scholarly journals Treatment of mineral-bone disorders in chronic kidney disease

2020 ◽  
Vol 29 (4) ◽  
pp. 85-90
Author(s):  
I.T. Murkamilov ◽  
K.A. Aitbaev ◽  
V.V. Fomin ◽  
Zh.A. Murkamilova ◽  
F.A. Yusupov

Mineral-bone disorders (MBD) in chronic kidney disease (CKD) manifest by hyperphosphatemia, vitamin D deficiency, overproduction of fibroblast growth factor-23, and secondary hyperparathyroidism. CKD-MBD also results in bone resorp-tion and ectopic calcification that is associated with an increased risk of cardiovascular events and mortality. Diet is the initial and obligatory approach to treatment for CKD-MBD. Sevelamer is frequently used for correction of hyperphosphatemia in patients with renal failure who present with calcification of arteries, adynamic bone disease and/or stably low serum parathyroid hormone levels. Calcimimetics, that is, cinacalcet and evocalcet, are widely used in hemodialysis patients who do not respond to treatment with vitamin D.

Author(s):  
Stuart M. Sprague ◽  
James M. Pullman

Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.


2018 ◽  
Vol 22 (3) ◽  
pp. 4-8
Author(s):  
V. Martina ◽  
M.A. Rizzo ◽  
C. Uggetti ◽  
L. Gravellone ◽  
A. Giordano ◽  
...  

La complessa patologia ossea dei pazienti affetti da insufficienza renale cronica è oggi definita Chronic Kidney Disease-Mineral and Bone Disorders (CKD-MBD) e comprende quadri patologici differenti tra i quali l'osso adinamico (Adynamic Bone Disease-ABD). Le conseguenze dell'ABD non sono meno invalidanti di quelle che insorgono in corso di iperparatiroidismo secondario. Talvolta le manife-stazioni cliniche di ABD, come le complicanze vertebrali a lungo temine qui descritte, possono avere ripercussioni extrascheletriche tali da richiedere necessariamente un approccio terapeutico neuro-chirurgico invasivo, ma l'esito negativo dell'inter-vento effettuato sulla nostra paziente, per l'insor-genza di un'instabilità secondaria, sottolinea la difficoltà di successo quando si opera selettivamente in una situazione clinica di globale deterioramento del tessuto osseo. A questo proposito potrebbe essere valorizzato l'utilizzo di tecniche chirurgiche meno rigide dell'artrodesi strumentata per compensare la minore elasticità e resistenza dell'osso. Da ciò si desume l'importanza di un attento follow-up clinico del paziente e della necessità di una fattiva collaborazione con altri specialisti (neurologo, neurochirurgo, radiologo) per la prevenzione delle complicanze a lungo termine della patologia ossea del paziente dializzato.


PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e79721 ◽  
Author(s):  
Juliana C. Ferreira ◽  
Guaraciaba O. Ferrari ◽  
Katia R. Neves ◽  
Raquel T. Cavallari ◽  
Wagner V. Dominguez ◽  
...  

2010 ◽  
Vol 29 (3) ◽  
pp. 293-299 ◽  
Author(s):  
Richard Amerling ◽  
Nikolas B. Harbord ◽  
James Pullman ◽  
Donald A. Feinfeld

Author(s):  
Anne Schön ◽  
Maren Leifheit-Nestler ◽  
Jennifer Deppe ◽  
Dagmar-Christiane Fischer ◽  
Aysun K Bayazit ◽  
...  

Abstract Background Uraemic cardiac remodelling is associated with vitamin D and Klotho deficiency, elevated fibroblast growth factor 23 (FGF23) and activation of the renin–angiotensin system (RAS). The cardioprotective properties of active vitamin D analogues in this setting are unclear. Methods In rats with 5/6 nephrectomy (5/6Nx) treated with calcitriol, the cardiac phenotype and local RAS activation were investigated compared with controls. A nested case–control study was performed within the Cardiovascular Comorbidity in Children with Chronic Kidney Disease (4C) study, including children with chronic kidney disease (CKD) Stages 3–5 [estimated glomerular filtration rate (eGFR) 25 mL/min/1.73 m2] treated with and without active vitamin D. Echocardiograms, plasma FGF23 and soluble Klotho (sKlotho) were assessed at baseline and after 9 months. Results In rats with 5/6Nx, left ventricular (LV) hypertrophy, LV fibrosis and upregulated cardiac RAS were dose-dependently attenuated by calcitriol. Calcitriol further stimulated FGF23 synthesis in bone but not in the heart, and normalized suppressed renal Klotho expression. In the 4C study cohort, treatment over a mean period of 9 months with active vitamin D was associated with increased FGF23 and phosphate and decreased sKlotho and eGFR compared with vitamin D naïve controls, whereas LV mass index did not differ between groups. Conclusions Active vitamin D ameliorates cardiac remodelling and normalizes renal Klotho expression in 5/6Nx rats but does not improve the cardiac phenotype in children with CKD Stages 3–5. This discrepancy may be due to further enhancement of circulating FGF23 and faster progression of CKD associated with reduced sKlotho and higher serum phosphate in vitamin D-treated patients.


2014 ◽  
Vol 34 (6) ◽  
pp. 626-640 ◽  
Author(s):  
Jordi Bover ◽  
Pablo Ureña ◽  
Vincent Brandenburg ◽  
David Goldsmith ◽  
César Ruiz ◽  
...  

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