We are analyzing https://link.springer.com/article/10.1007/s00223-024-01261-w.

Title:
The Relationship between Sclerostin and Kidney Transplantation Mineral Bone Disorders: A Molecule of Controversies | Calcified Tissue International
Description:
Kidney transplantation is the most effective treatment option for most patients with end-stage kidney disease due to reduced mortality, decreased cardiovascular events and increased quality of life compared to patients treated with dialysis. However, kidney transplantation is not devoid of both acute and chronic complications including mineral bone disorders (MBD) which are already present in patients with chronic kidney disease (CKD) before kidney transplantation. The natural history of MBD after kidney transplantation is variable and new markers are needed to define MBD after kidney transplantation. One of these promising molecules is sclerostin. The main action of sclerostin is to inhibit bone formation and mineralization by blocking osteoblast differentiation and function. In kidney transplant recipients (KTRs), various studies have shown that sclerostin is associated with graft function, bone parameters, vascular calcification, and arterial stiffness although non-uniformly. Furthermore, data for inhibition of sclerostin with monoclonal antibody romosozumab for treatment of osteoporosis is available for general population but not in KTRs which osteoporosis is highly prevalent. In this narrative review, we have summarized the studies investigating the change of sclerostin before and after kidney transplantation, the relationship between sclerostin and laboratory parameters, bone metabolism and vascular calcification in the context of kidney transplantation. We also pointed out the uncertainties, explained the causes of divergent findings and suggest further potential study topics regarding sclerostin in kidney transplantation.
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Keywords {🔍}

sclerostin, bone, pubmed, kidney, article, google, scholar, transplantation, cas, levels, vascular, patients, studies, calcification, increased, cardiovascular, transplant, central, serum, relationship, disease, ktrs, renal, mortality, study, role, mineral, pth, signaling, high, clin, treatment, chronic, showed, association, expression, nephrol, recipients, int, arterial, mass, circulating, evenepoel, function, afsar, stiffness, risk, fgf, mineralization, metabolism,

Topics {✒️}

wnt/β-catenin pathway inhibitors end-stage kidney disease chronic kidney disease-mineral chronic kidney disease–mineral wnt-β-catenin signaling preventing translocation beta-catenin osteo/chondrocytic transcription factors bone-related protein related wingless-related integration site protein–albumin/creatinine ratio long-term cardiovascular morbidity article download pdf chronic kidney disease dickkopf-related protein-1 proteins long-term renal transplantation noncardio-embolic ischemic stroke google scholar long-term period identified vascular calcification inhibitor early post-transplant period wnt signaling pathway early post-transplantation period chronic allograft failure dba/2j mice showed calcifying aortic tissue pre-transplant arterial stiffness monoclonal antibody romosozumab coronary heart disease large-scale prospective studies de novo hyperparathyroidism wingless-related wnt akt signaling pathway notch signaling pathway pulse wave velocity bone mineral density anti-catabolic signaling rengin elsurer afsar bone-related clinical parameters mineral bone disorders cardiovascular safety profile privacy choices/manage cookies full access technological research council long-term administration increased osteocyte number blocking wnt signaling suppressing wnt signaling patients receiving hemodialysis systemic disorder including signaling pathways occurs

Questions {❓}

Claes KJ, Viaene L, Heye S, Meijers B, d’Haese P, Evenepoel P (2013) Sclerostin: another vascular calcification inhibitor?
Elder GJ (2016) Decreased circulating sclerostin levels in renal transplant recipients with persistent hyperparathyroidism: who’s conducting the orchestra?
Magalhães J, Quelhas-Santos J, Pereira L, Neto R, Castro-Ferreira I, Martins S, Frazão JM, Carvalho C (2022) Could bone biomarkers predict bone turnover after kidney transplantation?
Moysés RM, Jamal SA, Graciolli FG, dos Reis LM, Elias RM (2015) Can we compare serum sclerostin results obtained with different assays in hemodialysis patients?
Viaene L, Behets GJ, Claes K, Meijers B, Blocki F, Brandenburg V, Evenepoel P, D’Haese PC (2013) Sclerostin: another bone-related protein related to all-cause mortality in haemodialysis?
Why does this dynamic changes occur?

Schema {🗺️}

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         description:Kidney transplantation is the most effective treatment option for most patients with end-stage kidney disease due to reduced mortality, decreased cardiovascular events and increased quality of life compared to patients treated with dialysis. However, kidney transplantation is not devoid of both acute and chronic complications including mineral bone disorders (MBD) which are already present in patients with chronic kidney disease (CKD) before kidney transplantation. The natural history of MBD after kidney transplantation is variable and new markers are needed to define MBD after kidney transplantation. One of these promising molecules is sclerostin. The main action of sclerostin is to inhibit bone formation and mineralization by blocking osteoblast differentiation and function. In kidney transplant recipients (KTRs), various studies have shown that sclerostin is associated with graft function, bone parameters, vascular calcification, and arterial stiffness although non-uniformly. Furthermore, data for inhibition of sclerostin with monoclonal antibody romosozumab for treatment of osteoporosis is available for general population but not in KTRs which osteoporosis is highly prevalent. In this narrative review, we have summarized the studies investigating the change of sclerostin before and after kidney transplantation, the relationship between sclerostin and laboratory parameters, bone metabolism and vascular calcification in the context of kidney transplantation. We also pointed out the uncertainties, explained the causes of divergent findings and suggest further potential study topics regarding sclerostin in kidney transplantation.
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      headline:The Relationship between Sclerostin and Kidney Transplantation Mineral Bone Disorders: A Molecule of Controversies
      description:Kidney transplantation is the most effective treatment option for most patients with end-stage kidney disease due to reduced mortality, decreased cardiovascular events and increased quality of life compared to patients treated with dialysis. However, kidney transplantation is not devoid of both acute and chronic complications including mineral bone disorders (MBD) which are already present in patients with chronic kidney disease (CKD) before kidney transplantation. The natural history of MBD after kidney transplantation is variable and new markers are needed to define MBD after kidney transplantation. One of these promising molecules is sclerostin. The main action of sclerostin is to inhibit bone formation and mineralization by blocking osteoblast differentiation and function. In kidney transplant recipients (KTRs), various studies have shown that sclerostin is associated with graft function, bone parameters, vascular calcification, and arterial stiffness although non-uniformly. Furthermore, data for inhibition of sclerostin with monoclonal antibody romosozumab for treatment of osteoporosis is available for general population but not in KTRs which osteoporosis is highly prevalent. In this narrative review, we have summarized the studies investigating the change of sclerostin before and after kidney transplantation, the relationship between sclerostin and laboratory parameters, bone metabolism and vascular calcification in the context of kidney transplantation. We also pointed out the uncertainties, explained the causes of divergent findings and suggest further potential study topics regarding sclerostin in kidney transplantation.
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         Chronic kidney disease
         Kidney transplantation
         Sclerostin
         Vascular calcification
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         general
         Endocrinology
         Orthopedics
         Cell Biology
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