Heart failure (HF) is a complex clinical syndrome characterized by the heart’s inability to maintain sufficient circulation, leading to inadequate organ perfusion and fluid buildup. A thorough understanding of the molecular, biochemical, and hemodynamic interactions that underlie this condition is essential for improving its management and enhancing patient outcomes. Recent advancements in cardiovascular research have emphasized the critical role of microRNAs (miRNAs) as post-transcriptional regulators of gene expression, playing an important part in the development and progression of HF. This review aims to explore the contributions of miRNAs, systemic congestion markers, and traditional biomarkers to the pathophysiology of heart failure, with the objective of clarifying their prognostic value and potential clinical applications. Among the miRNAs studied, miR-30d, miR-126-3p, and miR-483-3p have been identified as key players in processes such as left ventricular remodeling, regulation of pulmonary artery pressure, and adaptation of the right ventricle. These findings underscore the importance of miRNAs in modulating the structural and functional changes seen in HF. Beyond the heart, HF affects multiple organ systems, including the kidneys and liver, with markers of dysfunction in these organs—such as worsening renal function and liver stiffness—being closely linked to increased morbidity and mortality. This highlights the interdependence of the heart and other organs, where systemic congestion, indicated by elevated venous pressures, exacerbates organ dysfunction. In this context, traditional biomarkers like natriuretic peptides and cardiac troponins remain vital tools in the diagnosis and management of HF. Natriuretic peptides reflect ventricular strain, while troponins are indicators of myocardial injury, both of which are critical for risk stratification and monitoring disease progression. Emerging diagnostic techniques, such as lung ultrasonography and advanced echocardiographic methods, offer new ways to assess hemodynamic status, further aiding therapeutic decision-making. These techniques, alongside established biomarkers, provide a more comprehensive approach to understanding the complexities of heart failure and managing its impact on patients. In conclusion, miRNAs, systemic congestion markers, and traditional biomarkers are indispensable for understanding HF pathophysiology and determining patient prognosis. The integration of novel diagnostic tools with existing biomarkers holds the promise of improved strategies for the management of heart failure. However, further research is needed to validate their prognostic value and refine their role in optimizing treatment outcomes.

Heart failure (HF) is a challenging syndrome, affecting 64 million people worldwide, and is associated with high mortality rates. There are several potential biomarkers that help us diagnose the disease as well as help us assess the prognosis. Cardiac troponins I and T are effective tools for predicting poor outcomes in HF. Cardiac troponins are intracellular proteins responsible for regulating and conducting muscle contractions. They indicate cardiomyocyte injury caused by ischemia, toxins, inflammation, wall stress, and other factors. Some of these injuries may be reversible. The blood level of troponins is influenced by various factors, both physiological—such as sex, age, and weight—and pathological, including microbiological organisms, autoantibody complexes, and conditions like pulmonary embolism, stroke, sepsis, or kidney disease. Numerous studies demonstrate the effectiveness of troponin measurement in prognostication for patients with acute and chronic HF. However, it has been found that many patients with chronic heart failure have undetectable serum levels of cardiac troponins, leading to the adoption of high-sensitivity cardiac troponins (hs-cTn). Expanding this knowledge is crucial for enabling more intensive stratification and early identification of patients with poorer prognoses.

In recent years, significant advancements in the understanding of the processes underlying heart failure (HF) have been made, particularly regarding the role of chronic low-intensity inflammation or smoldering inflammation (SI). This review consolidates findings from the available literature and illustrates the relationships between inflammation, neurohormonal activation, metabolic derangements, and comorbidities in HF, with a focus on heart failure with preserved ejection fraction (HFpEF).A comprehensive literature search was conducted using PubMed®, Wiley Online Library, Scopus, and Web of Science (limited to 2025). The search terms included "heart failure", "HFpEF", "inflammation", "smoldering inflammation", "biomarkers", "cytokines", "fibrosis", and "comorbidities". Peer-reviewed articles, reviews, as well as clinical and observational studies describing the mechanistic, prognostic and therapeutic aspects of SI in HF were included. Studies limited to acute coronary syndrome (ACS) were excluded.Structural changes leading to hemodynamic perturbations in HFpEF are correlated with processes mediated by SI. Several biomarkers measure inflammation and provide diagnostic and prognostic value, including C-reactive protein (CRP), interleukin-6 (IL-6), soluble suppression of tumorigenicity 2 (sST2), galectin-3 (Gal-3), and iron homeostasis. Clinical trials demonstrate the efficacy of sodium-glucose cotransporter-2 (SGLT-2) inhibitors, glucagon-like peptide 1 (GLP-1) receptor agonists, and other targeted interventions in the modulation of SI.Smoldering inflammation is a key mechanism in the pathogenesis of HFpEF and the progression of comorbidities. Understanding SI may improve risk stratification and management strategies. Both established and emerging anti-inflammatory therapies, when administered alone or in combination, may target SI in order to enhance HF management.

Metabolic acidosis is a common complication of chronic kidney disease (CKD). The kidneys play a crucial role in acid–base balance, maintaining pH within the normal range (isohydria) by following mechanisms: bicarbonate reabsorption, ammogenesis, and titratable acidity. The anion gap describes the amount of unmeasured anions and is classically evaluated as the difference between the major cation (sodium) and the sum of the two major anions (chloride and bicarbonate). Metabolic acidosis can be divided into two types: normal anion gap metabolic acidosis and high anion gap metabolic acidosis. A high anion gap level is considered unfavorable in terms of prognosis as it is associated with increased mortality. Treatment of metabolic acidosis in patients with chronic kidney disease, despite available therapeutic options, is a challenge. Supplementation with bicarbonates does not improve prognosis on the one hand, and on the other hand, it may be harmful. The new KDIGO guidelines for 2024 have been significantly modified compared to 2012 after negative results of studies on bicarbonate supplementation. Bicarbonate supplementation is currently recommended only when levels are less than 18 mmol/L. This review provides an overview of the current knowledge on the pathophysiology, classification, and therapeutic options, including dietary recommendations and new pharmacology agents.

Background/Objectives: High-protein diets have gained increasing popularity in recent years. This trend has raised concerns regarding its impact on renal function, particularly among individuals with chronic kidney disease (CKD). The aim of this narrative review is to summarize current evidence on the effect of high-protein intake on kidney function. An analysis across species and age groups takes into account both theoretical and clinical perspectives. Methods: A literature search was conducted in PubMed, Scopus, and Web of Science to identify experimental and animal studies, as well as data concerning adult and pediatric populations, with special focus on those with CKD. Results: Experimental studies confirm protein-triggered adaptive increase in intraglomerular pressure and subsequent hyperfiltration, yet without any long-term negative effect on a healthy kidney. Human adult studies indicate that high-protein dietary content may accelerate the progression of CKD. Conversely, in older individuals, high protein intake combined with plant-rich diet appears to protect against sarcopenia and is associated with increased longevity. In children with CKD, protein intake should be adjusted according to growth requirements. In both pediatric and general populations, increasing the proportion of plant-based protein relative to animal protein may improve the health outcomes, although evidence on kidney function protection is insufficient. Conclusions: A balance should be maintained between excessive protein intake, which may aggravate existing dysfunctions, and overly restrictive protein consumption, which may lead to sarcopenia in older adults and impaired growth/development in children. A personalized approach is essential, taking into account age, kidney function/CKD stage, comorbidities, and, in the pediatric population, growth rate and developmental needs.