• Agatston score
• Coronary calcification
• Hemodialysis
• Vitamin K1

• Humans
• Renal Dialysis/adverse effects
• Male
• Female
• Middle Aged
• Vascular Calcification/etiology
• Vascular Calcification/prevention & control
• Vascular Calcification/diagnostic imaging
• Coronary Artery Disease/prevention & control
• Coronary Artery Disease/etiology
• Coronary Artery Disease/diagnostic imaging
• Vitamin K 1/administration & dosage
• Vitamin K 1/therapeutic use
• Vitamin K 1/adverse effects
• Aged
• Renal Insufficiency, Chronic/therapy
• Renal Insufficiency, Chronic/complications
• Dietary Supplements
• Treatment Outcome
• Mexico
• Disease Progression
• Double-Blind Method

• Adragão score
• Gla-rich protein
• biomarker
• peritoneal dialysis
• vascular calcification

• PhD grant 2020.07476.BD; the transitional provision DL57/2016/CP1361/CT0006, and projects EXPL/BTM-TEC/0990/2021, UIDB/04326/2020 (DOI:10.54499/UIDB/04326/2020), UIDP/04326/2020 (DOI:10.54499/UIDP/04326/2020) and LA/P/0101/2020 (DOI:10.54499/LA/P/0101/202 Fundação para a Ciência e Tecnologia
• AAC nº 41/ALG/2020-Project nº 072583-NUTRISAFE Portugal 2020; CRESC Algarve
• projects funding 2019 Sociedade Portuguesa de Nefrologia

• CKD
• PIVKA-II
• dp-ucMGP
• menaquinone-7
• vascular calcification
• vitamin K

• Humans
• Vascular Calcification/etiology
• Vitamin K
• Renal Insufficiency, Chronic/complications
• Matrix Gla Protein
• Vitamin K Deficiency/complications
• Extracellular Matrix Proteins/blood
• Extracellular Matrix Proteins/metabolism
• Calcium-Binding Proteins/blood
• Dietary Supplements
• Cardiovascular Diseases/etiology
• Cardiovascular Diseases/prevention & control
• Biomarkers/blood

• Calcium & bone
• Coronary heart disease
• Dialysis

• Humans
• Adolescent
• Calcium/therapeutic use
• Coronary Vessels
• Renal Dialysis
• Hyperparathyroidism, Secondary/drug therapy
• Hyperparathyroidism, Secondary/etiology
• Hyperparathyroidism, Secondary/prevention & control
• Randomized Controlled Trials as Topic
• Multicenter Studies as Topic
• Propionates

• The UPCOMING study will be funded by Sanwa Kagaku Kenkyusho Co., Ltd

• Kidney transplantation
• coronary artery calcification
• mineral and bone disorder
• thoracic aortic calcification
• vascular calcification

• Male
• Humans
• Kidney Transplantation/adverse effects
• Calcium
• Prediabetic State
• Collagen Type I
• Vascular Calcification/diagnostic imaging
• Vascular Calcification/etiology
• Vascular Calcification/metabolism
• Bone Density
• Minerals
• Bone Diseases, Metabolic
• Peptides

• Female
• Humans
• Magnesium
• Male
• Prospective Studies
• Renal Dialysis
• Renal Insufficiency, Chronic/drug therapy
• Renal Insufficiency, Chronic/therapy
• Vascular Calcification/etiology

Chronic Kidney Disease (CKD) patients are at high risk of presenting with arterial calcification or stiffness, which confers increased cardiovascular mortality and morbidity. In recent years, it has become evident that VC is an active process regulated by various molecules that may act as inhibitors of vessel mineralization. Matrix Gla Protein (MGP), one the most powerful naturally occurring inhibitors of arterial calcification, requires vitamin K as a co-factor in order to undergo post-translational γ-carboxylation and phosphrorylation and become biologically active. The inactive form of MGP (dephosphorylated, uncarboxylated dp-ucMGP) reflects vitamin K deficiency and has been repeatedly associated with surrogate markers of VC, stiffness, and cardiovascular outcomes in CKD populations. As CKD is a state of progressive vitamin K depletion and VC, research has focused on clinical trials aiming to investigate the possible beneficial effects of vitamin K in CKD and dialysis patients. In this study, we aim to review the current evidence regarding vitamin K supplementation in uremic patients.

