scholarly journals Plasma Exosomes Derived From Patients With End-Stage Renal Disease and Renal Transplant Recipients Have Different Effects on Vascular Calcification

2021 ◽  
Vol 8 ◽  
Author(s):  
Xiao Lin ◽  
Ting Zhu ◽  
Feng Xu ◽  
Jia-Yu Zhong ◽  
Fuxingzi Li ◽  
...  
Keyword(s):  
Vascular Calcification ◽  
End Stage Renal Disease ◽  
Annexin A2 ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Fetuin A ◽  
Calcification Inhibitors ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

End-stage renal disease (ESRD) patients usually develop extensive and progressive vascular calcification, and lots of calcification inhibitors as well as procalcifying factors are involved in the process. However, the mechanisms of vascular calcification in ESRD patients are still ill-defined. In the present study, we found that the plasma exosomes derived from ESRD patients (ESRD-Ex) promoted calcification of vascular smooth muscle cells (VSMCs) significantly, while plasma exosomes from renal transplant recipients (RTR-Ex) could partially attenuate VSMCs calcification. Moreover, the protein concentration of ESRD-Ex was significantly higher than plasma exosomes from the normal health control group (Nor-Ex) and RTR-Ex, and the content of both matrix gla protein (MGP) and Fetuin-A, the calcification inhibitors, were prominently lower in ESRD-Ex than those in Nor-Ex. The content of Annexin-A2, one of the calcification promoters, was significantly higher in ESRD-Ex and RTR-Ex than that in Nor-Ex. However, bone morphogenetic protein (BMP-2) and receptor activator for nuclear factor-κB ligand (Rankl) had no significant difference among the three groups. In addition, the content of Fetuin-A in RTR-Ex was higher than that in ESRD-Ex, although it was still lower than that in Nor-Ex. Furthermore, the levels of both Fetuin-A and MGP in plasma exosomes were negatively while the levels of Annexin-A2 in plasma exosomes was positively correlated to coronary artery calcification scores (CACS). These results indicated that ESRD-Ex significantly promoted VSMCs calcification, while renal transplantation could partially attenuate the procalcification effect of exosomes. Fetuin-A and MGP were decreased, but Annexin-A2 was increased in ESRD-Ex, and renal transplantation could increase the level of Fetuin-A rather than MGP.

scholarly journals Plasma exosomes derived from patients with end-stage renal disease and renal transplant recipients have different effects on vascular calcification

2020 ◽  
Author(s):  
xiao lin ◽  
Ting Zhu ◽  
Feng Xu ◽  
Jia-Yu Zhong ◽  
Fuxingzi Li ◽  
...  
Keyword(s):  
Vascular Calcification ◽  
End Stage Renal Disease ◽  
Annexin A2 ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Fetuin A ◽  
Calcification Inhibitors ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Abstract Background End-stage renal disease (ESRD) patients usually develop extensive and progressive vascular calcification, and lots of calcification inhibitors as well as pro-calcifying factors are involved in the process. However, the mechanisms of vascular calcification in ESRD patients are still ill-defined. Methods The participants in the study were selected at the Second Xiangya Hospital, Central South University, and the plasma exosomes derived from ESRD patients (ESRD-Ex), renal transplant recipients (RTR-Ex), and the normal health control group (Nor-Ex) were isolated by ExoQuick-TC kit. Transmission electron microscopy and molecular size analysis were used to assess the morphology and size of exosomes. Alizarin Red S staining was carried out to detect calcification of vascular smooth muscle cells (VSMCs). Protein levels of Fetuin-A, matrix gla protein (MGP), Annexin-A2, bone morphogenetic protein (BMP-2), and receptor activator for nuclear factor-κ B ligand (Rankl) were measured by Western Blot analysis and the contents of that were detected using ELISA. Coronary artery calcification scores (CACS) were quantified via Agaston and analysed by Siemens CaScoring software. Results Compared with Nor-Ex, the ESRD-Ex promoted calcification of VSMCs significantly, and RTR-Ex could attenuate VSMCs calcification. Moreover, the protein concentration of ESRD-Ex was significantly higher than Nor-Ex and RTR-Ex, and the content of both MGP and Fetuin-A, the calcification inhibitors, were prominently lower in ESRD-Ex than those in Nor-Ex. The content of Annexin-A2, one of the calcification promoters, was significantly higher in ESRD-Ex and RTR-Ex than that in Nor-Ex. But, BMP-2 and Rankl had no significant difference among the three groups. In addition, the content of Fetuin-A in RTR-Ex was higher than that in ESRD-Ex, though it was still lower than in Nor-Ex. Furthermore, the content of both plasma Fetuin-A and MGP were negatively while that of Annexin-A2 was negatively correlated to CACS. Conclusions These results indicated that ESRD-Ex significantly promoted VSMCs calcification while renal transplantation could partially attenuate the effect of exosomes. Fetuin-A and MGP were decreased but Annexin-A2 was increased in ESRD-Ex, and renal transplantation could increase the level of Fetuin-A rather than MGP.

