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By Isabel Acosta-Ochoa Nephrology senior staff. Valladolid. Spain
Fabiana G Graciolli, Katia R Neves, Fellype Barreto, Daniela V Barreto, Luciene M Dos Reis, Maria E Canziani, Yves Sabbagh, Aluizio B Carvalho, Vanda Jorgetti, Rosilene M Elias, Susan Schiavi, Rosa M A Moysés
Chronic Kidney Disease (CKD)-Mineral and Bone Disorder (CKD-MBD) is a complex disease that is not completely understood. However, some factors secreted by the osteocytes might play an important role in its pathophysiology. Therefore, we evaluated the bone expression of proteins in a group of patients with CKD 2-3, CKD 4, and CKD 5 on dialysis and healthy individuals. We also tested several bone remodeling markers, and correlated these levels with bone biopsy findings. As expected, as serum calcium decreased, serum phosphate, alkaline phosphatase, fibroblast growth factor-23 (FGF-23), parathyroid hormone, and osteoprotegerin increased, as CKD progressed...
March 15, 2017: Kidney International
Anuja Shah
As the prevalence of chronic kidney disease (CKD) increases and the population ages, there is an imperative to offer cost effective and patient specific therapeutic options for the management of advanced CKD. In cases where there is a desire to avoid or delay renal replacement therapy, conservative options need to be defined and strategies for delaying the need for renal replacement therapy should be offered. CKD-mineral bone disorders (MBD) refers to the constellation of disturbances in abnormal bone and soft tissue calcification along with abnormalities, in phosphorus, calcium, parathyroid hormone, vitamin D, and FGF-23...
June 2017: Panminerva Medica
Hirotaka Komaba, Takatoshi Kakuta, Masafumi Fukagawa
Secondary hyperparathyroidism (SHPT) is a common complication in chronic kidney disease. Currently, various treatment options are available, including vitamin D receptor activators, cinacalcet hydrochloride, and parathyroidectomy. These treatment options have contributed to the successful control of SHPT, and recent clinical studies have provided evidence suggesting that effective treatment of SHPT leads to improved survival. Although bone disease is the most widely recognized consequence of SHPT and remains a major target for treatment of SHPT, there is increasing evidence that parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23), both of which are markedly elevated in SHPT, have multiple adverse effects on extraskeletal tissues...
March 2017: Clinical and Experimental Nephrology
Marc G Vervloet, Siren Sezer, Ziad A Massy, Lina Johansson, Mario Cozzolino, Denis Fouque
The importance of phosphate homeostasis in chronic kidney disease (CKD) has been recognized for decades, but novel insights - which are frequently relevant to everyday clinical practice - continue to emerge. Epidemiological data consistently indicate an association between hyperphosphataemia and poor clinical outcomes. Moreover, compelling evidence suggests direct toxicity of increased phosphate concentrations. Importantly, serum phosphate concentration has a circadian rhythm that must be considered when interpreting patient phosphate levels...
January 2017: Nature Reviews. Nephrology
Kenneth R Phelps, Darius L Mason, Kim S Stote
AIMS: Increased concentrations of parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) often coincide with normal serum phosphorus ([P]s) in chronic kidney disease (CKD). We hypothesized that the phosphate concentration ([P]f) in the cortical distal nephron (CDN) determines [PTH] and [FGF23] in this circumstance. METHODS: We studied 29 patients with CKD at 4 visits and 28 controls at 1 visit. Assuming GFR = creatinine clearance (Ccr), we examined the following regressions: [P]s on its determinants, EP/Ccr and TRP/Ccr (P excretion and reabsorption per volume of filtrate); [PTH] and [FGF23] on [P]s and EP/Ccr; and TRP/Ccr on [PTH] and [FGF23]...
May 2016: Clinical Nephrology
Ljubica Djukanović, Nada Dimković, Jelena Marinković, Živka Djurić, Violeta Knežević, Tatjana Lazarević, Stanimir Ljubenović, Rodoljub Marković, Violeta Rabrenović
BACKGROUND: Increased mortality of hemodialysis (HD) patients is associated with chronic kidney disease-mineral and bone disorders (CKD-MBD), and therefore, their correction may improve patient survival. Differences in targets recommended by KDOQI and KDIGO CKD-MBD guidelines directed us to compare the relative numbers of patients achieving these targets and to examine possible associations between compliance with the targets and patient outcome. METHODS: A total of 1,744 patients (61...