• Matrix Gla Protein
• cardiovascular disease
• chronic kidney disease
• end-stage kidney disease
• hemodialysis
• menaquinone-7
• vascular calcification
• vitamin K

• Dietary Supplements
• Humans
• Renal Dialysis/adverse effects
• Renal Insufficiency, Chronic/complications
• Vascular Calcification/complications
• Vascular Calcification/prevention & control
• Vitamin K

Compared with the general population, the risk of death is substantially higher in renal transplant recipients than in age- and sex-matched individuals in the general population. In the general population, coronary artery calcification (CAC) predicts all-cause and cardiovascular mortality. In this study we aimed to analyse these relationships in renal transplant recipients.

We examined 178 renal transplant patients in this prospective observational cohort study. We measured CAC with multidetector spiral computed tomography using the Agatston score at multiple time points. Overall, 411 scans were performed in 178 patients over an average 12.8 years follow-up. The clinical endpoint was a composite including all-cause death and non-fatal cardiovascular events. Data analysis was performed by the joint model.

During a follow-up of 12.8 ± 2.4 years, coronary calcification progressed over time (P < 0.001) and the clinical endpoint occurred in 54 patients. In the analysis by the joint model, both the baseline CAC score and the CAC score progression were strongly associated with the incidence rate of the composite event [hazard ratio 1.261 (95% confidence interval 1.119–1.420), P = 0.0001].

CAC at baseline and coronary calcification progression robustly predict the risk of death and cardiovascular events in renal transplant recipients. These findings support the hypothesis that the link between the calcifying arteriopathy of renal transplant patients and clinical end points in these patients is causal in nature.

• cardiovascular disease
• coronary artery calcification
• joint model
• mortality
• renal transplantation

• Cardiovascular disease
• carbamylated albumin
• cardiac morphology
• home hemodialysis
• intensive hemodialysis
• myocardial stunning
• nocturnal hemodialysis
• vascular calcification

• CKD-MBD
• Calcification
• Children
• FGF23
• Growth
• Parathyroid hormone
• Renal transplantation

Cardiovascular disease is the leading cause of death in end-stage renal disease (ESRD) and is strongly associated with vascular calcification. An important driver of vascular calcification is high phosphate levels, but these become lower when patients initiate nocturnal hemodialysis or receive a kidney transplant. However, it is unknown whether nocturnal hemodialysis or kidney transplantation mitigate vascular calcification. Therefore, we compared progression of coronary artery calcification (CAC) between patients treated with conventional hemodialysis, nocturnal hemodialysis, and kidney transplant recipients.

We measured CAC annually up to 3 years in 114 patients with ESRD that were transplantation candidates: 32 that continued conventional hemodialysis, 34 that initiated nocturnal hemodialysis (≥4x 8 hours/week), and 48 that received a kidney transplant. We compared CAC progression between groups as the difference in square root transformed volume scores per year (ΔCAC SQRV) using linear mixed models. Reference category was conventional hemodialysis.

The mean age of the study population was 53 ±13 years, 75 (66%) were male, and median dialysis duration was 28 (IQR 12–56) months. Median CAC score at enrollment was 171 (IQR 10–647), which did not differ significantly between treatment groups (P = 0.83). Compared to conventional hemodialysis, CAC progression was non-significantly different in nocturnal hemodialysis -0.10 (95% CI -0.77 to 0.57) and kidney transplantation -0.33 (95% CI -0.96 to 0.29) in adjusted models.

Nocturnal hemodialysis and kidney transplantation are not associated with significantly less CAC progression compared to conventional hemodialysis during up to 3 years follow-up. Further studies are needed to confirm these findings, to determine which type of calcification is measured with CAC in end-stage renal disease, and whether that reflects cardiovascular risk.

• Adult
• Aged
• Coronary Vessels/diagnostic imaging
• Coronary Vessels/pathology
• Disease Progression
• Female
• Humans
• Kidney Failure, Chronic/therapy
• Kidney Transplantation
• Male
• Middle Aged
• Multidetector Computed Tomography
• Renal Dialysis/adverse effects
• Renal Dialysis/methods
• Vascular Calcification/diagnostic imaging
• Vascular Calcification/pathology

• Amgen Nederland
• Baxter Nederland
• Novartis Pharma
• Fresenius Medical Care
• Wellerdieck-de Goedefonds
• Roche
• Shire

• Chronic kidney disease-mineral and bone disorders
• RANK
• RANKL, OPG
• Renal Osteodystrophy
• Sclerostin
• Vascular calcification

• Agatston score
• Infrarenal abdominal aorta
• Kidney transplantation
• Multi-slice computed tomography
• Risk factor
• Vascular calcification

