Treatment with Cinacalcet in Hemodialysis Patients with Severe Secondary Hyperparathyroidism, Influences Bone Mineral Metabolism and Anemia Parameters

2020 ◽  
Vol 15 (3) ◽  
pp. 249-263
Author(s):  
Maria Aktsiali ◽  
Theodora Papachrysanthou ◽  
Ioannis Griveas ◽  
Christos Andriopoulos ◽  
Panagiotis Sitaras ◽  
...  
Keyword(s):  
Bone Mineral ◽  
Mineral Metabolism ◽  
Treatment Options ◽  
Dry Weight ◽  
Chronic Hemodialysis ◽  
Protective Agent ◽  
Positive Correlation ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Background: Due to the premium rate of Chronic Kidney Disease, we have increased our knowledge with respect to diagnosis and treatment of Bone Mineral Disease (BMD) in End- Stage Renal Disease (ESRD). Currently, various treatment options are available. The medication used for Secondary Hyper-Parathyroidism gives promising results in the regulation of Ca, P and Parathormone levels, improving the quality of life. The aim of the present study was to investigate the relation of cinacalcet administration to not only parathormone, Ca and P but also to anemia parameters such as hematocrit and hemoglobin. Materials and Methods: retrospective observational study was conducted in a Chronic Hemodialysis Unit. One-hundred ESRD patients were recruited for twenty-four months and were evaluated on a monthly rate. Biochemical parameters were related to medication prescribed and the prognostic value was estimated. Cinacalcet was administered to 43 out of 100 patients in a dose of 30-120 mg. Results: Significant differences were observed in PTH, Ca and P levels with respect to Cinacalcet administration. Ca levels appeared to be higher at 30mg as compared to 60mg cinacalcet. Furthermore, a decreasing age-dependent pattern was observed with respect to cinacalcet dosage. A positive correlation was observed between Dry Weight (DW) and cinacalcet dose. Finally, a positive correlation between Hematocrit and Hemoglobin and cinacalcet was manifested. Conclusions: Cinacalcet, is a potential cardiovascular and bone protective agent, which is approved for use in ESRD patients to assist SHPT. A novel information was obtained from this study, regarding the improvement of the control of anemia.

scholarly journals Serum Lipid Profile Constituents as Markers of Cardiovascular Morbidity in Patients on Chronic Hemodialysis

2006 ◽  
Vol 1 ◽  
pp. 117727190600100
Author(s):  
Dimitrios Kirmizis ◽  
Evangelia Koutoupa ◽  
Apostolos Tsiandoulas ◽  
Aphroditi Valtopoulou ◽  
Georgios Niavis ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Case Control Study ◽  
Case Control ◽  
Chronic Hemodialysis ◽  
Cardiovascular Morbidity ◽  
Confounding Effect ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients ◽  
Control Study

We designed the present case-control study in order to examine the validity of apolipoprotein (apo) A-I, B, apoB/apoA-I ratio and Lp(a) as alternative markers of cardiovascular morbidity in end-stage renal disease (ESRD) patients undergoing chronic hemodialysis (HD). Twenty-five HD patients (18 males, mean age 63, range 52–69 years) comprised the group with prevalent cardiovascular disease (CVD) and 50 HD patients (35 males, mean age 62, range 40–77 years) with non evident cardiovascular disease history constituted the second study group. Patients with CVD had significantly higher concentrations of serum apoB, apoB/apoA-I ratio and Lp(a), and lower levels of apoA-I compared to patients without incident CVD. All three parameters studied were correlated with cardiovascular morbidity, i.e. apoA-I negatively and apoB and apoB/apoA-I ratio positively (r = −0.6, P < 0.05; r = 0.659, P < 0.01; and r = 0.614, P < 0.01, respectively). Furthermore, logCRP exhibited as well a significant positive correlation with cardiovascular morbidity (r = 0.704, P < 0.001), not this being the case for Lp(a) which was not found to exhibit such a correlation (r = 0.05, P = NS). Among them, apoB and apoB/apoA-I ratio exhibited the characteristics most coherent to CVD. The age- and sex-adjusted OR for the presence of CVD was 2.3 and 2.0, respectively, which remained independent of any confounding effect of inflammation. In conclusion, serum apoB levels and apoB/apoA-I ratio exhibit characteristics of credible independent markers of in HD patients.