2016: Nephron
Tilman B Drüeke, Ziad A Massy
It is commonly held that osteitis fibrosa and mixed uremic osteodystrophy are the predominant forms of renal osteodystrophy in patients with chronic kidney disease. Osteitis fibrosa is a high-turnover bone disease resulting mainly from secondary hyperparathyroidism, and mixed uremic osteodystrophy is in addition characterized by a mineralization defect most often attributed to vitamin D deficiency. However, there is ancient and more recent evidence that in early chronic kidney disease stages adynamic bone disease characterized by low bone turnover occurs first, at least in a significant proportion of patients...
February 2016: Kidney International
Andrew L Lundquist, Sagar U Nigwekar
PURPOSE OF REVIEW: The review summarizes recent studies on chronic kidney disease-mineral bone disorders, with a focus on new developments in disease management. RECENT FINDINGS: The term chronic kidney disease-mineral bone disorder has come to describe an increasingly complex network of alterations in minerals and skeletal disorders that contribute to the significant cardiovascular morbidity and mortality seen in patients with chronic kidney disease and end stage renal disease...
March 2016: Current Opinion in Nephrology and Hypertension
W Charles O'Neill
Hypocalcemia is common in advanced chronic kidney disease (CKD) and end-stage renal disease (ESRD), and it is standard practice to correct this back to the normal range, presumably to prevent symptomatic hypocalcemia and help control hyperparathyroidism. However, there are few studies to support this approach, and recent data suggest that this promotes vascular calcification and adynamic bone disease. Whether setting a lower target will improve outcomes has not been tested, but existing data suggest that this may have minimal risks and substantial potential benefits and should be explored...
January 2016: Kidney International
Tamara Isakova
No abstract text is available yet for this article.
November 2015: Seminars in Dialysis
Michael E Seifert, Keith A Hruska
The last 25 years have been characterized by dramatic improvements in short-term patient and allograft survival after kidney transplantation. Long-term patient and allograft survival remains limited by cardiovascular disease and chronic allograft injury, among other factors. Cardiovascular disease remains a significant contributor to mortality in native chronic kidney disease as well as cardiovascular mortality in chronic kidney disease more than doubles that of the general population. The chronic kidney disease (CKD)-mineral bone disorder (MBD) is a syndrome recently coined to embody the biochemical, skeletal, and cardiovascular pathophysiology that results from disrupting the complex systems biology between the kidney, skeleton, and cardiovascular system in native and transplant kidney disease...
March 2016: Transplantation
Kathryn K Stevens, Rajan K Patel, Patrick B Mark, Christian Delles, Alan G Jardine
BACKGROUND: Hyperphosphataemia is a risk factor for accelerated cardiovascular disease in chronic kidney disease. The mechanism is poorly understood; it is unclear whether phosphate has direct effects or effects mediated via calcification or FGF23. We investigated direct effects of phosphate on endothelial function using myography to study rat and human blood vessels. In addition we assessed the effects of phosphate loading on endothelial function in a clinical study. METHODS: Resistance vessels from patients with (n=12) and without (n=13) chronic kidney disease were incubated in normal or high phosphate...
February 26, 2015: Lancet
Arnold J Felsenfeld, Barton S Levine, Mariano Rodriguez
Calcium, phosphorus, and magnesium homeostasis is altered in chronic kidney disease (CKD). Hypocalcemia, hyperphosphatemia, and hypermagnesemia are not seen until advanced CKD because adaptations develop. Increased parathyroid hormone (PTH) secretion maintains serum calcium normal by increasing calcium efflux from bone, renal calcium reabsorption, and phosphate excretion. Similarly, renal phosphate excretion in CKD is maintained by increased secretion of fibroblast growth factor 23 (FGF23) and PTH. However, the phosphaturic effect of FGF23 is reduced by downregulation of its cofactor Klotho necessary for binding FGF23 to FGF receptors...
November 2015: Seminars in Dialysis
Yueming Liu, Qiang He
BACKGROUND: Clinicians may use several biochemical markers of bone turnover to assess or guide the care of patients with chronic kidney disease (CKD). The aims of this study are to describe changes and correlations of markers of bone remodeling in patients with different stages of CKD. METHODS: A total of 317 Chinese patients with advanced CKD (stage 3-5) were enrolled. We measured serum levels of intact-parathyroid hormone (iPTH), N-terminal midfragment (N-MID) osteocalcin, procollagen type 1 amino-terminal propeptide (P1NP), β-isomerized C-terminal telopeptide (β-CTx), total alkaline phosphatase (ALP), and 25-hydroxyvitamin D (25[OH]D)...
