scholarly journals P0869EXOGENOUS OSTEOGENIC FACTOR 1 ADMINISTRATION ATTENUATED VASCULAR CALCIFICATION AND IMPROVED BONE DISORDERS IN CHRONIC UREMIC RATS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Chien-Te Lee ◽  
Hwee-Yeong Ng ◽  
Wen-Lin Chen ◽  
Yuai-Ting Lee
Keyword(s):  
Renal Failure ◽  
Vascular Calcification ◽  
Fibroblast Growth Factor 23 ◽  
Mineral Density ◽  
Bone Disorders ◽  
Trabecular Thickness ◽  
Bony Structure ◽  
Significant Difference ◽  
Fgf 23 ◽  
Osteogenic Factor

Abstract Background and Aims Hyperphosphatemia and secondary hyperparathyroidism are frequent complications in chronic kidney disease (CKD) which both contribute to increased morbidity and mortality in CKD. Osteogenic factor-1 (OP-1) is an important member of BMPs subfamily and its effects on CKD-associated mineral and bone disorders (MBD) is controversial. The study examined whether exogenous OP-1 administration can modulate disturbed CKD-MBD in adenine-induced chronic uremic rats Method Chronic renal failure was induced in adult male SD rats by feeding adenine-containing diet. After adenine diet feeding 3 weeks, animals were injected with OP-1 (5μg/kg/day) intraperitoneally for 2 weeks. The serum and urine phosphorus levels and associated mineral parameters, including fibroblast growth factor 23(FGF-23), DKK-1 and sclerostin were measured. Vascular calcification was assessed by immunohistochemistry staining on aortic tissue. Bony structure was evaluated by microCT (Bruker-microCT, Kontich, Belgium). Results A significant decrease of body weight and deteriorated renal function was observed in adenine and OP-1 treatment groups during study period and serum creatinine levels were similar (5.23 ±1.1 mg/dL vs. 5.4 ±1.2 mg/dL, p>0.05). Animals in OP-1 group had lower serum phosphorous (18.7±5.1 vs. 29.0±9.6 mg/dL, p<0.05) and intact parathyroid hormone levels (2906.1±1206.9 vs. 4669.7±2505.9 pg/dL, p<0.05) compared to adenine group. Decreased urine phosphorous excretion was noted in both groups without significant difference. Levels of serum FGF-23, sclerostin and DKK-1 were significantly lower in OP-1 treatment group (all p< 0.05). OP-1 administration diminished the staining of RUNX2 (59.1±3% of adenine-treated group), alkaline-phosphatase (49.4±5.7%), β-caterin (39.3±1.8%), BMP2 (43.2%±6.7%), and BMP7 (51.9±10%, all p <0.05). MicroCT revealed that bone mineral density was increased by OP-1 treatment (0.46±0.1 vs.0.39±0.06 g/cm3). Total volume was increased but bone volume was not changed. OP-1 administration did not affect trabecular thickness and trabecular number. Conclusion Our data indicated administration of exogenous OP-1 improved hyperparathyroidism and attenuated vascular calcification. OP-1 treatment was also associated with beneficial effects on bony structure in animals with renal failure.

P1823THE ROLE OF FGF-23 IN CKD PROGRESSION IN CHILDREN

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Altynay Balmukhanova ◽  
Kairat Kabulbayev ◽  
Assiya Kanatbayeva ◽  
Harika Alpay ◽  
Aigul Balmukhanova ◽  
...  
Keyword(s):  
Statistical Analysis ◽  
Fibroblast Growth Factor 23 ◽  
Public Health Issue ◽  
Control Group ◽  
Healthy Individuals ◽  
Ckd Progression ◽  
Average Value ◽  
Significant Difference ◽  
Fgf 23