Arrested Bone Growth and Mineral Maturation in Sub-Totally Nephrectomized Rats

1977 ◽  
Vol 53 (5) ◽  
pp. 479-484
Author(s):  
J. M. Letteri ◽  
R. M. Biltz ◽  
K. J. Ellis ◽  
A. Martino ◽  
S. Yasumura ◽  
...  
Keyword(s):  
Renal Failure ◽  
Bone Mineral ◽  
Bone Growth ◽  
Matched Control ◽  
Mineral Metabolism ◽  
Essential Feature ◽  
Renal Bone Disease ◽  
Maturation Defect ◽  
Stage Renal Disease ◽  
End Stage

1. Young, sub-totally nephrectomized rats were used to study the altered mineral metabolism of renal failure and its effects on bone growth and mineral maturation. 2. Rats killed at 4 weeks after sub-total nephrectomy demonstrated less bone growth than the age-matched control animals. These differences diminished in successive 4 week periods and were not significant at 12 weeks after operation. 3. The major differences in bone mineral composition between the uraemic rats and the control rats were: (i) lower CO23;− concentrations, and (ii) higher PO34;− and HPO24;− concentrations. 4. These differences are consistent with the view that bone mineral matures by the conversion of an acidic calcium phosphate precursor into a carbonate-containing apatite, an essential feature of this conversion being the replacement of PO34;− or HPO24;− by CO23;−. By this definition, uraemic rats at 4 weeks after operation contained more immature bone mineral than the control rats. These differences corresponded to the changes in bone weight, and were similarly unaffected at 12 weeks after operation. 5. The effects observed were transient and were reversed as renal function recovered. If renal failure is sustained, however, as in patients with end-stage renal disease, the maturation defect could become a feature of renal bone disease. Specific aetiological factors are discussed, but not identified.

scholarly journals Platelet Activation in End-Stage Renal Disease Is Mediated By Extracellular Nucleosomes That Originate from White Blood Cells

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 4909-4909
Author(s):  
Trung Phan ◽  
McMillan Ryan ◽  
Leonidas Skiadopoulos ◽  
Amanda Walborn ◽  
Debra Hoppensteadt ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Activation ◽  
Blood Cells ◽  
White Blood Cells ◽  
Positive Correlation ◽  
Cell Counts ◽  
Wbc Count ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Abstract Introduction Extracellular nucleosomes in plasma (PNs) are complexes of DNA and histones that are released during cell death and inflammatory responses. End-stage renal disease (ESRD) represents a complex syndrome where inflammation, endothelial dysfunction, and hemostatic aberrations contribute to the observed vascular manifestations. The purpose of this investigation is to profile PNs in patients with ESRD and to demonstrate their relevance to blood cells and platelet activation products. Methods Pre-dialysis plasma samples from patients undergoing maintenance hemodialysis (n = 90) at Loyola University outpatient dialysis unit were collected under an approved IRB protocol. Plasma samples from healthy individuals (n = 50) were purchased from a biobank as a control (George King Biomedical, Overland Park, Kansas). Complete blood count profiles, including white blood cells (WBCs), red blood cells (RBCs), and platelets were obtained from the patients' medical records. The levels of PNs in ESRD patients and healthy volunteers were measured using the Cell Death Detection ELISA PLUS assay (Roche Diagnostics, Mannheim, Germany). MP-TF levels were measured using the Zymuphen MP-TF kit (Hyphen BioMed, Neuville-sur-Oise, France). PDGF levels were measured using the Human PDGF-BB Quantikine ELISA Kit (R&D Systems, Minneapolis, Minnesota). Human PF4 levels were measured using the Zymutest PF4 ELISA Kit (Hyphen BioMed, Neuville-sur-Oise, France). All individual results were tabulated and analyzed using the statistical software GraphPad Prism 7. The Mann-Whitney test for non-parametric data was utilized in comparing ESRD to control groups. PN levels were correlated with cell counts and platelet activation factors using the non-parametric Spearman correlation. Individual cell counts were also correlated with platelet activating factors using the same method. Results In the ESRD patients, the average hematocrit was 31.7 ± 4.4 %, the average WBC count was 6.5 ± 4.0 K/uL, and the average platelet count was 179.4 ± 66.3 K/uL. The levels of PNs in the ESRD patients (15.5 ± 14.1 Arbitrary Units (AU)) were markedly higher in comparison to that of the controls (6.74 ± 13.7 AU; p < 0.0001). Similarly, MP-TF levels were significantly elevated in ESRD patients (3.00 ± 1.42 pg/mL) compared to normal (0.363 ± 0.263 pg/mL; p < 0.0001). PF4 levels were also significantly elevated in ESRD patients (95.3 ± 35.3 ng/mL) compared to normal (27.4 ± 19.8 ng/mL; p < 0.0001). While PDGF levels were higher in the ESRD group (116.0 ± 172.5 pg/mL) in comparison to the controls (82.7 ± 113.5 pg/mL), this increase was not statistically significant (p = 0.405). A positive correlation was observed between PNs and WBCs (p = 0.024; r = 0.244). PN levels did not show a correlation with RBC (p = 0.448; r = 0.083) and platelet levels (p = 0.545; r = 0.066). Furthermore, there was no correlation between PNs and MP-TF (p = 0.501; r = 0.077), PDGF (p = 0.314; r = 0.110) and PF4 (p = 0.524; r = -0.070) in the ESRD patients. However, the platelet count showed a positive correlation with PDGF (p = 0.044; r = 0.218) and MP-TF (p = 0.042; r = 0.237). Similarly, the WBC count showed a positive correlation with the platelet count (p < 0.0001; r = 0.476) and PDGF (p = 0.016; r = 0.260). Conclusion This study clearly demonstrates that extracellular nucleosomes are elevated in the plasma of patients with ESRD. The fact that the PN levels correlated with the number of circulating white blood cells suggest that the PNs originate from these cells. Since the ESRD patients exhibited platelet activation, as evident by the observed increase in PDGF, MP-TF and PF4, it is plausible that this activation is mediated by PNs originating from the WBCs. As observed by the positive correlation between WBCs, PDGF, and platelet count, this study underscores the potential role of nucleosomes originating from WBCs in the activation of platelets. These results are consistent with previously reported observations that extracellular histones can induce platelet activation in a TLR2 and TLR4 dependent manner (http://www.ncbi.nlm.nih.gov/pubmed/21673343). Disclosures No relevant conflicts of interest to declare.