Coronary artery calcifications(CACs), are related to the increased cardiovascular mortality during kidney transplantation(KTx). Using coronary-CT performed at 1 month(T0) and 5 years(T5) after KTx we evaluated: (1) the prevalence of CACs; (2) the clinical and biochemical factors related to CACs; 3) the factors implicated with CACs progression. We evaluated 67-pts selected from the 103-pts transplanted in our unit between 2007 and 2008. Clinical and biochemical parameters were recorded at the time of pre-KTx evaluation and for five years after KTx. Coronary-CT for the Agatson score (AS) evaluation was performed at T0 and at T5, and CACs progression was determined. At baseline AS was 45 [0–233]. At T5 AS was 119 [1–413]. At T0, 69% of patients had CACs. Age and dialytic vintage were the main independent variables related to CACs. At T5, CACs were present in 76% of patients. Age was the only independent factor in determining CACs. A progression of CACs was observed in 74% of patients. They were older, had higher CACs-T0 and higher SBP throughout the 5-years. The presence of CACs at T0 and age were the only independent factors in determining the CACs-progression. CACs-T0 had the best discriminative power for CACs progression. CACs prevalence is quite high in KTx patients; Age is strictly related to CACs; Age and the presence of CACs at baseline were the two major factors associated with the progression of CACs during the five years of follow up. CACs-T0 had the best discriminative power for progression of CACs.

• coronary artery calcification
• haemodialysis
• kidney transplantation
• peritoneal dialysis
• systematic review

• Calcific uremic arteriolopathy
• Calcification
• Chronic kidney disease
• Fibroblast growth factor 23
• Kidney transplantation
• Klotho
• Phosphate binders
• Sevelamer
• Uremia

• bone mineral metabolism
• dialysate calcium concentration
• nocturnal hemodialysis
• vascular calcification

Coronary calcification (CAC) is highly prevalent in kidney transplant recipients (KTRs) and has been associated with cardiovascular morbidity and mortality. Some studies have shown a reduction in CAC progression with statin therapy in the general and chronic kidney disease (CKD) populations.

The aim of the present study was to evaluate the effect of statins on CAC progression in incident kidney transplant recipients. Patients were randomly assigned to the statin (n = 61, 10 mg daily) and control group (n = 59). CAC and biochemical analyses were performed at baseline and 12 months.

At baseline, CAC was observed in 30% and 21% of patients in the statin and control groups, respectively (p = 0.39). The calcium score at baseline and its absolute and relative changes over 12 months of follow up were similar among the groups. In the statin group, total cholesterol (p < 0.001), low density lipoprotein cholesterol (p < 0.001) and triglycerides (p = 0.005) decreased, and the estimated glomerular function rate increased (p<0.001) significantly. CRP levels remained stable (p = 0.52) in the statin group but increased in the control group (p = 0.01). In the multivariate model, there was no difference in CAC progression between the groups (group effect p = 0.034; time-effect p = 0.23; interaction p = 0.74). Similar results were obtained when only patients with ≥ 10AU calcium score (calcified) were analyzed (group effect p = 0.051; time-effect p = 0.58; interaction p = 0.99).

Although statins reduce the levels of cholesterol, triglycerides, inflammation and improve graft function, the dose adopted in the current study did not delay CAC progression within 12 months of follow up.

Brazilian Clinical Trials Registry RBR-32RFMB

• ASCVD
• CKD
• Cholesterol
• atherosclerotic cardiovascular disease
• cardiovascular disease
• coronary heart disease
• drug safety
• guidelines
• high density lipoprotein cholesterol
• lipids
• low density lipoprotein cholesterol
• mortality
• review
• risk score
• statin
• treatment recommendations

• Atherosclerosis
• Cardiac imaging techniques
• Chronic kidney disease
• Coronary artery disease
• Vascular calcification

• aldosteronoma resolution score
• aortic calcification
• laparoscopic adrenalectomy
• persistent hypertension
• primary aldosteronism

• Atrioventricular block
• Chronic kidney disease
• Subcutaneous nerve activity
• Sudden death

The development of end stage renal failure can be seen as a catastrophic health event and patients with this condition are considered at the highest risk of cardiovascular disease among any other patient groups and risk categories. Although kidney transplantation was hailed as an optimal solution to such devastating disease, many issues related to immune-suppressive drugs soon emerged and it became evident that cardiovascular disease would remain a vexing problem. Progression of chronic kidney disease is accompanied by profound alterations of mineral and bone metabolism that are believed to have an impact on the cardiovascular health of patients with advanced degrees of renal failure. Cardiovascular risk factors remain highly prevalent after kidney transplantation, some immune-suppression drugs worsen the risk profile of graft recipients and the alterations of mineral and bone metabolism seen in end stage renal failure are not completely resolved. Whether this complex situation promotes progression of vascular calcification, a hall-mark of advanced chronic kidney disease, and whether vascular calcifications contribute to the poor cardiovascular outcome of post-transplant patients is reviewed in this article.

