Osteologie 2008; 17(03): 148-153
DOI: 10.1055/s-0037-1619861
Renale Osteopathie
Schattauer GmbH

Kalzimimetika zur Behandlung des sekundären Hyperparathyreoidismus

Calcimimetics for the therapy of secondary hyper parathyroidism
R. Fiedler
1   Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Klinik und Poliklinik für Innere Medizin II (Direktor: Prof. Dr. med. habil. Matthias Girndt)
› Author Affiliations
Further Information

Publication History

Publication Date:
28 December 2017 (online)

Zusammenfassung

Der sekundäre Hyperparathyreoidismus (sHPT) ist einer der wesentlichsten Folgen der chronischen Niereninsuffizienz. Er verursacht über den gestörten Kalzium-Phosphat-Stoff-wechsel nicht nur die Entstehung von ossären Veränderungen („renale Osteopathie”), sondern ist ebenso mitverantwortlich für extraossäre Kalzium-Phosphat-Ablagerungen, die zu einer erhöhten kardiovaskulären Morbidität und Mortalität des nierenkranken Patienten führen. Der kalziumsensible Rezeptor (CaSR) in der Nebenschilddrüse und seine therapeutische Stimulierung durch Kalzimimetika sind wichtige Stellgrößen zur Behandlung des sHPT. Für sogenannte Typ-II-Kalzimimetika (z. B. Cinacalcet) konnte die effektive und sichere Supprimierung des Parathormons und des Kalzium-Phosphat-Produktes nachgewiesen werden. Die additive niedrig dosierte Vitamin-D-Gabe sollteje doch nicht vergessen werden, da nicht nur dem Vitamin-D-Mangel, sondern auch dem schweren sHPT optimal entgegengewirkt wird. Zusammenfassend ist festzustellen, dass die Therapie mit Cinacalcet nicht nur häufiger zur Einhaltung der biochemischen Zielwerte der NKF-K/DOQI-Leitlinien führt, sondern auch die Inzidenz von kardiovaskulären Ereignissen und chirurgischen Parathyreoidektomien zu reduzieren scheint.

Summary

The secondary hyperparathyroidism (sHPT) is one of the most substantial consequences of chronic kidney disease (CKD). It is caused bya disturbanced calcium-phosphorus metabolism and responsible for the development of renal osteodystrophy as well as of extraosseous calcifications, which lead to an increased cardiovascular morbidity and mortality, in patients with CKD. The calcium-sensing receptor (CaSR) in the parathyroid glands and its therapeutic activation due to calcimimetics are important correcting variables for the treatment of sHPT. So-called type II calcimimetics (e. g. cinacalcet) are able to decrease parathyroid hormone level and calcium-phosphorus product, effectively and safely. In addition to, vitamin D metabolites should be given ina low dose to avoid vitamin D deficiency and aggravation of sHPT. In conclusion, the biochemical goal values of NKF-K/DOQI guidelines will be kept more frequently bya therapy with calcimimetic cinacalcet and the incidence of cardiovascular events and surgical parathyroidectomies seems to be reduced.

 
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