Abstract Background and Aims Chronic kidney disease (CKD) is considered a global medical and public health issue. CKD takes a special place among non-infectious diseases because of its prevalence (6-20% according to different surveys and studies) and is associated with a poor life quality, complications and high risk of mortality. In recent years, there have been new biomarkers requiring more research in this area. One of these biomarkers is Fibroblast growth factor-23 (FGF-23) which is found as a bone derived hormone and might be a predictor of progression. However, the role of FGF-23 in CKD progression in children has not been adequately studied, especially on the early stages. Nowadays, the study of FGF-23 in children and the question of the clinical importance of this marker are relevant. Therefore, the aim of our study was to establish the role of FGF-23 in CKD progression in children. Method A prospective study was conducted on 73 children with different stages of CKD and 14 healthy individuals (control group) matched by age and gender. There were approximately equal numbers of patients in study groups. An average age was 9.61±1.05 years. Exclusion criteria: active inflammatory, bone, infectious, oncological, immunological diseases, taking steroids and vitamin D supplements. Laboratory measurements included all common clinical and biochemical indicators. Serum concentration of intact FGF-23 was assessed by using the ELISA method (Biomedica Medizinprodukte GmbH, Austria). Statistical analysis was conducted in MS Excel 2016 and SPSS 18.0. Results The normal range of FGF-23 for this kit was 0.1-1.5 pmol/l. The average value of FGF-23 in the control group was 0.69±0.12 pmol/l. Further studies in the groups with different stages of CKD revealed that FGF-23 concentration gradually rose in parallel with stages of CKD, and it reached the maximum on the last stage. It should be noticed that the level of FGF-23 concentration on the first stage of CKD was normal (0.73±0.14 pmol/l) and the comparison with healthy individuals revealed no significant differences. What is remarkable, despite the fact that the average value of the second stage patients was normal (1.36±0.2 pmol/l), there was a statistically significant difference with the control group (p=0.008). The levels of FGF-23 on the next stages were 2.52±0.52 pmol/l, 5.42±1.61 pmol/l, and 12.16±1.55 pmol/l, respectively. The differences were considerable and proved by statistical analysis (p<0.01). Conclusion Our study showed that there is an upward trend of FGF-23 as CKD progresses from early to advanced stages. The results on the second and third stages indicate that FGF-23 should be considered as one of early biomarkers of CKD progression in children. Thus, there is a need for more studies in this area.

scholarly journals Role of Fibroblast Growth Factor- 23 in Coronary Artery Diseases and its Association with Apolipoprotein A1

2018 ◽  
Vol 9 (SPL1) ◽  
Author(s):  
Fadhil Jawad Al-Tu'ma ◽  
Anaam Hato Kadhim ◽  
Anaam Hato Kadhim ◽  
Saif Sami Al-Mudhaffar
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Apolipoprotein A1 ◽  
Control Group ◽  
Significant Difference ◽  
Artery Disease ◽  
Fgf 23

Coronary artery disease (CAD) is a clinical manifestation resulting from a narrowing of epicardial coronary arteries that supply blood and oxygen to the heart. Coronary artery disease is mostcommonlydue to atherosclerotic occlusion of the coronary arteries.Fibroblast growth factor 23 (FGF23) is a circulating peptide hormone secreted by bone cells,regulating phosphate and vitamin D metabolism. Several recent observational studies reported an independent association of circulating FGF23 with several cardiovascular disease (CVD) risk factors including left ventricular hypertrophy and vascular dysfunction,CVD progression and incident clinical CVD eventsand mortality.Apolipoprotein A1 (ApoA1) is the primary protein associated with high-density lipoprotein (HDL) particles,and plays a central role in reverse cholesterol transport. HDL cholesterol (HDL-C) and ApoA1 concentrations are inverlassely related to the risk for coronary artery disease. To find the role of fibroblast growth factor-23 in coronary artery disease and its associationwith Apolipoprotein-A1.This ccross –sectionalstudyincluded 42 elective patients attending the cardiology unit and the results of those patients were compared with 40 healthy control group. Blood samples were obtained for measurements of (FGF-23,troponin I,Apo-A1,total creatine kinase activity,urea,creatinine and lipid profile).The obtained results showed that there was a significant difference in serum FGF-23 in coronary artery disease (367.52 ± 128.52 pg/ml) as compared with the control (165.41 ± 53.65 pg/ml) (p< 0.05). There was a significant differences in Apo-A1 in coronary artery disease (2.03±0.90 mg/ml) as compared with the control (1.49 ± 0.25 mg/ml) (P = 0.014).There was a significant difference in age between CAD (58.66±8.85) and control group (51.125 ± 11.71) (P<0.005).There was a significant difference in TG where control (99.50 ± 21.59) differ from CAD (142.05 ± 66.24) (P = 0.006).According to the results that were shown in the tables, we can be conclude that higher levels of FGF23 and Apo-A1 may be associated with complications and mortality of CAD beside its associating with atherosclerosis in the Iraqi patients.

scholarly journals Effect of empagliflozin on phosphorus and calcium metabolism in patients with type 2 diabetes mellitus with preserved kidney function

