Calcification Of Blood Vessels Research Articles

Anaphylatoxins and their corresponding receptors as potential drivers in cartilage calcification during osteoarthritis progression

ObjectiveThe complement cascade as major fluid phase innate immune system is activated during progression of osteoarthritis (OA). Generated anaphylatoxins and the corresponding receptors C3aR and C5aR1 are associated with the calcification of blood vessels and involved in osteogenic differentiation. This study aims on elucidating whether complement activation products contribute to cartilage calcification of OA cartilage. MethodHuman articular chondrocytes were osteogenically differentiated in vitro in the presence or absence of C3a, C5a, and bone morphogenetic protein (BMP) 2. Furthermore, macroscopically intact (OARSI grade ≤ 1) and highly degenerated human cartilage (OARSI grade ≥ 3) was used for C3aR and C5aR1 histochemistry. Calcification of the cartilage was assessed by Alizarin Red S and von Kossa staining. ResultsC3a and C5a amplified matrix mineralization during in vitro osteogenesis, while inhibition of the corresponding receptors impaired calcium deposition. Moreover, C3aR and C5aR1 expression was upregulated during osteogenic differentiation and also in degenerated cartilage. Additionally, anaphylatoxin receptor expression was positively associated with calcification of native cartilage tissue and calcium deposition during osteogenic differentiation. Finally, the pro-hypertrophic growth factor BMP2 induced the expression of C5aR1. ConclusionsOur findings indicate that anaphylatoxins and their receptors play a decisive role in cartilage calcification processes during OA progression.

BRG1 is involved in vascular calcification in chronic renal disease via autophagy of vascular smooth muscle cells

We aimed to investigate the mechanisms of Brahma related gene 1 (BRG1) in promoting vascular calcification in chronic kidney disease (CKD). The expression of BRG1 was examined in high phosphorus stimulated rat aortic smooth muscle cells (RASMCs) and calcified artery tissues from rat models and hemodialysis patients. Autophagosome formation was measured in high phosphorus stimulated RASMCs with and without BRG1 knock-down. We also detected the coexistence of BGR1 and exosomes, and measured the circulatory levels of BRG1 in the hemodialysis patients. BRG1 promoted the osteogenic transdifferentiation of RASMCs. Silencing BRG1 prevented autophagy from being induced by high phosphorus stimulation in RASMCs. Increased expression of BRG1 was observed in calcified blood vessels. Serum BRG1 level increased in the hemodialysis patients. BRG1 was involved in the development of high phosphorus induced osteogenic phenotype invitro and invivo, and its underlying mechanism might be facilitating autophagy.

Prevention of calcium and vitamin D deficiency in osteoporosis: possibility of using combined drugs Osteomed, Osteomed Forte, Osteo-Vit D3

Objective. To analyse literature data reflecting the issue of prevention of calcium and vitamin D deficiency in osteoporosis. Material and methods. Analysis of 47 Russian and foreign publications on prevention of calcium and vitamin D deficiency in osteoporosis was carried out. Results and discussion. The role of vitamin D in maintenance of calcium homeostasis and bone metabolism has been shown. Lack of vitamin D is associated with the development of osteomalacia and osteoporosis in adults and rickets in children. It was noted that hypovitaminosis D was recognised as a worldwide pandemic. It was acknowledged that there was a need to develop dietary recommendations, supplementary intake of vitamin D to prevent, among other things, bone diseases in most countries of the world. The results of the study of the Russian drugs Osteomed, Osteomed Forte, Osteo-Vit D3 (Parapharm, Russia) were presented. Conclusions. Thus, combined preparations of Ca and vitamin D were of great importance for prevention and complex treatment of osteoporosis, for the compensation of calcium deficiency in adolescence, elderly, during pregnancy, lactation and after menopause. Combined calcium and vitamin D supplementation was more effective than monotherapy in slowing bone loss, reducing the risk of fractures, strengthening the skeletal musculature and reducing the probability of falls, disability and death, but promotes calcification of soft tissues and blood vessels. At the same time, the only osteoprotectors without the risk of calcification of blood vessels and soft tissue, as well as the development of atherosclerosis, to date recognized by the Russian line of drugs "Osteomed. The safety of this group of dietary supplements, including their use in the treatment of bone pathologies in children and adolescents, is ensured by the presence of a unique HDBA organic complex. This component, by correcting the hormonal status and maintaining an optimal level of androgens within the age norm, has an anabolic effect, stimulating the birth of new bone cells. It is activation of reparative processes at the cellular level that enables to realize the effect of targeted delivery of calcium into bone tissue.

