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By Venkatesh Ariyamuthu Transplant Nephrologist at UT Southwestern Medical Center
Peggy Perrin, Clotilde Kiener, Rose-Marie Javier, Laura Braun, Noelle Cognard, Gabriela Gautier-Vargas, Francoise Heibel, Clotilde Muller, Jerome Olagne, Bruno Moulin, Sophie Caillard
BACKGROUND: The management of chronic kidney disease-mineral and bone disorders (CKD-MBD) has recently changed. We investigated the modifications of CKD-MBD with a special focus on the incidence of fractures in the first year after kidney transplantation (KT). METHODS: We retrospectively compared 2 groups of patients who consecutively underwent transplantation at our center 5 years from each other. Group 1 consisted of patients (n=152) transplanted between 2004 and 2006, whereas patients in group 2 (n=137) underwent KT between 2009 and 2011...
August 19, 2016: Transplantation
Roland D Chapurlat, Cyrille B Confavreux
Biochemical markers of bone turnover have been used for decades in the management of bone diseases, to assess the prognosis of these conditions and to monitor treatments. The new markers, however, also reflect specific physiological mechanisms in the bone or other organs. Periostin may be more specific to the periosteum; cathepsin K is an osteoclastic enzyme that may be involved in the cardiovascular system and joints; Dickkopf-1 is involved in bone formation and vascular calcification; sclerostin is a major regulator of bone formation in response to mechanical loading and may also play a role in chronic kidney disease bone and mineral disorder; sphingosine-1-phosphate is a lipid mediator interacting with bone resorption...
October 2016: Rheumatology
Melissa Soohoo, Mingliang Feng, Yoshitsugu Obi, Elani Streja, Connie M Rhee, Wei Ling Lau, Jialin Wang, Vanessa A Ravel, Steven Brunelli, Csaba P Kovesdy, Kamyar Kalantar-Zadeh
BACKGROUND: Abnormalities in mineral and bone disorder (MBD) markers are common in patients with chronic kidney disease. However, previous studies have not accounted for their changes over time, and it is unclear whether these changes are associated with survival. METHODS: We examined the association of change in MBD markers (serum phosphorus (Phos), albumin-corrected calcium (Ca(Alb)), intact parathyroid hormone (iPTH) and alkaline phosphatase (ALP)) during the first 6 months of hemodialysis (HD) with all-cause mortality across baseline MBD strata using survival models adjusted for clinical characteristics and laboratory measurements in 102,754 incident HD patients treated in a large dialysis organization between 2007 and 2011...
2016: American Journal of Nephrology
Yukihiro Wada, Masayuki Iyoda, Ken Iseri, Noriko Arai-Nunota, Tomohiro Saito, Toma Hamada, Shohei Tachibana, Misa Ikeda, Takanori Shibata
Denosumab (DMAb), a complete human type monoclonal antibody directed against the receptor activator of nuclear factor-κB ligand, has gained attention as a novel treatment for osteoporosis. However, its efficacy in patients with chronic kidney disease (CKD) remains unclear. We describe a 64-year-old man with severe bone loss and persistent secondary hyperparathyroidism (SHPT) after renal transplantation, whose condition failed to respond to conventional pharmacologic or surgical interventions. He underwent parathyroidectomy with left forearm autograft of crushed tiny parathyroid gland (PTG) particles...
2016: Tohoku Journal of Experimental Medicine
Antoine Bouquegneau, Syrazah Salam, Pierre Delanaye, Richard Eastell, Arif Khwaja
Bone and mineral disorders occur frequently in kidney transplant recipients and are associated with a high risk of fracture, morbidity, and mortality. There is a broad spectrum of often overlapping bone diseases seen after transplantation, including osteoporosis as well as persisting high- or low-turnover bone disease. The pathophysiology underlying bone disorders after transplantation results from a complex interplay of factors, including preexisting renal osteodystrophy and bone loss related to a variety of causes, such as immunosuppression and alterations in the parathyroid hormone-vitamin D-fibroblast growth factor 23 axis as well as changes in mineral metabolism...