2021 ◽  
Vol 24 (1) ◽  
pp. 4-9
Author(s):  
D. A. Lebedev ◽  
N. V. Timkina ◽  
T. L. Karonova ◽  
A. T. Andreeva ◽  
M. A. Kokina ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Kidney Function ◽  
Trabecular Bone Score ◽  
Fibroblast Growth Factor 23 ◽  
Mineral Density ◽  
Increased Risk ◽  
Fgf 23

Background: Sodium glucose co-transporter type 2 inhibitors (iSGLT2) are antihyperglycemic drugs approved for the treatment of type 2 diabetes mellitus (T2DM). Clinical trials with these drugs have shown evidence of an increased risk of fractures and an effect on phosphorus, vitamin D and parathyroid hormone (PTH) levels.Aim: The aim of this study was to investigate the effect of the most selective iSGLT2 empagliflozin on the calcium and phosphorus metabolism in patients with T2DM and preserved kidney function.Materials and methods: Thirty-nine T2DM patients were received empagliflozin 10 mg in addition to their antihyperglycemic drugs for 12 weeks. Before starting treatment, a dual-energy X-ray absorptiometry (DXA) with an assessment of the trabecular bone score (TBS) was performed. The concentration of phosphorus (P), total (tCa) and ionized calcium (Ca++), fibroblast growth factor 23 (FGF-23), 25(OH)D and PTH were assessed.Results: According to the DXA results, only 2 patients had osteoporosis, 10 (25.6%) patients had bone mineral density (BMD) values below 1.35 g /cm2 on the TCI scale. Treatment with empagliflozin for 12 weeks was lead to significant increase in FGF-23. Compared to the baseline level, there were no statistically significant differences in the concentrations of P, oCa, Ca++, PTH and 25(OH)D after 12 weeks of treatment. The level of FGF-23 did not correlate with the level of glomerular filtration rate either before or after treatment (r = 0.31, p = 0.27 and r = 0.39, p = 0.55, respectively). In addition, baseline BMD adjusted for TBS and baseline 25(OH)D did not correlate with Ca, F, FGF-23, and PTH concentrations (p>0.05).Conclusion: Thus, empagliflozin has increased the level of FGF-23 without significant changes in the concentration of phosphorus, calcium, 25 (OH) D, and PTH after 12 weeks of treatment in patients with T2DM and preserved renal function. The obtained data confirmed the necessity to assess the TBS in patients with T2DM, because it’s provide additional information on the quality of bone tissue.

scholarly journals Tumor-induced osteomalacia with the culprit lesion located in the palm: a case report

2019 ◽  
Vol 47 (5) ◽  
pp. 2240-2247
Author(s):  
Yanying Qian ◽  
Zhijuan Dai ◽  
Cong Zhu ◽  
Luya Ruan ◽  
Saroj Thapa ◽  
...  
Keyword(s):  
Fibroblast Growth Factor 23 ◽  
Elevated Serum ◽  
Serum Phosphorus ◽  
Postoperative Phase ◽  
Phosphorus Level ◽  
Serum Phosphorus Level ◽  
Mineral Density ◽  
Metacarpal Bones ◽  
The Right ◽  
Fgf 23

Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome. We herein report a rare case of TIO in a 58-year-old Chinese man who presented with a large lump in the right palm. Clinical, biochemical, and radiological assessments were performed. Laboratory examination showed severe hypophosphatemia, phosphaturia, an elevated serum alkaline phosphatase level, and an elevated serum fibroblast growth factor 23 (FGF-23) level. Dual-energy X-ray absorptiometry showed low bone mineral density. Magnetic resonance imaging revealed an irregular mass located in the right palm and abnormal findings in several metacarpal bones. During the operation, the surgeons found that the tumor had penetrated the surrounding muscles. The tumor had unique characteristics of local tissue invasion. The patient’s symptoms fully resolved and his serum phosphorus level normalized, although his serum FGF-23 level remained slightly high in the postoperative phase. Our findings suggest that in some patients with TIO, the serum phosphorus level might return to the normal range despite a relatively high postoperative serum FGF-23 level. These patients should be kept under close observation and regularly surveyed for any evidence of a residual tumor.

scholarly journals The Serum Level of Fibroblast Growth Factor-23 and Calcium-Phosphate Homeostasis in Obese Perimenopausal Women