Диабетопороз и риск тромбозов

Aim. To assess the risk factors for thrombosis in patients with osteoporosis-induced diabetes mellitus. Key points. Osteoporosis is a common multifactorial disease with a high risk of venous thromboembolic complications (VTEС). This is due to the main pathology — diabetes mellitus, the use of medications for the prevention and treatment of osteoporosis. The main pathogenetic patterns of VTEС development in patients with diabetoporosis are considered. These include hemostasis disorders, the calcification or calcification of blood vessels, drug inducers, age-related estrogen deficiency, etc. Conclusion. Patients with diabetes mellitus, mainly type 2, on the background of obesity, older age and with osteoporosis have an increased risk of developing VTEС. Thorough examination of patients with thrombosis risk factors and dynamic monitoring of them, individualization and personification of approaches to the treatment of osteoporosis are advisable. Keywords: osteoporosis, diabetoporosis, thrombosis, therapy.

Correction of Vascular Calcification and Hyperphosphatemia in CKD Rats Treated with ASARM Peptide.

Abnormalities in calcium, phosphorus, PTH, vitamin D metabolism, bone, and vascular calcification occur in chronic kidney disease mineral bone disorder (CKD-MBD). Calciphylaxis, involving painful, ulcerative skin lesions, is also a major problem associated with CKD-MBD. There are no quality medical interventions to address these clinical issues. Bone ASARM peptides are strong inhibitors of mineralization and induce hypophosphatemia by inhibiting phosphate uptake from the gut. We hypothesize treatment of CKD-MBD rats with ASARM peptides will reverse hyperphosphatemia, reduce soft-tissue calcification, and prevent calciphylaxis. To test our hypothesis, we assessed the effects of synthetic ASARM peptide in rats that had undergone a subtotal 5/6th nephrectomy (56NEPHREX), a rodent model of CKD-MBD. All rats were fed a high phosphate diet (2% Pi) to worsen mineral metabolism defects. Changes in serum potassium, phosphate, BUN, creatinine, PTH, FGF23, and calcium were assessed in response to 28 days of ASARM peptide infusion. Also, changes in bone quality, soft-tissue calcification, and expression of gut Npt2b (Slc34a2) were studied following ASARM peptide treatment. Rats that had undergone 56NEPHREX treated with ASARM peptide showed major improvements in hyperphosphatemia, blood urea nitrogen (BUN), and bone quality compared with vehicle controls. Also, ASARM-infused 56NEPHREX rats displayed improved renal, brain, and cardiovascular calcification. Notably, ASARM peptide infusion prevented the genesis of subdermal medial blood vessel calcification and calciphylaxis-like lesions in 56NEPHREX rats compared with vehicle controls. ASARM peptide infusion corrects hyperphosphatemia and improves vascular calcification, renal calcification, brain calcification, bone quality, renal function, and skin mineralization abnormalities in 56NEPHREX rats. These findings confirm our hypothesis and support the utility of ASARM peptide treatment in patients with CKD-MBD.

Serum Homocysteine and Vascular Calcification: Advances in Mechanisms, Related Diseases, and Nutrition.

Identifying and preventing modifiable risk factors for cardiovascular disease is very important. Vascular calcification has been studied clinically as an asymptomatic preclinical marker of atherosclerosis and a risk factor for cardio-cerebrovascular disease. It is known that higher homocysteine levels are associated with calcified plaques and the higher the homocysteine level, the higher the prevalence and progression of vascular calcification. Homocysteine is a byproduct of methionine metabolism and is generally maintained at a physiological level. Moreover, it may increase if the patient has a genetic deficiency of metabolic enzymes, nutritional deficiencies of related cofactors (vitamins), chronic diseases, or a poor lifestyle. Homocysteine is an oxidative stress factor that can lead to calcified plaques and trigger vascular inflammation. Hyperhomocysteinemia causes endothelial dysfunction, transdifferentiation of vascular smooth muscle cells, and the induction of apoptosis. As a result of transdifferentiation and cell apoptosis, hydroxyapatite accumulates in the walls of blood vessels. Several studies have reported on the mechanisms of multiple cellular signaling pathways that cause inflammation and calcification in blood vessels. Therefore, in this review, we take a closer look at understanding the clinical consequences of hyperhomocysteinemia and apply clinical approaches to reduce its prevalence.

