Search Results (27)

Chronic kidney disease (CKD) is associated with a high burden of cardiovascular morbidity and mortality, while lipid disorders in renal failure differ substantially from the LDL-C-centered pattern observed in the general population. This narrative review aimed to synthesize recent evidence on the mechanisms, clinical implications, and therapeutic management of dyslipidemia in patients with renal failure, with emphasis on cardiovascular events and CKD progression. A structured literature search was conducted in PubMed/MEDLINE, Scopus, and Web of Science for publications from January 2018 to April 2026. The review shows that CKD-related dyslipidemia is characterized by triglyceride-rich lipoprotein and remnant particle accumulation, small dense and modified LDL, and dysfunctional HDL within a uremic-inflammatory environment that promotes endothelial injury, vascular calcification, and residual cardiovascular risk. These abnormalities may also contribute to renal lipotoxicity, proteinuria, glomerulosclerosis, tubulointerstitial injury, and fibrosis, although direct causal and therapeutic implications remain incompletely established. Statin-based therapy remains central in non-dialysis CKD, whereas lipid management in dialysis, transplantation, frailty, and severe hypertriglyceridemia requires individualized interpretation. Future risk assessment should integrate lipid, inflammatory, vascular, nutritional, and renal-trajectory markers rather than relying on LDL-C alone. Full article

Background: Atherosclerosis is a degenerative-proliferative disease that leads to lesions primarily in the tunica intima and media of the arteries. Atherosclerotic plaques undergo progressive calcification, and the hydroxyapatite deposited within them absorbs X-rays. The coronary artery calcification score (CAC-score) can be assessed using computed tomography. Intima–media thickness (IMT) and endothelial function, evaluated by flow-mediated dilatation (FMD) of the brachial artery, can be measured using ultrasound. This study aimed to assess the relationship between CAC-score, atherosclerosis risk factors, IMT, and FMD in women, with particular emphasis on the comparison of IMT measurement sites. Methods: The study included 124 women divided into three groups based on CAC-score. The following parameters were evaluated: risk factors for coronary artery disease (CAD), FMD, and IMT. CAD risk factors included age, BMI, smoking status, hypertension, diabetes, and lipid disorders, which were obtained from medical history. Results: A significant positive correlation was observed between CAC-score and IMT of the common carotid artery in women. IMT measured at the carotid bifurcation showed the strongest correlation with CAC-score. No correlation was found between CAC-score and endothelial dysfunction assessed by FMD. Conclusions: IMT, particularly when measured at the carotid bifurcation, was associated with CAC-score in women without diagnosed CAD, whereas no association was observed between FMD and CAC-score in this population. Full article

Self-healing materials have attracted increasing attention as a strategy to enhance durability, extend service life, and reduce maintenance in advanced material systems. Among these, cellulose-based self-healing materials represent a sophisticated intersection between sustainable macromolecular chemistry and adaptive materials science. This review provides a synthesis of recent advancements in the field, systematically categorizing materials derived from cellulose raw materials. We evaluate the fundamental chemical strategies employed to achieve autonomous repair, distinguishing between extrinsic mechanisms—utilizing cellulose-based micro/nano-capsules to sequester healing agents—and intrinsic mechanisms governed by dynamic covalent chemistry (Schiff-base, boronic ester, Diels–Alder) and supramolecular interactions (hydrogen bonding, metal–ligand coordination, and host–guest assemblies). The analysis highlights how cellulose’s hierarchical structure and abundant surface functionality are leveraged to overcome the traditional trade-off between mechanical toughness and healing efficiency. Particular emphasis is placed on the transition from simple structural hydrogels to sophisticated multifunctional systems. These include ultra-stretchable strain and pressure sensors for e-skin applications, biocompatible and injectable matrices for chronic wound management and stem cell delivery, and advanced anti-freezing eutectogels for performance in extreme environments. Furthermore, we explore the integration of cellulose into traditional sectors, such as self-healing concrete utilizing microbe-induced calcification and smart, eco-friendly coatings for corrosion protection. Finally, we discuss critical challenges, including environmental stability, scalability, and the development of standardized evaluation protocols, providing a roadmap for the next generation of bio-derived, sustainable and intelligent materials. Full article