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
M. Holecki ◽  
J. Chudek ◽  
A. Więcek ◽  
M. Titz-Bober ◽  
J. Duława
Keyword(s):  
Calcium Phosphate ◽  
Bone Turnover ◽  
Fibroblast Growth Factor 23 ◽  
Elevated Serum ◽  
Serum Phosphorus ◽  
Obese Women ◽  
Mineral Density ◽  
Phosphate Homeostasis ◽  
Hydroxyvitamin D ◽  
Fgf 23

Plasma FGF-23 concentrations and its relationship with calcium-phosphate homeostasis were evaluated in 48 perimenopausal obese women and in 29 nonobese controls. Serum parathyroid hormone, 25-hydroxyvitamin D3, CTX1, osteocalcin, total calcium, phosphorus, creatinine, and plasma intact FGF-23 concentrations were assessed. DXA of lumbar spine and femoral neck was performed to determine bone mineral density (BMD). Plasma iFGF-23 concentration was significantly higher in obese patients (by 42%) and correlated with age and BMD of proximal femur (R=-0.346;R=0.285, resp.) but not with markers of bone turnover. However, serum phosphorus level in obese subjects was significantly lower. iFGF-23 concentration correlated significantly with body mass index (R=0.292) and fat content (R=0.259) in all study subjects. Moreover, a significant correlation between iFGF-23 and iPTH (R=0.254) was found. No correlation between serum phosphorus or eGFR and plasma iFGF-23 and between eGFR and serum phosphorus was found. Elevated serum iFGF-23 concentration may partially explain lower phosphorus levels in the obese and seems not to reflect bone turnover.

scholarly journals Gender-Related Differences in Chronic Kidney Disease-Associated Vascular Calcification Risk and Potential Risk Mediators: A Scoping Review

Healthcare ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 979
Author(s):  
Patrick Yihong Wu ◽  
Szu-Ying Lee ◽  
Ke-Vin Chang ◽  
Chia-Ter Chao ◽  
Jenq-Wen Huang
Keyword(s):  
Chronic Kidney Disease ◽  
At Risk ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Large Scale ◽  
Fibroblast Growth Factor 23 ◽  
Vascular Wall ◽  
Matrix Gla Protein ◽  
Phenotypic Change ◽  
Fgf 23

Vascular calcification (VC) involves the deposition of calcium apatite in vascular intima or media. Individuals of advanced age, having diabetes mellitus or chronic kidney disease (CKD) are particularly at risk. The pathogenesis of CKD-associated VC evolves considerably. The core driver is the phenotypic change involving vascular wall constituent cells toward manifestations similar to that undergone by osteoblasts. Gender-related differences are observed regarding the expressions of osteogenesis-regulating effectors, and presumably the prevalence/risk of CKD-associated VC exhibits gender-related differences as well. Despite the wealth of data focusing on gender-related differences in the risk of atherosclerosis, few report whether gender modifies the risk of VC, especially CKD-associated cases. We systematically identified studies of CKD-associated VC or its regulators/modifiers reporting data about gender distributions, and extracted results from 167 articles. A significantly higher risk of CKD-associated VC was observed in males among the majority of original investigations. However, substantial heterogeneity exists, since multiple large-scale studies yielded neutral findings. Differences in gender-related VC risk may result from variations in VC assessment methods, the anatomical segments of interest, study sample size, and even the ethnic origins of participants. From a biological perspective, plausible mediators of gender-related VC differences include body composition discrepancies, alterations involving lipid profiles, inflammatory severity, diversities in matrix Gla protein (MGP), soluble Klotho, vitamin D, sclerostin, parathyroid hormone (PTH), fibroblast growth factor-23 (FGF-23), and osteoprotegerin levels. Based on our findings, it may be inappropriate to monotonously assume that male patients with CKD are at risk of VC compared to females, and we should consider more background in context before result interpretation.

scholarly journals Using Transgenic Mice to Explore the Effect of il-17rc Gene Knockout on Bone Metabolism

2021 ◽  
Author(s):  
Fan Yu ◽  
Bo Li ◽  
Guoliang Zhang ◽  
Song Zhou
Keyword(s):  
Transgenic Mice ◽  
Bone Metabolism ◽  
Gene Knockout ◽  
Control Group ◽  
Signal Pathways ◽  
Interleukin 17 ◽  
Micro Ct ◽  
Mineral Density ◽  
Trabecular Thickness ◽  
Significant Difference