Fractures in patients with chronic kidney disease

Abstract. Despite rapid progress in improving dialysis technology in recent years, the mortality of patients treated with renal replacement therapy remains quite high. Mineral and bone disease is omnipresent in patients with chronic kidney disease (CKD) and leads to a diverse range of clinical manifestations, including bone pain and fractures. Mineral bone disorders (MBD), as well as changes in bone structure, develop at the beginning of CKD. Osteoporosis can progress according to declining of the glomerular filtration rate and contribute to the deterioration of bone strength resulted in a high risk of fracture. In CKD patients, the most common are hip fractures, femur, humerus, compression fractures of the vertebrae and pelvic fractures. CKD-MBD is characterized by disorders of calcium, phosphate, parathyroid hormone and/or vitamin D metabolism, as well as, bone regeneration, mineralization, volume, linear growth and strength violation, calcification of blood vessels, or other soft tissues. Medications that correct systemic mineral metabolism can improve bone histology in patients with CKD. However, clinical and biochemical targets used in clinical practice remain controversial, resulting in an undermanagement of bone fragility. The clarifying of the appropriateness of medicines that act directly on the bone or affect the mineral and hormonal metabolism could be a promising strategy to prevent pathological fractures due to fragility among CKD patients.

Relationship between the level of vitamin D in bloof flow and skin dermatosis

Vitamin D is vital for bone health and its deficiency deemed as a disease of the past has re-emerged as an important health concern. Thanks to modern research, the role of vitamin D has been studied in detail and goes far beyond the concepts of regulating the mineral composition of bones. A small amount of active vitamin in the form of cholecalciferol is obtained by the body with food of animal origin, in the form of ergocalciferol and previtamin D ― with food of plant origin. Another way to get vitamin D is exposure to solar radiation. Both insufficient and excessive levels of vitamin D have adverse effects on the body. A constant blood level above 200 ng/ml is considered toxic and is manifested by anorexia, weight loss, polyuria and cardiac arrhythmia. Vitamin D toxicity increases the risk of kidney stones, calcification of blood vessels and tissues, as well as complications associated with these changes.
 The growing interest in the role played by vitamin D in skin disease has given rise to the publication of many studies of the relationship between this vitamin and cutaneous dermatoses. Undoubtedly, a complete understanding of the synthesis of vitamin D, the main sources of its production by the body, indicators of the normal content of vitamin D levels in the blood, as well as factors that can influence their changes, are important. Of particular interest are the latest discoveries about the role of vitamin D in skin diseases such as lupus erythematosus, ichthyosis, atopic dermatitis, hidradenitis suppurativa, acne, alopecia areata, androgenetic alopecia, melanoma, and nonmelanoma skin cancer.
 Also of interest is the importance of vitamin D as adjuvant therapy in patients on long-term treatment with corticosteroids. In this review, we provide an overview of the most important and most recent information regarding the relationship between vitamin D and skin disease and discuss the importance of assessing individual vitamin D status and correcting deficiencies.

Role of Fibroblast Growth Factor-23 in Coronary Slow Flow Phenomenon Pathogenesis

The phenomenon of angina chest pain without significant epicardial coronary artery stenosis, but accompanied by a slowdown in coronary blood flow is often found in patients with symptoms of acute coronary syndrome who undergoing invasive coronary angiography. This phenomenon of slow coronary blood flow is then called the coronary slow flow phenomenon (CSFP). The pathogenesis mechanism of CSFP remains unclear. The pathogenesis of CSFP is thought to be multifactorial. Endothelial dysfunction, small vessel disease, inflammation, renin system angiotensin aldosterone, atherosclerosis are thought to be involved in the pathogenesis of CSFP. Cardiovascular disease incidence and death were associated with elevated levels of Fibroblast growth factor-23 (FGF-23). High levels of FGF-23 can lead to formation of blood vessel calcification, left ventricular hypertrophy, arterial stiffness, endothelial dysfunction, increased inflammatory markers and elevated levels of angiotensin II. It is suspected that FGF-23 has a role in this event other than as a regulator of bone and mineral metabolism. This literature review aims to determine the relationship between fibroblast growth factor-23 and the pathophysiology of CSFP. Based on the broad role of FGF-23, it is possible that FGF-23 is involved in the pathogenesis of CSFP.

