follow-up, thyroid function had normalized, and hepatic lesions showed significant regression. This case highlights the necessity of systematic thyroid function screening in all infants with IHH and illustrates the efficacy of propranolol in managing this rare but potentially life-threatening condition.

Infective endocarditis is an infection of the endocardium and cardiac valves. Fungal etiologies are rare, accounting for 1-3% of cases, and affect prosthetic valves in 0.1% of cases. We present a case of recurrent fungal endocarditis, caused by Candida parapsilosis in a patient with a mechanical mitral prosthetic valve successfully managed with medical therapy alone in a resource-limited setting. This report highlights the diagnostic and therapeutic challenges of fungal endocarditis and demonstrates that under appropriate clinical conditions, such as the absence of congestive heart failure, heart block, thrombotic events, and close monitoring with appropriate antifungal therapy, favorable outcomes may be achieved even in the absence of surgical intervention.

Heart transplantation offers the only life-saving option for patients with terminal heart failure; yet, the sequential "innate-adaptive" avalanche initiated by ischemia-reperfusion injury (IRI) remains the Achilles' heel of long-term graft acceptance. Current regimens overwhelmingly focus on either the adaptive or the IRI-triggered innate arm, failing to interrupt the positive-feedback loop that amplifies allo-rejection. To address this unmet need, we herein present a single ROS-responsive nanoplatform that weds dual immunosuppression with on-demand oxygenation Fe3O4@CaO2@Tac@HA. The core-shell Fe3O4@CaO2 carrier simultaneously loads hyaluronic acid (HA), which is a potent dampener of innate inflammatory signaling, and tacrolimus (Tac), which is a calcineurin inhibitor that arrests adaptive T-cell activation. Upon exposure to the ROS-rich milieu of the reperfused graft, CaO2 undergoes conversion to O2, promptly relieving tissue hypoxia while reducing oxidative stress. In vitro, the nanocomposite exhibits rapid ROS scavenging, sustained oxygen release and inhibit T cell activation; in vivo, it markedly prolongs cardiac-allograft survival by synchronously suppressing innate immune cells infiltration and CD8+ T-cell cytotoxicity. Collectively, Fe3O4@CaO2@Tac@HA offers a translatable "one-two punch" strategy that unites innate and adaptive immunomodulation, setting the stage for precision nanotherapy in cardiac transplantation.