scholarly journals Plasma Calcium Concentration Modifies the Blood Sodium During Hemodialysis: Lessons from Hard Water Syndrome

2017 ◽  
Vol 15 (1) ◽  
pp. 29-32
Author(s):  
Davide Viggiano ◽  
Pietro Anastasio
Keyword(s):  
Hard Water ◽  
Chronic Hemodialysis ◽  
Hormonal Control ◽  
Water Control ◽  
Plasma Calcium Concentration ◽  
Acute Changes ◽  
Stage Renal Disease ◽  
End Stage ◽  
Na Release ◽  
Esrd Patients

AbstractIntroduction. Extracellular sodium (Na+) concentration is maintained within a tight physiological range due to hormonal control, that mainly modulates thirst, Na+ and water renal excretion. Extra-renal regulation of Na+ and water homeostasis is only partially understood. Recently it has been debated whether the osmotically inactive Na+ storage is fixed or variable. Methods. In the present study, fourteen End-Stage Renal Disease (ESRD) patients treated by chronic hemodialysis underwent by accident to a sharp increase in plasmatic calcium (Ca+2) levels due to the failure of the water control system, leading to the so-called hard water syndrome. The levels of plasmatic Ca+2 after 1 hr of hemodialysis were correlated with urea, Na+, potassium (K+) and creatinine levels. Eleven ESRD patients treated with hemodialysis under similar conditions were used as controls. Results. The hard water syndrome resulted in hypercalcemia, while mean plasma levels of Na+, K+ and urea were not different compared to controls. Plasma creatinine levels were slightly but significantly higher that control. A correlation analysis on the measured variables has showed a positive correlation between plasma Ca+2 and Na+ levels (Pearson=0.428, p=0.032), and the absence of any correlation with K+, creatinine and urea concentration. Conclusions. Our study suggests that acute changes in plasmatic Ca+2 levels may affect Na+ concentration in the absence of renal function; it is possible that hypercalcemia may trigger Na+ release from the osmotically inactive storage. These data further support previous observations on the interplay of sodium and calcium at extrarenal sites.

scholarly journals Bone mineral density in Palestinian patients with end-stage renal disease and the related clinical and biochemical factors: Cross-sectional study