CALCIFICATION OF ARTERIES IN PATIENTS WITH ATHEROSCLEROSIS: CAUSES AND MECHANISMS OF DEVELOPMENT

The paper shows analogies between the mechanisms of calcification of arteries, various tissues and bone mineralization. In calcification the same mechanisms are involved, as at ossification of an organic matrix of a bone, including participation of stem cells. In the arteries and capillaries of various organs found polypotent precursors – mesenchymal stem cells, presumably responsible for the pathological mineralization of the arterial wall. Circulating in the blood and present in the intima of the human atheromatous aorta colony-forming stem cells of the stromal line of differentiation. Adventitia cells or pericytes are considered as a pluripotent mesenchymal reserve for replenishment of some cellular forms of connective tissue. Bone marrow stem cells of the stromal line of differentiation with the presence of pluripotent stromal cells in the blood and granulomas (plaques) and their transformation into bone tissue cells are involved in atherogenesis. Smooth muscle cells (SMCs) and myofibroblasts of the arterial wall adventitia have an osteoblast-like phenotype. Collagen and elastic fibers are involved in the calcification of blood vessels and soft tissues. Calcification of granulomas (plaques) accompanies their inflammatory morphogenesis, accompanied by the development of scar tissue. It often accompanies and completes the inflammation in them. This process is observed with the gradual replacement of the parenchyma of some organs with connective tissue. The mineral phase in bones and soft tissues, represented by calcium (Ca) and phosphate (P), contacts with nucleators - specific areas of collagen fibers. Non-collagen proteins are also involved in arterial calcification. With the progression of atherosclerosis and calcification of granulomas/plaques by cells present in the arterial wall, osteonectin is expressed. Osteopontin content is associated with Ca deposits in them; in particular, it correlates with the Ca level in the coronary arteries. In the processes of ossification and calcification, phosphatases play a certain role. In areas of calcification of granulomas/plaques, osteoprotegerin is found, which inhibits the activity of alkaline phosphatase in the aorta and prevents calcification of the media. Arterial wall calcification and inflammation are inhibited by fetuin-A and matrix γ-carboxyglutaric protein (MGP). The rate of bone formation and tissue calcification depends on the concentration of Ca and P in plasma and extracellular fluid. With their high concentration in the extracellular fluid, the mineral phase appears where it normally does not exist. Lipids are among the initiators of granuloma / plaque calcification in the arteries. The role of inflammation and necrosis in the calcification of the arteries is confirmed by experiments on animals with repeated intravenous injections of adrenaline, which causes focal necrosis of the middle membrane, which then undergoes calcification. In arterial walls, heart muscle, bone and cartilage tissue, osteonectin, osteocalcin, osteopontin, bone sialoprotein are often formed. In general, the mechanisms of arterial and soft tissue calcification are poorly understood. There are no effective remedies for calcification.

Association of Diabetes With Lower Back Pain: A Narrative Review.

Diabetes mellitus with its increasing prevalence is one of the four major non-communicable diseases. It is characterized by hyperglycemia, which may progress to chronic complications such as peripheral vascular disease and neuropathy. This paper highlights the pathophysiology associated with diabetes, which is restricted to not only hyperglycemia but also other comorbidities including chronic lower back pain.Diabetes is a metabolic disorder associated with hypercholesteremia, hypertriglyceridemia, and hypertension. This chain of events leads to free plasma fatty acids and a pro-inflammatory state, therefore promoting calcification of blood vessels, which may block the blood supply to vertebral discs and thereby increase vulnerability in the patients with ongoing inflammatory disease such as osteoarthritis and also causing costochondritis. Functional limitation due to increased load on the weight-bearing joints is a common mechanical complication of diabetes. Obesity in diabetes is more prevalent due to a disturbed metabolism, which is aggravated with a persistent inflammatory state.Moreover, the aim of this review is to encourage further conduction of clinical studies to explore the definite cause and potential therapy for chronic lower back pain in diabetes, thereby investigating the association of lipid metabolism and skeletal muscle atrophy leading to chronic back pain, the role of diabetic medications, and vulnerability in the female gender. Diminished physical activity and depression in diabetic patients disrupt the hypothalamic-pituitary-adrenal axis (HPA), which further contributes to lower back pain. Further clinical investigation and research in this regard will establish substantial data for the linkage between depression in diabetes and back pain. However, despite all the advancements of medical literature, the exact cause of lower back pain in diabetes is arguable.Pain impedes the health status and life quality; therefore, it is essential to maintain the quality of health in patients with diabetes by treating not only hyperglycemia but also other multifactorial causes leading to lower back pain.

