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Dialyse aktuell 2013; 17(8): 426-436
DOI: 10.1055/s-0033-1359377
Nephrologie
© Georg Thieme Verlag Stuttgart · New York

Kalzium- und Phosphatbilanz bei Niereninsuffizienz – Wann und wie soll therapiert werden?

Calcium and phosphate homeostasis in chronic kidney disease –When and how is a treatment necessary?
Patrick Biggar
1   Medizinische Klinik III – Nephrologie, Klinikum Coburg GmbH, Coburg (ärztliche Leitung: Prof. Dr. Markus Ketteler)
,
Markus Ketteler
1   Medizinische Klinik III – Nephrologie, Klinikum Coburg GmbH, Coburg (ärztliche Leitung: Prof. Dr. Markus Ketteler)
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Publication History

Publication Date:
15 October 2013 (online)

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In den letzten 2 Jahrzehnten hat sich unser Verständnis für den menschlichen Kalzium- und Phosphathaushalt wesentlich geändert. Noch vor nicht allzu langer Zeit ging man davon aus, dass eine erhöhte Kalziumzufuhr günstig sei, um einen gesunden Knochenaufbau zu ermöglichen, und dass zumindest leicht erhöhte Serum-Phosphat-Werte keine nachteiligen Wirkungen bei Patienten mit chronischer Niereninsuffizienz hätten. Heute weiß man aus zahlreichen Beobachtungs- sowie In-vitro-Studien, dass sowohl Kalzium als auch Phosphat eine zentrale Triggerfunktion für den Prozess der Weichteil- bzw. der Gefäßverkalkung und somit für die Prognose haben. Dementsprechend werden neben anderen therapeutischen Optionen auch kalziumfreie Phosphatbinder eingesetzt, um die Kalziumbeladung und die Phosphataufnahme zu reduzieren. Angesichts der derzeit widersprüchlichen Datenlage bezüglich der Applikation von Phosphatsenkern bei präterminaler Niereninsuffizienz und nur tendenziell erhöhtem Serumphosphat sollten Phosphatbinder momentan nur bei sichtbarer Hyperphosphatämie verabreicht werden. Darüber hinaus bleibt jedoch eine Reduktion des Phosphatgehalts in der täglichen Nahrung eine Herausforderung, solange keine adäquate Kennzeichnung der Lebensmittel erfolgt.

In the last 2 decades, our understanding of the human calcium and phosphate homeostasis has changed dramatically. Following initial perceptions that calcium supplementation was advantageous for normal bone development and that moderately elevated phosphate levels were not detrimental to patients with chronic kidney disease, numerous observational and in vitro studies have shown that calcium and phosphate possess a central trigger function regarding initiation of soft tissue calcification, i. e. in the vessels, and thus are both determinants of prognosis. In this context, calcium-free phosphate binders are employed among other interventions to reduce corporeal calcium and phosphate loading. In view of present contradictory data regarding phosphate binder therapy in patients with preterminal chronic kidney disease but only marginally elevated serum phosphate levels, phosphate binders should presently only be administered when hyperphosphatemia is visible. Furthermore, however, a reduction in the daily nutrition remains enigmatic as long as adequate food supplement declaration is not enforced.

Key words

calcium and phosphate homeostasis - chronic kidney disease - hyperphosphatemia - soft tissue calcification - phosphate binder
 

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