Abstract ObjectiveTo investigate whether interleukin-17 receptor C (il-17rc) gene knockout leads to systemic osteoporosis in transgenic mice. MethodsThe immunohistochemistry and micro computed tomography (micro-CT) were used to analyze the condition of vertebral cancellous bone in 3-month healthy female wild-type C57BL/6 mice (control group) and il-17rc gene knockout C57BL/6 mice (experimental group). ResultsWild type C57BL/6 mice had higher bone density per unit volume (0.52 ± 0.12 vs. 0.47 ± 0.05, P = 0.028) (g/cm3), more trabecular connections (8.97 ± 1.46 vs. 5.59 ± 3.15, P = 0.017) (1/mm), thicker trabecular thickness (0.16 ± 0.08 vs. 0.10 ± 0.04, P = 0.029) (1/mm) and the number of trabeculae was more (5.01 ± 0.33 vs. 3.16 ± 0.37, P = 0.038) (1/mm) than mut-il-17rc mice. In addition, the results of micro-CT also showed that the osteoporosis of il-17rc gene knockout C57BL/6 mice was mainly manifested in T13 (P = 0.039), L1 (P = 0.035), L3 (P = 0.018), L5 (P = 0.021) and L6 (P = 0.036), but the mean bone mineral density between L2 (P = 0.317) and L4 (P = 0.242) was no significant difference between the two groups. ConclusionIL-17/il-17rs signal axis is widely distributed in the animal skeletal system and is one of the important signal pathways regulating bone metabolism. Knockout of il-17rc gene can lead to the occurrence of osteoporosis in model animals.

scholarly journals Phosphate and Cardiovascular Disease beyond Chronic Kidney Disease and Vascular Calcification

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Sinee Disthabanchong
Keyword(s):  
Vascular Calcification ◽  
Early Stage ◽  
Subclinical Atherosclerosis ◽  
Fibroblast Growth Factor 23 ◽  
Left Ventricular ◽  
Normal Serum ◽  
Serum Phosphate ◽  
Calciprotein Particles ◽  
Habitual Intake ◽  
Fgf 23

Phosphate is essential for life but its accumulation can be detrimental. In end-stage renal disease, widespread vascular calcification occurs as a result of chronic phosphate load. The accumulation of phosphate is likely to occur long before the rise in serum phosphate above the normal range since several observational studies in both general population and early-stage CKD patients have identified the relationship between high-normal serum phosphate and adverse cardiovascular outcomes. Consumption of food high in phosphate increases both fasting and postprandial serum phosphate and habitual intake of high phosphate diet is associated with aging, cardiac hypertrophy, endothelial dysfunction, and subclinical atherosclerosis. The decline in renal function and dietary phosphate load can increase circulating fibroblast growth factor-23 (FGF-23) which may have a direct impact on cardiomyocytes. Increased FGF-23 levels in both CKD and general populations are associated with left ventricular hypertrophy, congestive heart failure, atrial fibrillation, and mortality. Increased extracellular phosphate directly affects endothelial cells causing cell apoptosis and vascular smooth muscle cells (VSMCs) causing transformation to osteogenic phenotype. Excess of calcium and phosphate in the circulation can promote the formation of protein-mineral complex called calciprotein particles (CPPs). In CKD, these CPPs contain less calcification inhibitors, induce inflammation, and promote VSMC calcification.

scholarly journals P1098THE CHANGE OF PLASMA SCLEROSTIN AND OTHER BIOMARKERS IN HEMODIALYTIC PATIENTS USING DIALYZER WITH MEDIUM CUT-OFF MEMBRANE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Jong Hwan Jung ◽  
Seon-Ho Ahn ◽  
Ju Hung Song
Keyword(s):  
Molecular Weight ◽  
Vascular Calcification ◽  
Plasma Levels ◽  
Cardiovascular Complications ◽  
Uremic Toxins ◽  
Control Group ◽  
High Flux ◽  
Middle Molecules ◽  
Significant Difference ◽  
Fgf 23