Schistosomiasis (bilharzia) is a parasitic infection caused by trematodes of the Schistosoma genus and remains a significant health burden in endemic regions. Granulomatous host responses to deposited Schistosoma eggs in small veins and tissues result in progressive changes and characteristic imaging findings. This diagnostic radiological review synthesizes the published literature and highlights key and robust imaging findings that facilitate the diagnosis of Schistosoma mansoni and Schistosoma haematobium, with emphasis on modality-specific patterns and disease staging. Schistosoma mansoni primarily affects the liver, causing periportal fibrosis visible as “pipe-stem” echogenic thickening upon ultrasonography, which may progress to portal hypertension and chronic liver disease. Liver cirrhosis is the end-stage disease manifested as an irregular liver contour with surface nodularity and lobar redistribution as right lobe atrophy with left and/or caudate lobe hypertrophy. Schistosoma haematobium predominantly affects the genitourinary system, causing urinary bladder wall thickening and calcification. Early disease, within three months of infection, may present with fine calcification, firstly in the bladder base and then extending to the whole bladder and even to the ureters. Calcification appears as a line or two parallel lines on radiography and as a circle in axial computed tomography (CT) images, which is pathognomonic for early-stage Schistosomiasis. In contrast studies, including conventional urography and CT urography, Schistosoma eggs appear as bubble-like filling defects in the ureter, kidney, and bladder, manifested as ureteritis, pyelitis, and cystitis cystica. Late stages appear as coarse calcification, fibrosis, strictures, and reduced bladder capacity and are associated with an increased risk of bladder squamous cell carcinoma. Moreover, Schistosomiasis calcification can present in genital organs, especially in the seminal vesicles; in the prostate in males; and in the vulva, cervix, and perineum in females. Ultimately, Schistosoma mansoni and haematobium eggs can reach the spinal cord, leading to acute myelopathy with paraparesis, urinary retention, or paraplegia. Recognition of characteristic imaging patterns of Schistosomiasis is essential for early diagnosis, accurate staging, and prevention of long-term complications. Full article

Gla-rich protein (GRP), also known as UCMA, is a vitamin K-dependent protein that has emerged as an important regulator of pathological calcification and inflammation. Vascular calcification is a major complication of chronic kidney disease and cardiovascular disorders and is now recognized as an active and tightly regulated process rather than a passive accumulation of minerals. Increasing evidence indicates that GRP plays a protective role in mineral homeostasis through its strong calcium-binding capacity and its dependence on vitamin K-mediated gamma carboxylation. This work represents a comprehensive narrative review aimed at summarizing and critically discussing the current scientific knowledge on GRP. Available experimental and clinical data are analyzed with respect to gene expression, molecular regulation, vitamin K dependency, and underlying mechanisms of action. Particular emphasis is placed on the dual function of GRP in inhibiting ectopic calcification and modulating inflammatory responses. The evidence linking altered GRP levels or changes in its carboxylation status with chronic kidney disease, vascular calcification, calcific aortic valve disease, osteoarthritis, and tumor-associated microcalcifications is systematically examined. Current findings collectively support the concept that GRP is a multifunctional protein operating at the interface of mineral metabolism, inflammation, and tissue remodeling. Despite promising experimental data, important knowledge gaps remain, including the absence of standardized assays capable of distinguishing different GRP forms and the lack of longitudinal clinical studies evaluating its predictive value. This manuscript highlights the potential of GRP as a biomarker of disturbed mineral homeostasis and cardiovascular risk, while emphasizing the need for further research to clarify its precise biological functions and clinical relevance. Full article

Large animal models are a critical component of the preclinical evaluation of mechanical cardiac implants, enabling assessment of safety and performance under physiological conditions that cannot be adequately reproduced in vitro. Choosing a suitable animal model is important for both scientifically valid and ethically responsible preclinical evaluation. However, interspecies differences between animal models and humans pose significant challenges for relevant translation of preclinical findings to clinical outcomes. This narrative review provides a comprehensive overview of commonly used large animal models (sheep, goats, pigs, and calves) for the preclinical assessment of mechanical cardiac implants, including prosthetic heart valves, ventricular assist devices, and total artificial hearts. We summarize key anatomical and physiological characteristics that influence device implantation, chronic follow-up, and translational value. Emphasis is placed on three critical outcome domains for preclinical evaluation of mechanical cardiac implants: calcification, thrombogenicity, and hemodynamic performance. Species- and age-dependent differences in calcification are reviewed, identifying juvenile sheep as a worst-case model for early manifestation and detection of graft mineralization. Interspecies differences in coagulation biology are examined, showing attenuated platelet responses in sheep and closer similarity between porcine and human platelet behavior, supporting pigs as the preferred thrombogenicity model. Hemodynamic evaluation strategies in acute and chronic large-animal studies are discussed, with particular emphasis on circulatory demands influenced by somatic growth and on device adaptability under varying loading conditions. Overall, this review provides practical, outcome-driven guidance for large animal model selection and experimental design in mechanical cardiac implant research, while identifying key limitations, knowledge gaps, and the need for standardized reporting to improve the translational reliability of preclinical studies. Based on the findings presented in this review, we conclude that there is no single animal model capable of evaluating all relevant aspects of a device. Instead, different animal models provide distinct advantages depending on the outcomes of interest. Full article