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0241201
Author(s):  
Zaher Nazzal ◽  
Shahd Khader ◽  
Hiba Zawyani ◽  
Mazen Abdallah ◽  
Osama Sawalmeh ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Mineral ◽  
End Stage Renal Disease ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Mineral Density ◽  
Cross Sectional ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Introduction End-Stage Renal Disease (ESRD) is the ultimate result of chronic kidney disease (CKD). In Palestine, the prevalence of ESRD was 240.3 PMP which is comparable with the nearby countries. Accelerated bone loss among ESRD patients is attributed to abnormal bone turn over that leads to osteoporosis and osteopenia. The risk of fractures is increased four-fold in men and women on hemodialysis, which explains the importance of assessing the bone mineral density among these population. The goals of this study were to find the prevalence of osteoporosis in ESRD patients as determined by bone mineral density (BMD) at different sites and to determine whether BMD correlates with many other clinical parameters. Methods A cross-sectional study of 194 ESRD patients were recruited from the dialysis unit in An-Najah National University Hospital, Nablus, Palestine. The patients were on regular hemodialysis or peritoneal dialysis. BMD was measured at the lumbar spine and the hip using the dual-energy X-Ray absorptiometry (DEXA) and the value is expressed as T-score. The data were analyzed using SPSS, version 26. The relationship between BMD and the clinical and biochemical parameters among the ESRD patients was assessed. Results We found that 42.8% of ESRD patient had osteoporosis and 40.2% had osteopenia. There were significantly higher proportions of osteoporosis and osteopenia among patients >60 years of age (p<0.005). Patients with osteoporosis and osteopenia had significantly higher serum levels of PTH (792.9 and 469.7) (p<0.05). BMD decreases as the duration of dialysis (39.0 months Vs. 56.8 months), (p<0.05). We found no significant difference between patients on hemodialysis or peritoneal dialysis. Conclusion This study showed that Palestinian patients with ESRD have low BMD at the hip and spine. The observed high serum level of PTH was associated with low BMD. Those patients should be closely monitored especially those with more than one risk factor. Moreover, more attention should be paid for these category of patients to decrease the incidence of falling down and the resulting fractures that might lead to mortality and morbidity.

scholarly journals Frailty severity is significantly associated with electrocardiographic QRS duration in chronic dialysis patients

PeerJ ◽  
2015 ◽  
Vol 3 ◽  
pp. e1354 ◽  
Author(s):  
Chia-Ter Chao ◽  
Jenq-Wen Huang
Keyword(s):  
Regression Analysis ◽  
Chronic Hemodialysis ◽  
Self Report ◽  
Qtc Interval ◽  
Dialysis Patients ◽  
Increased Risk ◽  
Qrs Duration ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

End-stage renal disease (ESRD) patients are at increased risk of sudden cardiac death, the risk of which is presumably related to arrhythmia. Electrocardiographic (ECG) parameters have been found to correlate with arrhythmia and predict cardiovascular outcomes in ESRD patients. Frailty is also a common feature in this population. We investigate whether the severity of dialysis frailty is associated with ECG findings, including PR interval, QRS duration, and QTc interval. Presence and severity of frailty was ascertained using six different self-report questionnaires with proven construct validity. Correlation analysis between frailty severity and ECG was made, and those with significant association entered into multiple regression analysis for confirmation. Among a cohort of chronic hemodialysis patients, we found that frailty severity, assessed by the Edmonton frailty scale, is significantly associated with QRS duration (r= − 0.3,p< 0.05). Dialysis patients with QRS longer than 120 ms had significantly lower severity of frailty than those with QRS less than 120 ms (p= 0.01 for the Edmonton frailty scale and 0.05 for simple FRAIL scale). Regression analysis showed that frailty severity, assessed by the Edmonton frailty scale and simple FRAIL scale, was significantly associated with QRS duration independent of serum electrolyte levels. In conclusion, a significant relationship exists between the severity of frailty and QRS duration in ESRD patients. This might be an under-recognized link between frailty and its adverse cardiovascular impact in these patients.

scholarly journals A Review of Sevelamer Hydrochloride in End-Stage Renal Disease Patients on Dialysis

2011 ◽  
Vol 3 ◽  
pp. CMT.S5990 ◽  
Author(s):  
Goce Spasovski
Keyword(s):  
Mineral Metabolism ◽  
Treatment Options ◽  
Phosphate Removal ◽  
Phosphate Binders ◽  
Systemic Complication ◽  
Clinical Scenarios ◽  
Main Culprit ◽  
Calcium Phosphorus ◽  
Stage Renal Disease ◽  
End Stage