July 7, 2016: Clinical Journal of the American Society of Nephrology: CJASN
Jürgen Floege
Hyperphosphatemia is common in chronic kidney disease (CKD) and is treated by dietary measures, dialysis techniques and/or phosphate binders. For the present review PubMed was searched for new publications on phosphate binders appearing between January 2010 and October 2015. This review summarizes the latest information on non-pharmacological measures and their problems in lowering phosphate in CKD patients, effects of phosphate binders on morbidity and mortality, adherence to phosphate binder therapy as well as new information on specific aspects of the various phosphate binders on the market: calcium acetate, calcium carbonate, magnesium-containing phosphate binders, polymeric phosphate binders (sevelamer, bixalomer, colestilan), lanthanum carbonate, ferric citrate, sucroferric oxyhydroxide, aluminum-containing phosphate binders, and new compounds in development...
June 2016: Journal of Nephrology
Dennis M Black, Clifford J Rosen
Key Clinical Points Postmenopausal Osteoporosis Fractures and osteoporosis are common, particularly among older women, and hip fractures can be devastating. Treatment is generally recommended in postmenopausal women who have a bone mineral density T score of -2.5 or less, a history of spine or hip fracture, or a Fracture Risk Assessment Tool (FRAX) score indicating increased fracture risk. Bisphosphonates (generic) and denosumab reduce the risk of hip, nonvertebral, and vertebral fractures; bisphosphonates are commonly used as first-line treatment in women who do not have contraindications...
January 21, 2016: New England Journal of Medicine
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
Masafumi Fukagawa, Tilman B Drüeke
No abstract text is available yet for this article.
August 2016: Journal of the American Society of Nephrology: JASN
M Bonani, D Frey, J Brockmann, T Fehr, T F Mueller, L Saleh, A von Eckardstein, N Graf, R P Wüthrich
We conducted an open-label, prospective, randomized trial to assess the efficacy and safety of RANKL inhibition with denosumab to prevent the loss of bone mineral density (BMD) in the first year after kidney transplantation. Ninety kidney transplant recipients were randomized 1:1 2 weeks after surgery to receive denosumab (60 mg at baseline and 6 months) or no treatment. After 12 months, total lumbar spine areal BMD (aBMD) increased by 4.6% (95% confidence interval [CI] 3.3-5.9%) in 46 patients in the denosumab group and decreased by -0...
June 2016: American Journal of Transplantation
Leena Patel, Lisa M Bernard, Grahame J Elder
BACKGROUND AND OBJECTIVES: People with CKD stages 3-5 and on dialysis (5D) have dramatically increased mortality, which has been associated with hyperphosphatemia in many studies. Oral phosphate binders are commonly prescribed to lower serum phosphate. We conducted an updated meta-analysis of the noncalcium-based binder (non-CBB) sevelamer versus CBBs in CKD stages 3-5D. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Randomized, controlled trials comparing sevelamer with CBBs were identified through MEDLINE and the Cochrane Central Register of Controlled Trials...
February 5, 2016: Clinical Journal of the American Society of Nephrology: CJASN
Renata C Pereira, David S Bischoff, Dean Yamaguchi, Isidro B Salusky, Katherine Wesseling-Perry
BACKGROUND AND OBJECTIVES: Computed tomography (CT) measurements can distinguish between cortical and trabecular bone density in vivo. High-resolution CTs assess both bone volume and density in the same compartment, thus potentially yielding information regarding bone mineralization as well. The relationship between bone histomorphometric parameters of skeletal mineralization and bone density from microcomputed tomography (μCT) measurements of bone cores from patients on dialysis has not been assessed...
March 7, 2016: Clinical Journal of the American Society of Nephrology: CJASN
Bryan Kestenbaum
Phosphate binders are prescribed to chronic kidney disease (CKD) patients based on associations of serum phosphate concentrations with mortality and calcification, experimental evidence for direct calcifying effects of phosphate on vascular smooth muscle tissue and the central importance of phosphate retention in CKD-mineral and bone disorder (CKD-MBD). Current knowledge regarding phosphate metabolism in CKD provides important insight into disease mechanisms and supports future clinical trials of phosphate binders in CKD patients to determine the impact of these medications on clinically relevant outcomes...
