title: Adynamic bone disease: from bone to vessels in chronic kidney disease.
abstract: Adynamic bone disease (ABD) is a well-recognized clinical entity in the complex chronic kidney disease (CKD)-mineral and bone disorder. Although the combination of low intact parathyroid hormone (PTH) and low bone alkaline phosphatase levels may be suggestive of ABD, the gold standard for precise diagnosis is histomorphometric analysis of tetracycline double-labeled bone biopsies. ABD essentially is characterized by low bone turnover, low bone volume, normal mineralization, and markedly decreased cellularity with minimal or no fibrosis. ABD is increasing in prevalence relative to other forms of renal osteodystrophy, and is becoming the most frequent type of bone lesion in some series. ABD develops in situations with reduced osteoanabolic stimulation caused by oversuppression of PTH, multifactorial skeletal resistance to PTH actions in uremia, and/or dysregulation of Wnt signaling. All may contribute not only to bone disease but also to the early vascular calcification processes observed in CKD. Various risk factors have been linked to ABD, including calcium loading, ageing, diabetes, hypogonadism, parathyroidectomy, peritoneal dialysis, and antiresorptive therapies, among others. The relationship between low PTH level, ABD, increased risk fracture, and vascular calcifications may at least partially explain the association of ABD with increased mortality rates. To achieve optimal bone and cardiovascular health, attention should be focused not only on classic control of secondary hyperparathyroidism but also on prevention of ABD, especially in the steadily growing proportions of diabetic, white, and elderly patients. Overcoming the insufficient osteoanabolic stimulation in ABD is the ultimate treatment goal.
authors.affiliation: Fundació Puigvert, Department of Nephrology, IIB Sant Pau, RedinRen, Barcelona, Catalonia, Spain. Electronic address: jbover@fundacio-puigvert.es.
authors.forename: Jordi
authors.initials: J
authors.lastname: Bover
authors.affiliation: Department of Nephrology and Dialysis, Clinique du Landy, Department of Renal Physiology, Necker Hospital, University of Paris Descartes, Paris, France.
authors.forename: Pablo
authors.initials: P
authors.lastname: Ureña
authors.affiliation: Department of Cardiology and Intensive Care Medicine, Rheinisch-Westfälische Technische Hochschule (RWTH) University Hospital, Aachen, Germany.
authors.forename: Vincent
authors.initials: V
authors.lastname: Brandenburg
authors.affiliation: King's Health Partners Academic Health Sciences Centre (AHSC), London, United Kingdom.
authors.forename: David
authors.initials: D
authors.lastname: Goldsmith
authors.affiliation: Fundació Puigvert, Department of Nephrology, IIB Sant Pau, RedinRen, Barcelona, Catalonia, Spain.
authors.forename: César
authors.initials: C
authors.lastname: Ruiz
authors.affiliation: Fundació Puigvert, Department of Nephrology, IIB Sant Pau, RedinRen, Barcelona, Catalonia, Spain.
authors.forename: Iara
authors.initials: I
authors.lastname: DaSilva
authors.affiliation: Fundació Puigvert, Department of Nephrology, IIB Sant Pau, RedinRen, Barcelona, Catalonia, Spain.
authors.forename: Ricardo J
authors.initials: RJ
authors.lastname: Bosch
mesh_terms: D002118:Calcium / Q000097:blood; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy*; D048909:Diabetes Complications / Q000150:complications; D050723:Fractures, Bone / Q000209:etiology; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000097:blood / Q000150:complications; D010011:Osteocytes / Q000502:physiology; D010281:Parathyroid Hormone / Q000097:blood; D051436:Renal Insufficiency, Chronic / Q000150:complications* / Q000628:therapy; D012307:Risk Factors; D014511:Uremia / Q000150:complications; D061205:Vascular Calcification / Q000209:etiology
chemical_list: D010281:Parathyroid Hormone; D002118:Calcium
keywords: Adynamic bone disease; CKD-MBD; PTH; renal osteodystrophy; sclerostin