• morbidity
• Chronic kidney disease-mineral bone disorder
• cardiovascular disease
• chronic kidney disease
• Mortality
• Bone fractures

• hemodialysis
• mineral metabolism
• vascular calcification

• Adaptor Proteins, Signal Transducing
• Adult
• Aged
• Aorta/pathology
• Bone Morphogenetic Proteins/blood
• Cohort Studies
• Disease Progression
• Female
• Genetic Markers
• Humans
• Kidney Transplantation
• Longitudinal Studies
• Male
• Middle Aged
• Risk Factors
• Tomography, X-Ray Computed
• Transplant Recipients
• Vascular Calcification/blood
• Vascular Calcification/pathology

• Calcification
• Vascular calcification
• Vascular smooth muscle cells

• Bone Diseases, Metabolic/metabolism
• Bone Remodeling
• Cell Differentiation
• Chondrocytes/metabolism
• Core Binding Factor Alpha 1 Subunit/metabolism
• Humans
• Hypercalcemia/metabolism
• Hyperphosphatemia/metabolism
• Muscle, Smooth, Vascular/cytology
• Muscle, Smooth, Vascular/metabolism
• Myocytes, Smooth Muscle/metabolism
• Osteocytes/metabolism
• Renal Insufficiency, Chronic/complications
• Renal Insufficiency, Chronic/metabolism
• Vascular Calcification/complications
• Vascular Calcification/metabolism

Despite limitations of routine methods, Clinical Practice Guidelines support the assessment of bone mineral density (BMD) and vascular calcification in renal transplant recipients. Changes in fat mass also occur post-transplantation, although they are traditionally difficult to measure accurately. We report the feasibility, convenience and accuracy of measuring the above 3 parameters using a novel CT protocol.

We conducted a cross-sectional study of 64 first renal allograft recipients (eGFR > 30 ml/min/1.73 m²). Quantitative CT (QCT) BMD analysis was conducted using CT lumbar spine (GE Medical Systems Lightspeed VCT & Mindways QCT Pro Bone Mineral Densitometry System Version 4.2.3) to calculate spinal volumetric BMD and compared with standard DXA calculated areal BMD at the spine, hip and distal forearm. Abdominal aortic calcification was assessed by semi-quantitative Aortic Calcification Index (ACI) method and compared with lateral lumbar x-ray Kappuila score and pulse wave velocity (PWV). Visceral and subcutaneous adipose tissue volume (Osirix 16 Ver 3.7.1) was compared with BMI.

Participants were 61 % male, had a mean age of 47 years, median ESKD duration of 5.4 years and a mean eGFR of 54 ml/min. iDXA median T-score at proximal femur was −1.2 and at lumbar spine was −0.2. Median QCT Trabecular T-score at lumbar spine was −1.2. The percent of subjects with a T-score of <2.5 by site and method was DXA Proximal Femur: 7 %, DXA distal radius: 17 %, DXA spine: 9 %, QCT (American College of Radiology cutoffs): 9 %. CT derived ACI correlated with PWV (r = 0.29, p = 0.02), pulse wave pressure (r = 0.51, p < 0.001), QCT Trabecular (−0.31, p = 0.01) and cortical volumetric BMD and history of cardiovascular events (Mann–Whitney U, p = 0.02). Both visceral and subcutaneous adipose tissue correlated with BMI (r = 0.63 & 0.64, p < 0.001).

Single CT scan triple assessment of BMD, vascular calcification and body composition is an efficient, accurate and convenient method of risk factor monitoring post renal transplantation.

Arterial stiffness is closely associated with cardiovascular disease (CVD) in end stage renal disease (ESRD) patients. However, the clinical significance of pre-transplant arterial stiffness and the impact of kidney transplantation (KT) on arterial stiffness have not yet been determined.