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 One-Year Mortality Rates in US Children with End-Stage Renal Disease

2015 ◽  
Vol 41 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Blanche M. Chavers ◽  
Julia T. Molony ◽  
Craig A. Solid ◽  
Michelle N. Rheault ◽  
Allan J. Collins
Keyword(s):  
Peritoneal Dialysis ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Mortality Rates ◽  
Transplant Recipients ◽  
Dialysis Patients ◽  
One Year ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Background/Aims: Few published data describe survival rates for pediatric end-stage renal disease (ESRD) patients. We aimed to describe one-year mortality rates for US pediatric ESRD patients over a 15-year period. Methods: In this retrospective cohort study, we used the US Renal Data System database to identify period-prevalent cohorts of patients aged younger than 19 for each year during the period 1995-2010. Yearly cohorts averaged approximately 1,200 maintenance dialysis patients (60% hemodialysis, 40% peritoneal dialysis) and 1,100 transplant recipients. Patients were followed for up to 1 year and censored at change in modality, loss to follow-up, or death. We calculated the unadjusted model-based mortality rates per time at risk, within each cohort year, by treatment modality (hemodialysis, peritoneal dialysis, transplant) and patient characteristics; percentage of deaths by cause; and overall adjusted odds of mortality by characteristics and modality. Results: Approximately 50% of patients were in the age group 15-18, 55% were male, and 45% were female. The most common causes of ESRD were congenital/reflux/obstructive causes (55%) and glomerulonephritis (30%). One-year mortality rates showed evidence of a decrease in the number of peritoneal dialysis patients (6.03 per 100 patient-years, 1995; 2.43, 2010; p = 0.0263). Mortality rates for transplant recipients (average 0.68 per 100 patient-years) were consistently lower than the rates for all dialysis patients (average 4.36 per 100 patient-years). Conclusions: One-year mortality rates differ by treatment modality in pediatric ESRD patients.

P1732RECURRENCE OF GLOMERULONEPHRITIS POST TRANSPLANT

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Umesh Lingaraj ◽  
Ricken Mehta ◽  
Shivaprasad SM ◽  
Kishan A ◽  
Leelavathi V ◽  
...  
Keyword(s):  
Kidney Transplantation ◽  
Renal Disease ◽  
Kidney Transplant ◽  
End Stage Renal Disease ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Kidney Transplant Recipients ◽  
Post Transplant ◽  
Stage Renal Disease ◽  
End Stage

Abstract Background and Aims Glomerulonephritis (GN) is a major cause of end stage renal disease (ESRD)1. It represents the primary cause of end stage renal disease (ESRD) for 25% of the dialysis population1 and 45% of the transplant population. For patients with GN requiring renal replacement therapy, kidney transplantation is associated with superior outcomes compared with dialysis2. The possibility of recurrence of the original disease after transplantation was described in a seminal paper more than 40 years ago, and it is now clear that all forms of GN may recur after kidney transplantation.3 To study the recurrence of glomerulonephritis post-transplant in a tertiary care centre. Method 120 renal transplant recipients were analyzed from September 2015 to August 2019 at the Institute of Nephro-Urology, Bangalore. It was a retrospective analysis of data Results 120 adult patients underwent kidney transplantation, out of these 70 had GN as primary cause of kidney disease. 85.8% were males, 14.2 % females. 58.9 % were biopsy proven GN, remaining 41.1 % diagnosed based on history and clinical presentation. All but one patient had their first transplant. Out of these kidney transplant recipients 08 (11.4%) had recurrence of GN.  From these 4/08 was recurrent IgA N, 2/08 were PGNMID, 1/08 MGN, 1/08 aHUS. Graft loss due to recurrent GN was seen in 1/08 patients (12.5%). Conclusion Our study showed that 11.4 % of kidney transplant recipients with GN as their cause of ESRD had recurrent GN post kidney transplantation. IgAN was the most type of GN that recurred most frequently followed by PGNMID. Recurrence of GN was in par with other studies and did not affect graft survival

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