It is known that in the presence of even subtle kidney dysfunction an intensive prevention of cardiovascular risk is required. Apart from the conventional factors which contribute to cardiovascular disease (CVD), there are also some specific conditions of the chronic kidney disease (CKD) population such as oxidative stress of uremia and dialysis (D). However, hyperphosphatemia, hypercalcemia, and elevated calcium-phosphorus product remain as major contributors to the development of vascular calcification (VC) in this population, as part of the systemic complication known as mineral and bone disorders (MBD) in CKD patients. Importantly, the retention of phosphate remains as main culprit in the pathogenesis of CKD–-MBD. Over the years, various treatment options for phosphate removal and controlling mineral metabolism, bone health, VC and CVD have failed, mainly through an over-suppression of PTH, development of ABD and promotion of VC and mortality. Although KDOQI and KDIGO published CKD–-MBD guidelines has clearly stated where calcium-based phosphate binders should not be used in D patients (hypercalcemia and low PTH) and where non calcium-containing phosphate binders are preferred (patients with severe vascular and/or other soft tissue calcifications), the greatest controversy and disagreements within the nephrological community still exists upon the cost-effectiveness of non calcium binder (sevelamer) use. Indeed, despite the evidence and recognised trend towards both a decrease in VC and CVD associated with sevelamer use, it is still an ongoing matter of debate. The magnitude of this controversy is increased when the issue of advanced medical and/or budgetary evaluation related to the implementation of clinical guidelines for CKD–-MBD treatment is considered. Despite advocated use of sevelamer across a range of common clinical scenarios in CKD, its widespread utilization is challenged as exceeding what would usually be considered good value for money. If so, it is questionable whether the recommendations and suggestions from the guidelines should be followed, and further, do we need guidelines and innovative drugs for treatment of hyperphosphatemia? While awaiting the answer, as clinicians we should proceed with a treatment to “do no harm”, trying to at least limit the calcium exposure of our dialysis patients.

scholarly journals Bone mineral density and mortality in end-stage renal disease patients

2020 ◽  
Vol 13 (3) ◽  
pp. 307-321 ◽  
Author(s):  
Ken Iseri ◽  
Lu Dai ◽  
Zhimin Chen ◽  
Abdul Rashid Qureshi ◽  
Torkel B Brismar ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Renal Disease ◽  
Cortical Bone ◽  
Vascular Calcification ◽  
Bone Mineral ◽  
End Stage Renal Disease ◽  
Mineral Density ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Abstract Osteoporosis characterized by low bone mineral density (BMD) as assessed by dual-energy X-ray absorptiometry (DXA) is common among end-stage renal disease (ESRD) patients and associates with high fracture incidence and high all-cause mortality. This is because chronic kidney disease-mineral bone disorders (CKD-MBDs) promote not only bone disease (osteoporosis and renal dystrophy) but also vascular calcification and cardiovascular disease. The disturbed bone metabolism in ESRD leads to ‘loss of cortical bone’ with increased cortical porosity and thinning of cortical bone rather than to loss of trabecular bone. Low BMD, especially at cortical-rich bone sites, is closely linked to CKD-MBD, vascular calcification and poor cardiovascular outcomes. These effects appear to be largely mediated by shared mechanistic pathways via the ‘bone–vascular axis’ through which impaired bone status associates with changes in the vascular wall. Thus, bone is more than just the scaffolding that holds the body together and protects organs from external forces but is—in addition to its physical supportive function—also an active endocrine organ that interacts with the vasculature by paracrine and endocrine factors through pathways including Wnt signalling, osteoprotegerin (OPG)/receptor activator of nuclear factor-κB (RANK)/RANK ligand system and the Galectin-3/receptor of advanced glycation end products axis. The insight that osteogenesis and vascular calcification share many similarities—and the knowledge that vascular calcification is a cell-mediated active rather than a passive mineralization process—suggest that low BMD and vascular calcification (‘vascular ossification’) to a large extent represent two sides of the same coin. Here, we briefly review changes of BMD in ESRD as observed using different DXA methods (central and whole-body DXA) at different bone sites for BMD measurements, and summarize recent knowledge regarding the relationships between ‘low BMD’ and ‘fracture incidence, vascular calcification and increased mortality’ in ESRD patients, as well as potential ‘molecular mechanisms’ underlying these associations.

scholarly journals Lower Gastrointestinal Bleeding in Chronic Hemodialysis Patients

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Fahad Saeed ◽  
Nikhil Agrawal ◽  
Eugene Greenberg ◽  
Jean L. Holley
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Gastrointestinal Bleeding ◽  
Chronic Hemodialysis ◽  
Lower Gastrointestinal Bleeding ◽  
Gi Bleeding ◽  
Common Causes ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Gastrointestinal (GI) bleeding is more common in patients with chronic kidney disease and is associated with higher mortality than in the general population. Blood losses in this patient population can be quite severe at times and it is important to differentiate anemia of chronic diseases from anemia due to GI bleeding. We review the literature on common causes of lower gastrointestinal bleeding (LGI) in chronic kidney disease (CKD) and end-stage renal disease (ESRD) patients. We suggest an approach to diagnosis and management of this problem.

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