Klotho Protein and Cardio-Vascular System.

Klotho protein affects a number of metabolic pathways essential for pathogenesis of cardio-vascular diseases and their prevention. It inhibits lipid peroxidation and inflammation, as well as prevents endothelial injury and calcification of blood vessels. Klotho decreases rigidity of blood vessels and suppresses development of the heart fibrosis. Low level of its expression is associated with a number of diseases. Cardioprotective effect of klotho is based on its ability to interact with multiple receptors and ion channels. Being a pleiotropic protein, klotho could be a useful target for therapeutic intervention in the treatment of cardio-vascular diseases. In this review we present data on pharmaceuticals that stimulate klotho expression and suggest some promising research directions.

Excessive calcium consumption as a risk factor for cardiovascular diseases

Calcium is the most abundant mineral in the human body that participates in the construction of bones and teeth, nerve impulse transmission, intracellular signaling, hormone secretion, muscle contraction, coagulation, ensuring normal heart rhythm and physiological values of blood pressure. Excessive calcium concentration, predominantly caused by improper use of supplements, predisposes to the development of cardiovascular disease. High serum calcium induces reprogramming and differentiation of smooth muscle cells into an osteoblast-like phenotype, translocation of prohypertrophic cardiomyocyte transcription factors, compromise of diastolic relaxation of the myocardium and necrosis of its contractile girdle, stimulation of coagulation reactions, stimulation of platelet aggregation, hemodynamic changes and metabolic abnormalities. Acute intoxication with calcium supplements results in an increase in blood pressure. Chronic consumption of excessive calcium concentration predisposes to atherosclerosis and calcification of blood vessels, heart attack and stroke, hypertrophy and heart failure, and heart rhythm disorders. There is a need to strengthen the response and role of the health system in informing the public about the side effects of excessive calcium consumption, limiting the widespread prescribing of supplements, as well as a possible comprehensive reassessment of the same.

Characteristic of warfarin

In modern pharmacology, compounds of natural origin are gaining more and more recognition. One of them is warfarin, which is a compound of organic coumarin derivatives. It is used medicinally in the anticoagulant doctor. This compound was commercially introduced to the United States in the 1950s. It has been available on the Polish market since 2006. Warfarin is an antagonist of vitamin K. It works by inhibiting the synthesis of vitamin K in the liver and thus blocking the synthesis of vitamin K dependent blood clotting factors (II, VII, IX, X). It is widely used by people suffering from cardiovascular diseases such as venous thrombosis and venous embolism. Adopted by patients with suspected or after a heart attack. Despite its undisputed positive effect, one should remember about the numerous side effects resulting from long-term use of warfarin. They may be due to intolerance to this compound, which causes nausea, vomiting, and allergic reactions. Moreover, recent studies show that it may have a destructive effect on the liver and cause calcification of blood vessels. Keep in mind that warfarin can interact with many substances you are taking for other medical conditions. Agents that increase the effects of warfarin include antibiotics such as erythromycin, deoxicillin, commonly used drugs containing caffeine, acetylsalicylic acid and naturally derived compounds found in ginkgo, garlic and sage. Compounds that weaken the effect of warfarin are barbiturates, cyclosporine, vitamin C, and St. John's wort.