We measured the brachial-ankle pulse wave velocity (baPWV) before KT and one year after KT. We evaluated the potential utility of pre-transplant baPWV as a screening test to predict CVD. The impact of KT on progression of arterial stiffness was evaluated according to changes in baPWV after KT. The factors that influence the change of baPWV after KT were also examined.

The mean value of pre-transplant baPWV was 1508 ± 300 cm/s in ESRD patients; 93.4% had a higher baPWV value than healthy controls. Pre-transplant baPWV was higher in patients with CVD than in those without CVD (1800 ± 440 vs. 1491 ± 265 cm/s, p<0.05), and was a strong predictive factor of CVD (OR 1.003, p<0.05). The optimal cut-off value of baPWV for the detection of CVD was 1591 cm/s, and this value was an independent predictor of CVD in KT recipients (OR 6.3, p<0.05). The post-transplant baPWV was significantly decreased compared to that of pre-transplant rates (1418 ± 235 vs. 1517 ± 293 cm/s, p<0.05), and progression of arterial stiffness was not observed in 86.9% patients. Logistic regression analysis revealed that higher body mass index and the degree of increase in calcium levels were independent risk factors that affected baPWV after KT.

Evaluation of arterial stiffness with baPWV is a useful screening test for predicting CVD after KT, and KT is effective in preventing the progression of arterial stiffness in ESRD patients.

• Adult
• Ankle Brachial Index
• Blood Pressure
• Brachial Artery/physiopathology
• Calcium/metabolism
• Cardiovascular Diseases/diagnosis
• Cardiovascular Diseases/epidemiology
• Case-Control Studies
• Demography
• Disease Progression
• Female
• Hemodynamics
• Humans
• Incidence
• Kidney Failure, Chronic/physiopathology
• Kidney Transplantation
• Male
• Middle Aged
• Pulse Wave Analysis
• ROC Curve
• Reference Values
• Risk Factors
• Vascular Stiffness

• Coronary artery calcification
• Epicardial adipose tissue
• Hemodialysis
• Survival

Previous research on vascular calcification has mainly focused on the vascular intima and media. However, we show here that vascular calcification may also occur in the adventitia. The purpose of this work is to help elucidate the pathogenic mechanisms underlying vascular calcification. The calcified lesions were examined by Von Kossa staining in ApoE−/− mice which were fed high fat diets (HFD) for 48 weeks and human subjects aged 60 years and older that had died of coronary heart disease, heart failure or acute renal failure. Explant cultured fibroblasts and smooth muscle cells (SMCs)were obtained from rat adventitia and media, respectively. After calcification induction, cells were collected for Alizarin Red S staining. Calcified lesions were observed in the aorta adventitia and coronary artery adventitia of ApoE-/-mice, as well as in the aorta adventitia of human subjects examined. Explant culture of fibroblasts, the primary cell type comprising the adventitia, was successfully induced for calcification after incubation with TGF-β1 (20 ng/ml) + mineralization media for 4 days, and the phenotype conversion vascular adventitia fibroblasts into myofibroblasts was identified. Culture of SMCs, which comprise only a small percentage of all cells in the adventitia, in calcifying medium for 14 days resulted in significant calcification.Vascular calcification can occur in the adventitia. Adventitia calcification may arise from the fibroblasts which were transformed into myofibroblasts or smooth muscle cells.

• Adventitia/metabolism
• Adventitia/pathology
• Aged
• Aged, 80 and over
• Animals
• Aorta/metabolism
• Aorta/pathology
• Apolipoproteins E/deficiency
• Cells, Cultured
• Coronary Vessels/metabolism
• Coronary Vessels/pathology
• Female
• Fibroblasts/metabolism
• Fibroblasts/pathology
• Humans
• Male
• Mice
• Mice, Knockout
• Middle Aged
• Muscle, Smooth, Vascular/metabolism
• Muscle, Smooth, Vascular/pathology
• Myocytes, Smooth Muscle/metabolism
• Myocytes, Smooth Muscle/pathology
• Rats
• Rats, Sprague-Dawley
• Transforming Growth Factor beta1/metabolism
• Vascular Calcification/genetics
• Vascular Calcification/metabolism
• Vascular Calcification/pathology

The objective of the study was to determine the relationship between common carotid artery intima-media thickness (CCA-IMT) and histologically assessed calcification of radial artery in relation to clinical features and laboratory markers of bone and mineral metabolism, inflammation, and oxidative stress in patients with stage 5 chronic kidney disease (CKD).