February 2016: Nephrology, Dialysis, Transplantation
Antonio Bellasi
Convincing epidemiological data have repeatedly shown that increased phosphate levels as well as generous phosphate intakes are associated with unfavourable outcome both in normal and chronically impaired kidney disease (CKD) individuals. Indeed, evidence suggest that impaired phosphate metabolism is associated with markers of cardiovascular damage such as left ventricular hypertrophy, arterial stiffness or vascular calcification as well as mortality. Although current guidelines suggest phosphate control in CKD, evidence on the impact of different approaches to minimize phosphate burden on clinically meaningful outcome are still lacking...
February 2016: Nephrology, Dialysis, Transplantation
Carmine Zoccali, Francesca Mallamaci
Particularly because the risk of harm cannot be safely excluded, the use of phosphate binders in chronic kidney disease (CKD) patients demands caution. Yet, the clinical inertia concerning phosphate burden is unjustified. Inorganic, phosphate esters added to preserve food represent an important component of dietary phosphate load. These compounds are easily absorbable and have a measurable effect on serum phosphate, and therefore their use should be avoided in CKD patients. The ongoing CKD Optimal management with Binders and NicotinamidE (COMBINE) study, applying chelation by phosphate binders and intestinal Na-P channel blockade by nicotinamide, will establish whether this combination may effectively reduce serum phosphate and fibroblast growth factor 23 in pre-dialysis CKD patients and produce improvements in surrogate measures of cardiovascular and renal damages...
February 2016: Nephrology, Dialysis, Transplantation
Josep M Cruzado, Pablo Moreno, José V Torregrosa, Omar Taco, Richard Mast, Carmen Gómez-Vaquero, Carolina Polo, Ignacio Revuelta, José Francos, Joan Torras, Arantxa García-Barrasa, Oriol Bestard, Josep M Grinyó
Tertiary hyperparathyroidism is a common cause of hypercalcemia after kidney transplant. We designed this 12-month, prospective, multicenter, open-label, randomized study to evaluate whether subtotal parathyroidectomy is more effective than cinacalcet for controlling hypercalcemia caused by persistent hyperparathyroidism after kidney transplant. Kidney allograft recipients with hypercalcemia and elevated intact parathyroid hormone (iPTH) concentration were eligible if they had received a transplant ≥6 months before the study and had an eGFR>30 ml/min per 1...
August 2016: Journal of the American Society of Nephrology: JASN
Revekka Babayev, Thomas L Nickolas
Renal osteodystrophy (ROD) is a bone disorder that occurs in chronic kidney disease (CKD) patients and is associated with 2- to 14-fold increased fracture risk compared to the general population. Risk of fractures is also increased in kidney transplant recipients especially within the first 5 years after transplantation. Fractures in CKD patients are associated with increased morbidity and mortality; thus, proper screening and management of CKD bone complications is critical to improving clinical outcomes. Tetracycline double-labeled transiliac crest bone biopsy with histomorphometry is the gold standard for the diagnosis and classification of ROD...
November 2015: Seminars in Dialysis
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
Radwa El Borolossy, Lamia Mohamed El Wakeel, Ihab El Hakim, Nagwa Sabri
BACKGROUND: Hyperphosphatemia is a common problem in patients with end-stage renal disease (ESRD) who are on maintenance hemodialysis (HD) and contributes to the development of secondary hyperparathyroidism and cardiovascular complications. Nicotinamide (NAM) has been shown in some studies to inhibit intestinal and renal sodium/phosphorus co-transporters and reduce serum phosphorus levels. We have therefore evaluated the efficacy and safety of NAM as adjunctive therapy to calcium-based phosphate binders to control hyperphosphatemia in hemodialysis patients...
February 2016: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
Leandro C Baia, Ita Pfeferman Heilberg, Gerjan Navis, Martin H de Borst
Dysregulated phosphate metabolism is a common consequence of chronic kidney disease, and is characterized by a high circulating level of fibroblast growth factor (FGF)-23, hyperparathyroidism, and hyperphosphataemia. Kidney transplantation can elicit specific alterations to phosphate metabolism that evolve over time, ranging from severe hypophosphataemia (<0.5 mmol/l) to hyperphosphataemia (>1.50 mmol/l) and high FGF-23 levels. The majority of renal transplant recipients develop hypophosphataemia during the first 3 months after transplantation as a consequence of relatively slow adaptation of FGF-23 and parathyroid hormone levels to restored renal function, and the influence of immunosuppressive drugs...
November 2015: Nature Reviews. Nephrology
2015-10-01 17:46:52
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