The potential role of miRNAs in calcification of cardiovascular diseases

MicroRNA is a class of endogenous noncoding 17-25 nucleotides RNAs that regulate gene expression. Recently, more and more works have been appeared confirming the important role of miRNAs in the development and progression of cardiovascular diseases. Calcification mechanisms include impaired regulation of calcium and phosphate metabolism, activation of the signaling pathways that regulate bone formation, and suppression of the signaling pathways responsible for maintaining the smooth muscle cell phenotype. The involvement of microRNAs was demonstrated for each of these mechanisms, which emphasizes the significant contribution of microRNAs to the development of calcification of blood vessels. This review summarizes the scientific data on microRNAs that are proven to be involved in the development of in vitro and in vivo calcification of their targets, as well as the latest achievements in microRNA studies in the context of vascular calcification. We also discuss the possibility of their use for early diagnostics and treatment of calcification in cardiovascular diseases.

Maladaptive neuropathological syndrome of blood vessel aging

This article discusses the relationship between maladaptation and blood vessel aging. The work shows that upright posture created an additional load on the circulatory system, and the lifestyle of a modern human is an additional risk factor of cardiovascular diseases. It has been suggested that a disorder of the nervous regulation of vascular tone is the main etiopathogenetic mechanism of morphofunctional changes in blood vessels and their aging. We discussed the statute that vascular reactions in humans is based on the formation of a maladaptive circuit in the cerebral cortex, consisting of a matrix of motor, sensory and associative cortical neurons involved in the maladaptive process. This hypothesis is based on the fact that any irritations entering the cerebral cortex from the periphery (thermal, pain, and others) cause cortical-vascular reflex reactions that change their tonic activity. Based on this principle, a model of vascular aging is further constructed, which is based on the maladaptive damage to all layers of the vascular wall (intima, media and adventitia). The opinion is expressed about the need for early diagnosis and prevention of vascular disorders to maintain human health. In conclusion, it is concluded that if the age of a person is really determined by the age of his blood vessels, then in order to achieve active longevity it is necessary to normalize the relationship in the adaptation-maladaptation-environment. Detailed study of hypertrophy and calcification of blood vessels is needed, since aging always reveals vascular wall thickening and stiffness increase.

Elastolytic activity of cysteine cathepsins K, S, and V promotes vascular calcification

Elastin plays an important role in maintaining blood vessel integrity. Proteolytic degradation of elastin in the vascular system promotes the development of atherosclerosis, including blood vessel calcification. Cysteine cathepsins have been implicated in this process, however, their role in disease progression and associated complications remains unclear. Here, we showed that the degradation of vascular elastin by cathepsins (Cat) K, S, and V directly stimulates the mineralization of elastin and that mineralized insoluble elastin fibers were ~25–30% more resistant to CatK, S, and V degradation when compared to native elastin. Energy dispersive X-ray spectroscopy investigations showed that insoluble elastin predigested by CatK, S, or V displayed an elemental percentage in calcium and phosphate up to 8-fold higher when compared to non-digested elastin. Cathepsin-generated elastin peptides increased the calcification of MOVAS-1 cells acting through the ERK1/2 pathway by 34–36%. We made similar observations when cathepsin-generated elastin peptides were added to ex vivo mouse aorta rings. Altogether, our data suggest that CatK-, S-, and V-mediated elastolysis directly accelerates the mineralization of the vascular matrix by the generation of nucleation points in the elastin matrix and indirectly by elastin-derived peptides stimulating the calcification by vascular smooth muscle cells. Both processes inversely protect against further extracellular matrix degradation.

Thermodynamic and experimental modeling of the formation of the mineral phase of calcification