Lipoprotein(a) [Lp(a)] is a low-density lipoprotein-like particle that contains a unique apolipoprotein(a) [apo(a)] component covalently bound to apolipoprotein B-100. Elevated levels of Lp(a) have been identified as a well-established and genetically determined risk factor for atherosclerotic cardiovascular disease, including coronary artery disease, stroke, and calcific aortic valve stenosis. In contrast to other lipids, Lp(a) concentrations are minimally influenced by lifestyle or traditional lipid-lowering therapies, emphasizing the necessity for novel treatment approaches. This narrative review summarizes current and emerging therapeutic strategies for reducing Lp(a) levels. Such strategies include traditional agents such as niacin and PCSK9 inhibitors, as well as innovative therapies such as antisense oligonucleotides, RNA interference-based molecules, and small-molecule inhibitors. The mechanisms of action of these agents, in addition to clinical trial data and their capacity to modify cardiovascular outcomes, are explored in further detail. Furthermore, the current status of clinical guidelines and the evolving role of Lp(a)-targeted therapies in cardiovascular risk stratification are reviewed. A particular emphasis is placed on therapies that are in the advanced stages of clinical development. These include late-phase outcome trials and orally administered agents, which have the potential to significantly impact future clinical practice. The integration of mechanistic data with ongoing and completed clinical studies has been undertaken in order to provide a comprehensive framework for understanding the therapeutic potential of Lp(a) in the context of cardiovascular prevention. Full article

Atherosclerosis is a chronic, progressive disease of the arterial wall and the principal pathological substrate underlying most cardiovascular diseases, including ischemic heart disease, stroke, and peripheral arterial disease. Despite advances in prevention, imaging, and therapy, atherosclerosis remains the leading cause of cardiovascular morbidity and mortality worldwide. From a pathological perspective, the disease represents a dynamic and heterogeneous process characterized by endothelial dysfunction, lipid retention and modification, chronic inflammation, immune activation, smooth muscle cell phenotypic modulation, extracellular matrix remodeling, and thrombogenic surface alterations. This review provides a comprehensive overview of atherosclerosis from a pathologist’s perspective, integrating classical morphological concepts with contemporary insights into immunopathology, plaque classification, and mechanisms of plaque instability. We summarize the structure and function of the arterial wall, the stepwise pathogenesis of lesion initiation and progression, and the histopathological classification systems established by the American Heart Association and subsequently refined through Virmani’s framework. Particular emphasis is placed on plaque instability, highlighting the qualitative features—such as fibrous cap thinning, necrotic core expansion, macrophage-driven inflammation, plaque erosion, and calcification patterns—that determine clinical outcomes rather than luminal stenosis alone. Furthermore, the review discusses the expanding role of immunohistochemical markers in defining plaque biology, including lineage markers and functional indicators of inflammation, matrix integrity, osteogenic signaling, and local anticoagulant balance. These pathological insights are integrated with contemporary risk assessment tools, imaging modalities, preventive strategies, and therapeutic interventions, including emerging lipid-lowering and RNA-based therapies. In conclusion, pathology remains central to understanding atherosclerosis as a biologically active disease and to refining concepts of plaque instability. Integrating histopathology with molecular profiling, imaging, and clinical data is essential for advancing precision prevention and targeted treatment strategies in atherosclerotic cardiovascular disease. Full article

