Der Nephrologe

, Volume 8, Issue 1, pp 21–27 | Cite as

High-turnover-Osteodystrophie

Leitthema

Zusammenfassung

Bei chronischer Niereninsuffzienz kommt es durch Hyperphosphatämie, Vitamin-D-Mangel und ansteigende FGF-23-Spiegel zu einem Anstieg von Parathormon (PTH). Ein über längere Zeit bestehender und progressiver Hyperparathyreoidismus verursacht eine Erhöhung des Knochenumsatzes (High-turnover-Osteodystrophie, HTO), der in den überwiegenden Fällen zu einer relevanten Entkalkung des Skeletts, zu Frakturen sowie zu Gefäß- und Weichteilverkalkungen führen kann. Eine Senkung des PTH durch aktive Vitamin-D-Metabolite und/oder Cinacalcet sowie eine gute Kontrolle der Hyperphosphatämie unter Beachtung der Kalziumbilanz sind wirksame Therapieoptionen zur Behandlung der HTO. Unter Beachtung der Zielwerte für Kalzium, Phosphat und PTH gilt es, die HTO so zu behandeln, dass der Knochenstoffwechsel in einem leicht gesteigerten Bereich gehalten wird und eine Low-turnover-Osteodystrophie (LTO) vermieden wird.

Schlüsselwörter

Chronische Niereninsuffizienz Sekundärer Hyperparathyreoidismus Hyperphosphatämie Knochenstoffwechsel Knochenhistologie Verkalkung 

High turnover osteodystrophy

Abstract

In chronic kidney disease hyperphosphatemia, vitamin D deficiency and rising fibroblast growth factor (FGF) 23 levels lead to increased parathyroid hormone (PTH) levels. Progressive hyperparathyroidism which has been present for long periods of time leads to an increase in bone turnover (high turnover osteodystrophy, HTO) which in turn leads to demineralization of the skeleton, bone fractures and calcification of soft tissue and blood vessels. A decrease in PTH and treatment of HTO can be achieved by administration of vitamin D and/or cinacalcet as well as optimized phosphate control and balanced calcium metabolism. In HTO therapy, target levels of phosphate, calcium and PTH should be considered and bone metabolism should be maintained at a slightly elevated level in order to prevent low turnover osteodystrophy.

Keywords

Chronic kidney disease Secondary hyperparathyreoidism Hyperphosphatemia Bone metabolism Bone histology Calcification 

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Copyright information

© Springer-Verlag Berlin Heidelberg 2012

Authors and Affiliations

  1. 1.Klinik für Innere Medizin I und KfH-NierenzentrumEvangelisches Krankenhaus Paul Gerhardt Stift, Paul Gerhardt Diakonie und Pflege GmbH Berlin und Wittenberg e.V.Lutherstadt WittenbergDeutschland

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