Vascular calcification is the process of calcium salt precipitation in vessel walls. In-depth understanding of the mechanisms of crystallization of calcifications in blood vessels is crucial for developing effective protective therapy. Calcification processes reduce the life span of implanted heart valves. The purpose of this paper is a comprehensive study of calcification processes. We calculated the solubility diagrams of the basic poorly soluble compounds formed in the prototype human plasma, performed laboratory modeling of crystallization of calcification mineral phases under conditions typical of human blood plasma solution (ionic composition, pH), and verified the obtained theoretical and experimental modeling results for adequacy to pathogenic phase formation from human blood plasma solution. The paper presents the results of the thermodynamic calculation of the formation of calcification mineral phases and experimental results of phase formation under conditions typical of the human blood plasma prototype. The laboratory tests showed that dopants of the biological solution (magnesium ions and glutamic acid) affect phase composition and solubility of the samples. The bioactivity of synthetic samples was studied in solutions of different composition and in Verapamil. The results indicate that the model studies of the crystallization of pathogenic formations in the cardiovascular system performed to identify the mechanisms that control their genesis are significant and will provide timely diagnosis of calcification and development of new approaches in cardiology aimed to reduce the incidence of these diseases. Statement of significanceThe processes of crystallization of organo-mineral associations (OMA) that are part of the physiogenetic (bone, teeth) and pathogenic minerals (urinary, dental, calcifications etc.) are currently one of the crucial study areas. These studies are of essential interest since pathogenic OMA are primarily considered to be human diseases, for example, arteriosclerosis, which is associated with precipitation of calcium salts in blood vessels. It is the second most common disease after atherosclerosis among all lesions of arterial vessels. It should be noted that the percentage of calcification in blood vessels, heart valves and operating stents has increased in recent years.Vascular calcification is a complex process that involves a number of mechanisms responsible for the precipitation of calcium salts in vessel walls. As a result, arterial stiffness and pulse wave velocity increase, which in turn increases the rate of morbidity and mortality from cardiovascular diseases. The study and in-depth understanding of the mechanisms of calcification crystallization in blood vessels can be crucial for developing effective protective therapy.

Prediction model for successful radiocephalic arteriovenous fistula creation in patients with diabetic nephropathy

Arteriovenous fistula (AVF) is the most appropriate vascular access for all chronic kidney disease patients for hemodialysis. However, patients with diabetic nephropathy are at increased risk for primary failure after AVF creation, mainly due to atherosclerosis and calcification of blood vessels. We conducted this study to find out the risk factors for primary failure of radiocephalic AVF in end-stage renal disease (ESRD) patients due to diabetic nephropathy and develop a risk predicting model. This study was conducted at a tertiary care teaching hospital of South India. Patients with ESRD due to diabetic nephropathy whom underwent left radiocephalic AVF at wrist were enrolled. Risk factors for primary failure were analyzed by univariate and multivariate logistic regression models. Sixty-six patients were included in the study. Thirty-one patients had a primary failure. Independent risk factors for primary failure were palpable vessel wall of the radial artery (P = 0.003, odds ratio [OR] = 15.317), smaller radial artery diameter (P = 0.001, OR = 16.526), radial artery peak systolic velocity (PSV) <45 cm/s (P = 0.005, OR = 8.494), and linear radial artery calcification (P = 0.006, OR = 7.942). The risk predicting model obtained by adding the score given for each risk factors (vessel wall not palpable = 0, palpable = 1, no linear calcification in digital X-ray = 0, linear calcification = 1, PSV ≥45 cm/s = 0, <45 cm/s = 1 and 2.5 - radial artery diameter in mm) had an area under receiver-operating characteristic curve of 0.886. Cutoff score of 1.5 had sensitivity of 83.9% and specificity of 80.0% for primary failure. Risk predicting model for primary failure based on condition of the vessel wall on palpation, radial artery diameter, flow velocity, and calcification may be helpful for suitable patient selection.

Calcification of abdominal aorta in patients recently starting hemodialysis: A single-center experience from Egypt.

Vascular calcification (VC) is a well-known complication in patients with chronic kidney disease (CKD). Keeping in mind, the end goal to assess the genuine effect of mineral bone disease in the pathogenesis of blood vessel calcification during the pre-dialysis course of CKD, we assessed the prevalence and extent of abdominal aortic calcification (AAC) in nondiabetic CKD patients recently starting hemodialysis (HD). Eighty-one patients with end-stage renal disease beginning HD over a one-month period were selected. They underwent a detailed clinical examination and laboratory evaluation, including serum calcium, phosphorus, parathyroid hormone, fibroblast growth factor (FGF-23), and alkaline phosphatase were measured, and spiral computed tomography was performed to evaluate AAC score. AAC was present in 64 patients (79%). There was a significant correlation between the AAC score and age (r = 0.609, P <0.001) and FGF-23 (r = 0.800, P <0.001). This study suggests that the prevalence and extent of AAC are critical in incident HD patients. Serum FGF-23 level is the sole statistically significant correlate of AAC in these patients.