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Hamostaseologie 2015; 35(01): 73-76
DOI: 10.5482/HAMO-14-08-0032
Review
Schattauer GmbH

Kidney and haemostasis

A (personal) time-journeyNiere und HämostaseEine (persönliche) Zeitreise
K. Andrassy
1   Med Universitätsklinik – Nephrologie, Heidelberg, Germany
› Author Affiliations
Further Information

Publication History

received: 21 August 2014

accepted in revised form: 29 October 2014

Publication Date:
28 December 2017 (online)

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Summary

Renal insufficiency is characterized by thrombocytopathy, caused by the accumulation of water soluble and protein bound waste products of protein metabolism, which are not adequately eliminated by the kidney. The kidneys also excrete drugs and their metabolites, which accumulate if dosages are not adjusted to the renal function and may cause clinically relevant bleeding (i. e. synthetic penicillins, vitamin K antagonists, new oral anticoagulants). Therefore, each patients kidney function (GFR) ought to be evaluated by the KDIGO guidelines. The survival of chronic renal patients is lowered by increasing cardiovascular complications. Particularly frequent is non-valvular atrial fibrillation. The recommended prophylaxis with vitamin K antagonists for renal insufficiency is hampered by increased bleeding as well as by augmented (coronary) vascular and valvular calcification. It is not known yet whether prophylaxis with vitamin K may prevent this complication. Conclusion: Because new oral anticoagulants are equally or even more effective and cause less bleeding, they may be favoured in future and even in end-stage renal failure if more is known about dosing, safety and efficacy. The measurement of serum FGF 23 concentration may be helpful as a marker for their use.

Zusammenfassung

Die Niereninsuffizienz ist durch eine Thrombozytopathie gekennzeichnet und wird durch Kumulation von Abbauprodukten aus dem Eiweißstoffwechsel hervorgerufen. Die Niere ist aber auch Ausscheidungsorgan für Medikamente und ihre Metabolite. Ohne Dosisanpassung kumulieren sie bei eingeschränkter Nierenfunktion und können Blutungen hervorrufen (z. B. synthetische Penicilline, Vitamin-K-Antagonisten, neue orale Antikoagulanzien). Daher ist bei jedem Patienten die Nierenfunktion nach den KDIGO-Richtlinien zu ermitteln. Das Überleben des chronisch Nierenkranken ist durch gesteigerte kardiovaskuläre Komplikationen limitiert. Vor allem Vorhofflimmern ist gegenüber dem Nierengesunden gehäuft. Die empfohlenen Vitamin K-Antagonisten führen bei Niereninsuffizienz zu vermehrten Blutungen und zu gesteigerter (koronarer) Gefäßund Herzklappenverkalkung. In wie weit die Substitution mit Vitamin K diese Verkalkung vermindern kann, wird zurzeit geprüft. Schlussfolgerung: Nachdem die neuen oralen Antikoagulanzien bei gleicher oder besserer Wirkung die Blutungsgefährdung in der Niereninsuffizienz reduzieren, könnten sie in Zukunft nach Dosisanpassung und Ausschluss unerwünschter Arzneimittelwirkungen möglicherweise gegenüber den Vitamin-K-Antagonisten bevorzugt werden. Als Marker für ihren Einsatz könnte die FGF-23-Serumkonzentration dienen.

Keywords

Uremic bleeding - FGF 23 - vitamin K antagonists - myocardial infarction

Schlüsselwörter

Urämie - Blutung - FGF 23 - Vitamin-K-Antagonisten - Myokardinfarkt
 

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