2015: Clinical Laboratory
Rosa M A Moysés, Susan C Schiavi
Osteocytes respond to kidney damage by increasing production of secreted factors important to bone and mineral metabolism. These circulating proteins include the antianabolic factor, sclerostin, and the phosphaturic hormone, fibroblast growth factor 23 (FGF23). Elevated sclerostin levels correlate with increased FGF23, localized reduction in Wnt/β-catenin signaling in the skeleton and reduced osteoblast differentiation/activity. Decreased Wnt/β-catenin signaling occurs regardless of the overall changes in bone formation rates, suggesting that a reduction in the anabolic response may be a common feature of renal bone disorders but additional mechanisms may contribute to the diversity of osteodystrophy phenotypes...
November 2015: Seminars in Dialysis
Yoshiko Iwasaki, Junichiro J Kazama, Hideyuki Yamato, Aira Matsugaki, Takayoshi Nakano, Masafumi Fukagawa
Chronic kidney disease (CKD) is associated with an increased risk of fragility fractures, but the underlying pathophysiological mechanism remains obscure. We performed an in vivo experimental study to examine the roles of uremia and abnormal mineral/parathyroid metabolism in the development of bone metabolic abnormalities in uremic rats. Male Sprague-Dawley rats were divided into four groups, comprising sham operation (high turnover bone control=HTB-Cont), 5/6-nephrectomy (high turnover bone nephrectomized=HTB-Nx), thyroparathyroidectomy (low turnover bone control=LTB-Cont), and thyroparathyroidectomy plus 5/6 nephrectomy (low turnover bone nephrectomized=LTB-Nx), and maintained for 16 weeks...
December 2015: Bone
Keith A Hruska, Michael Seifert, Toshifumi Sugatani
PURPOSE OF REVIEW: The causes of excess cardiovascular mortality associated with chronic kidney disease (CKD) have been attributed in part to the CKD-mineral bone disorder syndrome (CKD-MBD), wherein, novel cardiovascular risk factors have been identified. The causes of the CKD-MBD are not well known and they will be discussed in this review RECENT FINDINGS: The discovery of WNT (portmanteau of wingless and int) inhibitors, especially Dickkopf 1, produced during renal repair and participating in the pathogenesis of the vascular and skeletal components of the CKD-MBD implied that additional pathogenic factors are critical, leading to the finding that activin A is a second renal repair factor circulating in increased levels during CKD...
July 2015: Current Opinion in Nephrology and Hypertension
Aline G Costa, John P Bilezikian, E Michael Lewiecki
PURPOSE OF REVIEW: Sclerostin is a regulator of the osteoanabolic canonical Wnt signaling pathway, and thus helps to govern rates of bone formation. The Wnt pathway is also recognized as playing an important role in the pathophysiology of the chronic kidney disease-mineral and bone disorder (CKD-MBD). It also may serve as an interface between bone and the vascular system. Pharmacological inhibition of sclerostin has shown promise as an osteoanabolic approach to the treatment of osteoporosis...
July 2015: Current Opinion in Nephrology and Hypertension
Ken Tsuchiya, Nobuo Nagano, Kosaku Nitta
The sequential bone disorders, serum parameter abnormalities and vascular calcification that are associated with chronic kidney disease (CKD) have come to be generally known as CKD-mineral bone disorder (MBD). Klotho, a causative protein of aging, and fibroblast growth factor 23 (FGF23), a bone-derived phosphaturic factor, have been reported to be involved in CKD-MBD, and their relationship to the pathophysiology of this disease is gradually being elucidated. Klotho functions as a cofactor of FGF receptors and has been reported to cause FGF23 action and specificity in the kidney...
2015: Contributions to Nephrology
Masaaki Inaba
Increases in serum calcium and phosphate are known as main risk factors for cardiovascular mortality in hemodialysis patients. However, increased phosphate, a definite mortality risk in the general population, should be more remarkable in hemodialysis patients, as their renal capacity to excrete phosphate into urine is negligible. Phosphate acts directly and indirectly to cause vascular injury by stimulating the apoptosis of vascular endothelial cells and the vascular calcification of vascular smooth muscle cells...
2015: Contributions to Nephrology
2015-06-02 11:29:08
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