Summary
The high incidence of cardiac complications in endstage renal failure is not only related to the chronic pressure load of the left ventricle, although the proportion of patients with elevated blood pressure increases from 53 to 81% as reno-parenchymal disease progresses. Other factors as anemia, hyperparathyroidism, autonomic neuropathy and retention of electrolytes, metabolic products or toxins may cause damage to the heart. It is a matter of discussion whether uremia itself causes cardiomyopathy. Findings of a reduced Ca++-uptake during β-adrenergic stimulation and a reduced reaction of (Na+, K+)-ATPase to digitalis suggest a basic change of myocardial membrane metabolism. Retention of an “endogenous digitalis” could help to explain some contradictory results.
Zusammenfassung
Die Häufung kardialer Komplikationen bei terminaler Niereninsuffizienz ist nicht nur Folge einer chronischen Druckbelastung des linken Ventrikels, obwohl sich der Anteil der Hypertoniker mit fortschreitender renoparenchymatöser Erkrankung von 53 auf 81% erhöht. Andere Faktoren wie Anämie, Hyperparathyreoidismus, autonome Neuropathie und Retention von Elektrolyten, Stoffwechselprodukten oder Toxinen können das Herz schädigen. Ob die Urämie selbst eine Kardiomyopathie verursacht, ist noch nicht geklärt. Befunde über eine verminderte Ca++-Aufnahme während β-adrenerger Stimulation und über eine verminderte Reaktion der Membran-(Na+, K+)-ATPase auf Digitalis lassen eine tiefgreifende Änderung des myokardialen Membranstoffwechsels vermuten. Eine Retention von “endogenem Digitalis” bei Niereninsuffizienz könnte eine Reihe widersprüchlicher Befunde erklären.
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Mit Unterstützung der Deutschen Forschungsgemeinschaft im Rahmen des SFB-89 Kardiologie Göttingen
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Kramer, P., Schmidt-Lauber, M., Langenheim, N. et al. Reno-kardiale Wechselwirkungen bei Niereninsuffizienz. Klin Wochenschr 58, 1043–1050 (1980). https://doi.org/10.1007/BF01476875
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DOI: https://doi.org/10.1007/BF01476875