Adynamic bone disease is a predominant bone pattern in early stages of chronic kidney disease
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Chronic kidney disease (CKD) is complicated by disturbances of mineral and bone metabolism which start early in the course of the disease. It has long been assumed that high turnover bone lesions induced by secondary hyperparathyroidism are the predominant type of renal osteodystrophy from the start. However, there is increasing evidence in favor of the view that in early CKD stages low bone turnover is prevailing, with adynamic bone disease being the predominant form. Since serum parathyroid hormone levels increase progressively early on, and the most probable explanation is resistance to the skeletal action of this hormone. An early inhibition of the Wnt pathway with an increase in sclerostin and other inhibitors of Wnt signaling may be involved. Finally, a variety of other uremic toxins such as indoxyl sulfate and phosphate may play an important role in the pathogenesis of the low turnover bone disease observed in early stages of CKD. The optimal strategies to prevent and to treat adynamic bone disease in incipient CKD yet need to be defined. Targeting uremic toxins such as sclerostin, phosphate, and indoxyl sulfate may be relevant.
KeywordsRenal osteodystrophy Adynamic bone disease Early CKD PTH FGF23 Uremic toxins Indoxyl sulfate
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Conflict of interest
The authors declare that they have no conflict of interest.
This article does not contain any studies with human participants performed by any of the authors.
- 1.Kidney Disease-Improving Global Outcomes (KDIGO) CKD-MBD Work Group (2009) KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Kidney Int Suppl:S1–S130Google Scholar
- 2.National Kidney Foundation (2003) K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis 42:S1–201Google Scholar
- 9.Barreto FC, Barreto DV, FernandesCanziani ME, Tomiyama C, Higa A, Mozar A, Glorieux G, Vanholder R, Massy ZA, BarbosaDeCarvalho A (2014) Association between indoxyl sulfate and bone histomorphometry in pre-dialysis chronic kidney disease patients. J Braz Nefrol 36:289–296Google Scholar
- 12.Graciolli FG, Neves KR, Barreto F, Barreto DV, Dos Reis LM, Canziani ME, Sabbagh Y, Carvalho AB, Jorgetti V, Elias RM, Schiavi S, Moysés RM (2017) The complexity of chronic kidney disease-mineral and bone disorder across stages of chronic kidney disease. Kidney Int. doi: 10.1016/j.kint.2016.12.029 PubMedGoogle Scholar
- 20.Ferreira JC, Ferrari GO, Neves KR, Cavallari RT, Dominguez WV, Dos Reis LM, Graciolli FG, Oliveira EC, Liu S, Sabbagh Y et al (2013) Effects of dietary phosphate on adynamic bone disease in rats with chronic kidney disease—role of sclerostin? PLoS One 8:e79721CrossRefPubMedPubMedCentralGoogle Scholar
- 21.Nikolov IG, Joki N, Nguyen-Khoa T, Guerrera IC, Maizel J, Benchitrit J, Machado dos Reis L, Edelman A, Lacour B, Jorgetti V et al (2012) Lanthanum carbonate, like sevelamer-HCl, retards the progression of vascular calcification and atherosclerosis in uremic apolipoprotein E-deficient mice. Nephrol Dial Transpl 27:505–513CrossRefGoogle Scholar
- 29.Prisby R, Guignandon A, Vanden-Bossche A, Mac-Way F, Linossier MT, Thomas M, Laroche N, Malaval L, Langer M, Peter ZA et al (2011) Intermittent PTH(1–84) is osteoanabolic but not osteoangiogenic and relocates bone marrow blood vessels closer to bone-forming sites. J Bone Miner Res 26:2583–2596CrossRefPubMedGoogle Scholar
- 34.Ketteler M, Elder GJ, Evenepoel P, Ix JH, Jamal SA, Lafage-Proust MH, Shroff R, Thadhani RI, Tonelli MA, Kasiske BL et al (2015) Revisiting KDIGO clinical practice guideline on chronic kidney disease-mineral and bone disorder: a commentary from a kidney disease: improving global outcomes controversies conference. Kidney Int 87:502–528CrossRefPubMedGoogle Scholar