Background/Objectives: Calcinosis cutis universalis is a rare and severe manifestation of dystrophic calcification, most associated with connective tissue diseases such as dermatomyositis, systemic sclerosis, and systemic lupus erythematosus. It is characterized by widespread deposition of calcium salts throughout the soft tissues, leading to pain, recurrent infections, restricted mobility, and significant impairment in daily functioning and quality of life. Management remains challenging due to the absence of standardized treatment guidelines with risks including delayed wound healing and recurrence. Adjunctive therapies may support symptom control in refractory cases. Conclusions: Management of calcinosis cutis universalis requires an individualized, multimodal strategy. Based on available evidence and expert opinion, a stepwise therapeutic decision-making algorithm integrating medical, minimally invasive, and surgical approaches is proposed to guide clinical practice and the variable efficacy of available therapies. This review aims to summarize current therapeutic strategies and to propose a pragmatic approach to clinical decision-making. Methods: A narrative review of the literature was conducted using PubMed and Google Scholar. The review focused primarily on calcinosis cutis universalis and severe or extensive forms of calcinosis cutis, with particular emphasis on surgical management and its integration with medical and minimally invasive treatments. Results: Pharmacological treatments—including bisphosphonates, calcium-channel blockers, tetracyclines, phosphate binders, probenecid, immunomodulatory agents, biologics, colchicine, sodium thiosulfate and JAK inhibitors—show heterogeneous and often partial efficacy, with more favorable responses in early or localized disease. Surgical interventions such as excision, curettage, CO₂ laser ablation, and reconstructive procedures provide meaningful symptomatic relief in selected patients but are associated. Full article

Chronic kidney disease (CKD), which affects over 850 million individuals globally, is increasingly regarded as a systemic condition in which the gut microbiota represents a key pathogenic node. This review provides an integrated overview of mechanistic, translational and clinical data implicating the gut–kidney axis in CKD. The CKD-associated microbiota displays a characteristic dysbiosis, marked by depletion of short-chain fatty acid–producing commensals, overgrowth of proteolytic and urease-expressing taxa and disruption of epithelial barrier integrity. These disturbances favor the generation and systemic accumulation of gut-derived uremic toxins, most notably indoxyl sulfate, p-cresyl sulfate, indole-3-acetic acid and trimethylamine-N-oxide, which promote endothelial dysfunction, vascular calcification, fibrosis and chronic inflammation, thereby hastening renal function loss and heightening cardiovascular risk. Microbiome-directed interventions, including dietary modification, prebiotics, probiotics, synbiotics, intestinal dialysis, fecal microbiota transplantation, gut-acting sorbents and nephroprotective phytochemicals, are summarized with emphasis on their effects on uremic toxin burden and clinical surrogates. System-level implications of the gut–kidney axis for cardiovascular disease, immunosenescence and sarcopenia are discussed, together with future priorities for integrating multi-omics profiling and precision microbiome-based strategies into nephrology practice. Full article

Coronary artery disease remains the leading cause of cardiovascular morbidity and mortality worldwide, affecting millions of individuals each year. Coronary artery calcification is a common finding in patients with advanced atherosclerosis and represents an important determinant of procedural success during percutaneous coronary intervention. Severe calcifications are associated with increased procedural complexity and elevated complication rates due to challenging lesion preparation, suboptimal stent expansion, and less favorable long-term clinical results. This review summarizes the present understanding of vascular calcification mechanisms, discusses relevant diagnostic imaging modalities, and describes current plaque modification techniques used to optimize procedural outcomes. Methods such as rotational, orbital, and laser atherectomy, as well as specialized balloon technologies and intravascular lithotripsy, are discussed with regard to their mechanisms of action, clinical effectiveness, and safety profiles. Particular emphasis is placed on the integration of advanced imaging for precise lesion assessment, improved patient selection, and the use of combination strategies in complex cases. Finally, emerging technologies and future directions are highlighted, with the goal of enhancing procedural safety, device deliverability, and treatment outcomes in the evolving field of interventional cardiology. Full article