Abstract Background and Aims Protein-bound toxins and uremic toxins with middle molecular weight usually develop uremic symptoms in patients with advanced chronic kidney disease (CKD) or end-stage renal disease (ESRD). Although the effect on uremic toxicity of the molecules is not proven yet, middle molecules or larger middle molecules is regarded with important substance concerning of development of uremic symptoms and cardiovascular complication, particularly in CKD patients. Hemodialysis (HD) or hemodiafiltration (HDF) using dialyzer with high flux membrane provided improved clearance for uremic toxins with middle molecular weights. However, uremic toxins with larger middle molecular weight could not be easily removed through above methods. Medium cut-off (MCO) membrane can remove larger middle molecules which can be not removed through high flux membrane and HDF. From this perspective, chronic use of MCO membrane lowering the plasma concentration of larger middle molecules associated with cardiovascular complications including vascular calcification may give beneficial effect, particularly in patients with ESRD. Method Twenty-five patients undergoing chronic hemodialysis were prospectively analyzed for 6 months. We randomly divided enrolled patients into two groups: control group and MCO group. Patients in the control group used dialyzer with high flux membrane and patients in MCO group used dialyzer with MCO membrane. The enrolled patients performed hemodialysis thrice a week during 6 months. We measured plasma levels of several biomarkers at baseline and 3-month and 6-month through the multiplexing using Luminex® technology. In this prospective study, we performed comparative analysis with larger middle molecules, such as CXCL16, sclerostin, and FGF-23, in both groups. Results The plasma levels of all biomarkers at baseline did not show significant difference between two groups (CXCL16: p =0.904, Sclerostin: p =0.322, FGF-23: p =0.065, respectively). However, plasma sclerostin levels at 3-month and 6-month were significantly lower in MCO group (p = 0.060, p &lt;0.005, respectively). In addition, even after analysis of covariance through ANCOVA analysis, plasma sclerostin levels at 3-month and 6-month were significantly lower in MCO group compared with the control group (p = 0.042, p =0.001, respectively). But, there was no a significant decrease of plasma sclerostin levels according to time, particularly in MCO group (p = 0.157, p =0.412, respectively) (Figure 1). Conclusion This study showed the 6-month outcome for changes of the plasma levels of larger middle molecules, including CXCL16, sclerostin, and FGF-23, particularly in dialytic patients using dialyzer with MCO membrane. Plasma sclerostin associated with vascular calcification showed decreasing tendency during 6 months after application of MCO membrane, but, there was no statistical significance. However, plasma levels of sclerostin were significantly lower in dialytic patients using MCO membrane than those using high flux membrane at 3 and 6 months, respectively. Therefore, hemodialysis using dialyzer with MCO membrane may be an option to attenuate cardiovascular complications in ESRD patients.

scholarly journals Gla-Rich Protein (GRP) as an Early and Novel Marker of Vascular Calcification and Kidney Dysfunction in Diabetic Patients with CKD: A Pilot Cross-Sectional Study

2020 ◽  
Vol 9 (3) ◽  
pp. 635 ◽  
Author(s):  
Ana P. Silva ◽  
Carla S.B. Viegas ◽  
Filipa Mendes ◽  
Ana Macedo ◽  
Patrícia Guilherme ◽  
...  
Keyword(s):  
Vascular Calcification ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Positive Association ◽  
Serum Levels ◽  
Diabetic Patients ◽  
Mineral And Bone Disorder ◽  
Cross Sectional ◽  
Low Levels ◽  
Fgf 23

Vascular calcification (VC) is one of the strongest predictors of cardiovascular risk in chronic kidney disease (CKD) patients. New diagnostic/prognostic tools are required for early detection of VC allowing interventional strategies. Gla-rich protein (GRP) is a cardiovascular calcification inhibitor, whose clinical utility is here highlighted. The present study explores, for the first time, correlations between levels of GRP in serum with CKD developmental stage, mineral metabolism markers, VC and pulse pressure (PP), in a cohort of 80 diabetic patients with mild to moderate CKD (stages 2–4). Spearman’s correlation analysis revealed a positive association of GRP serum levels with estimated glomerular filtration rate (eGFR) and α-Klotho, while a negative correlation with phosphate (P), fibroblast growth factor 23 (FGF-23), vascular calcification score (VCS), PP, calcium (x) phosphate (CaxP) and interleukin 6 (IL-6). Serum GRP levels were found to progressively decrease from stage 2 to stage 4 CKD. Multivariate analysis identified low levels of eGFR and GRP, and high levels of FGF-23 associated with both the VCS and PP. These results indicate an association between GRP, renal dysfunction and CKD-mineral and bone disorder. The relationship between low levels of GRP and vascular calcifications suggests a future, potential utility for GRP as an early marker of vascular damage in CKD.

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