The study comprised 59 patients (36 hemodialyzed, 23 predialysis). CCA-IMT was measured by ultrasonography; the biochemical parameters examined were assessed using routine laboratory methods, ELISA micro-plate immunoassays and spectrophotometry. Fragments of radial artery obtained during creation of hemodialysis access were cryosectioned and stained for calcifications using von Kossa method and alizarin red.

Glucose, osteoprotegerin, pentraxin 3 and Framingham risk score significantly correlated with CCA-IMT. In multiple regression analysis, OPG positively predicted CCA-IMT. Radial artery calcifications were found in 34 patients who showed higher CCA-IMT (0.98 ± 0.13 vs 0.86 ± 0.14 mm; P = 0.006). Higher CCA-IMT values were also associated with more advanced calcifications. CCA-IMT and the presence of plaques in common carotid artery were positive predictors of radial artery calcifications, independent of dialysis status, Framingham risk score, CRP and Ca x Pi [OR for calcifications 2.19 (1.08-4.45) per 0.1 mm increase in CCA-IMT]. The presence of radial artery calcifications was a significant predictor of mortality, independent of dialysis status and Framingham risk score [HR 3.16 (1.03-9.64)].

In CKD patients, CCA-IMT examination can be used as a surrogate measure to assess the incidence and severity of arterial medial calcification which is associated with poor clinical outcome in these patients.

• MGP
• VSMC
• cardiovascular diseases
• phenotype switch
• vitamin K

• Adult
• Aorta/pathology
• Cadaver
• Calcinosis
• Cardiovascular System/physiopathology
• Female
• Humans
• Kidney/physiopathology
• Kidney Transplantation
• Living Donors
• Male
• Middle Aged

• Calcium-Binding Proteins/blood
• Dietary Supplements
• Extracellular Matrix Proteins/blood
• Female
• Hemostatics/administration & dosage
• Humans
• Male
• Renal Dialysis
• Vitamin K 2/administration & dosage
• Vitamin K 2/analogs & derivatives
• Matrix Gla Protein

• Dialysis
• High-resolution peripheral quantitative computed tomography
• Renal osteodystrophy
• Vascular calcification

• Absorptiometry, Photon
• Aged
• Bone Density
• Bone and Bones/diagnostic imaging
• Bone and Bones/pathology
• Calcinosis/complications
• Calcinosis/diagnostic imaging
• Calcinosis/pathology
• Coronary Vessels/pathology
• Female
• Humans
• Kidney Failure, Chronic/complications
• Kidney Failure, Chronic/pathology
• Male
• Middle Aged
• Tomography, X-Ray Computed/methods

• aortic calcification
• atherosclerosis
• coronary calcification
• dialysis
• pelvic calcification

• Adult
• Female
• Humans
• Kidney Transplantation/adverse effects
• Male
• Middle Aged
• Prevalence
• Renal Dialysis/adverse effects
• Renal Insufficiency, Chronic/diagnosis
• Renal Insufficiency, Chronic/epidemiology
• Renal Insufficiency, Chronic/surgery
• Risk Factors
• Severity of Illness Index
• Thailand/epidemiology
• Time Factors
• Treatment Outcome
• Vascular Calcification/diagnosis
• Vascular Calcification/epidemiology
• Waiting Lists

Vascular calcifications (VCs) are a cardiovascular risk factor in patients affected by chronic kidney disease and after kidney transplantation (KTx). We evaluated the prevalence of VCs at the abdominal aortic site in KTx patients at the time of transplantation and 1 year after KTx, exploring the possibly associated factors.

In 107 transplanted patients, the following parameters were evaluated at the first and twelfth month after KTx: the aortic calcification index (ACI), fibroblast growth factor 23, osteoprotegerin (OPG), fetuin A, and clinical and biochemical parameters. Patients were followed up for 2 years after KTx.

At the time of KTx, 60% of patients had some degree of VC (ACI>0), whereas 40% had no VC. One year after KTx, VCs worsened in 26% of patients, whereas in 74%, VCs remained stable or improved. The progression of VC was observed almost exclusively in patients with a positive ACI score at the first month. At the multivariate analysis, serum calcium, OPG, and estimated glomerular filtration rate were the only variables independently associated with the progression of VC.

VCs at the aortic site are frequent in KTx patients, and in a significant percentage of them, they tend to progress even in the short time. High levels of serum calcium and OPG are significantly associated with the progression of VCs. Whether these associations are based on a cause-effect relationship and their correction might impact on the calcification process could be ascertained by prospective interventional studies.