Fragility fractures are a major complication in chronic kidney disease (CKD), yet therapeutic strategies for their prevention remain highly controversial. The unique pathophysiology of CKD–mineral and bone disorder (CKD-MBD), coupled with the paucity of dedicated clinical trials, create substantial uncertainty regarding the efficacy and safety of medical interventions established in the general osteoporosis population. This review summarizes the available evidence regarding fracture risk and bone mineral density including pragmatic clinical guidance for the use of calcium, vitamin D, phosphate binders, calcimimetics, bisphosphonates, denosumab, romosozumab, and teriparatide in patients with advanced non-dialysis CKD, on dialysis, and after kidney transplantation. For calcium, the conflicting balance between skeletal needs and risk of vascular calcification in the setting of declining kidney function and limited evidence for fracture prevention is outlined. For vitamin D, the gap between its widespread clinical use and the inconsistent data on fracture prevention is analyzed including a discussion of target levels in progressive kidney dysfunction. For phosphate binders, the evidence for fracture prevention, showing benefits in dialysis populations, is summarized together with a synthesis of data on potential risks of calcium-based agents. For calcimimetics, the available evidence on their role in fracture prevention, PTH, and calcium control is reviewed. For bisphosphonates, the unresolved question of benefit versus harm in advanced CKD stages are discussed and the evidence regarding efficacy and safety for various clinical settings is disentangled. For denosumab, the current data on fracture prevention is presented with emphasis on its renal-independent pharmacokinetics and strategies to mitigate hypocalcemia and rebound fracture risk. For romosozumab, the promising effects on bone health are reviewed alongside an analysis of cardiovascular safety data. For teriparatide, the limited evidence in patients with low bone turnover disease is evaluated. The review navigates the available evidence and unresolved controversies across therapeutic options, and provides pragmatic guidance to support individualized clinical decision-making. Full article

Tertiary hyperparathyroidism (THPT) arises in patients with chronic kidney disease (CKD) as a consequence of prolonged secondary hyperparathyroidism and is marked by autonomous parathyroid hormone (PTH) secretion. In some cases, parathyroid hyperplasia persists even after successful renal transplantation, resulting in sustained PTH elevation and hypercalcaemia. These alterations contribute to bone loss, vascular calcification, and increased cardiovascular risk. Management includes medical therapy with calcimimetics or vitamin D analogues and surgical intervention via parathyroidectomy. However, optimal timing and treatment strategy remain uncertain. This review examines the pathophysiology, clinical manifestations, and current management paradigms of THPT, with an emphasis on areas that require further research and consensus. Full article

This study presents the living coccolithophore communities and the morphological variability of Emiliania huxleyi in the South Aegean Sea from three sampling regions during winter-early spring (March 2017, March 2019) and summer (August 2019). Emphasis is given to March 2017 to monitor the variations in coccolithophore assemblages after an exceptionally cold event in December 2016, which resulted in newly produced dense waters that ventilated the Aegean deep basins. The assemblages displayed distinct seasonality with the predominance of E. huxleyi and Syracosphaera molischii during winter-early spring, associated with the water column mixing. By contrast, summer assemblages were featured by holococcolithophores and typical taxa of warm, oligotrophic upper waters. It seems that the phytoplanktonic succession as well as the nutrient supply to the upper euphotic layers were affected by the water column perturbation during the extreme winter of 2016–2017, which led to strong convective mixing and dense water formation. The decreased coccosphere densities during March 2017, accompanied by the notable presence of diatoms, were most probably associated with a prolonged diatom bloom, causing delay in the development of the coccolithophore community and resulting in a nitrogen-limited setting. Emiliania huxleyi morphometry showed the characteristic seasonal calcification trend of the Aegean, with the dominance of smaller coccoliths in the summer and increased coccolith length and width during the cold season. The intense cold conditions and wind-induced mixing during the winter of 2016–2017 possibly increased the absorption of atmospheric CO₂ in surface waters, causing increased acidity and the subsequent presence of etched/undercalcified E. huxleyi coccoliths and other taxa, most probably implying in situ calcite dissolution. Full article

Bioprosthetic aortic valve degeneration (BAVD) is a significant clinical concern following both transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR). The increasing use of bioprosthetic valves in aortic valve replacement in younger patients and the subsequent rise in cases of BAVD are acknowledged in this review which aims to provide a comprehensive overview of the incidence, diagnosis, predictors, and management of BAVD. Based on a thorough review of the existing literature, this article provides an updated overview of the biological mechanisms underlying valve degeneration, including calcification, structural deterioration, and inflammatory processes and addresses the various risk factors contributing to BAVD, such as patient demographics, comorbidities, and procedural variables. The difficulties in early detection and accurate diagnosis of BAVD are discussed with an emphasis on the need for improved imaging techniques. The incidence and progression of BAVD in patients undergoing TAVR versus SAVR are compared, providing insights into the differences and similarities between the two procedures and procedural impacts on valve longevity. The current strategies for managing BAVD, including re-intervention options of redo surgery and valve-in-valve TAVR, along with emerging treatments are discussed. The controversies in the existing literature are highlighted to offer directions for future investigations to enhance the understanding and management of BAVD. Full article