Zusammenfassung
Hintergrund
1929 erstmals beschrieben, ist das Tumorlysesyndrom (TLS) bis heute ein lebensbedrohliches Erkrankungsbild. Sowohl im Kindes- als auch im Erwachsenenalter führt es gehäuft nach Einleitung einer Chemotherapie zu metabolischen Veränderungen und Organdysfunktionen.
Methoden
Selektive Literaturrecherche, Stichwörter „tumor lysis syndrome“, „acute kidney injury“, „rasburicase“, „allopurinol“.
Ergebnisse
Der Schlüssel jedes TLS-Managements liegt in der Prävention. An das jeweilige TLS-Risiko adaptiert werden Maßnahmen 24 h vor Induktionstherapie eingeleitet. Die Basistherapie bildet die i.v.-Hydrierung, ergänzt je nach Risikoprofil um Allopurinol oder Rasburicase. Elektrolytentgleisungen sollten symptomkorreliert therapiert werden, v. a. bei Hypokalzämie und einem Kalzium-Phosphat-Produkt > 60 mg2/dl2. Bei manifestem TLS mit progredientem Nierenversagen oder konservativ nicht beherrschbaren Elektrolytentgleisungen ist die Indikation zur Nierenersatztherapie großzügig zu stellen. Sowohl Hyperurikämie, Hyperphosphatämie als auch Hyperxanthinämie können eigenständig ein akutes Nierenversagen induzieren.
Schlussfolgerung
Das primäre Ziel ist die Vermeidung eines manifesten TLS mit konsekutivem Nierenversagen. Letzteres kompromittiert die körpereigenen Kompensationsmechanismen entscheidend und aggraviert das Erkrankungsbild. Unter Rasburicase-Therapie spielt vor allem das durch Kalzium-Phosphat-Ablagerungen induzierte Nierenversagen eine entscheidende Rolle. Suffizient behandelt, ist jedes Nierenversagen reversibel.
Abstract
Background
First described in 1929, the tumor lysis syndrome (TLS) is still a life-threatening medical condition. In both adults and children, it causes severe metabolic disorders and organ dysfunction after chemotherapeutic therapy induction.
Methods
A selective literature search was performed with the keywords “tumor lysis syndrome”, “acute kidney injury”, “rasburicase”, and “allopurinol”.
Results
Prevention plays a pivotal role in TLS management. Adapted to the particular TLS risk, specific measures are initiated 24 h before induction of therapy. Hydration is the basal therapy. Allopurinol or rasburicase are added according to the TLS risk profile. Electrolyte abnormalities are adjusted depending on clinical symptoms, particularly in hypocalcemia combined with a calcium phosphate product > 60 mg2/dl2. In the case of manifest TLS with progressive kidney injury or uncontrolled electrolyte abnormalities, renal replacement therapy should be applied generously. Hyperuricemia, hyperphosphatemia, and hyperxanthinemia are able to induce kidney failure.
Conclusion
Avoiding TLS in combination with renal failure is the central aim. The latter compromises the body’s compensatory mechanisms and thereby aggravates the medical condition. Especially under rasburicase treatment, renal injury induced by calcium phosphate precipitates plays a key role. Under sufficient management the renal injury can be reversed.
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C. Nusshag, S. Fink und M. Zeier geben an, dass kein Interessenkonflikt besteht.
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Nusshag, C., Fink, S. & Zeier, M. Das Tumorlysesyndrom. Nephrologe 11, 6–13 (2016). https://doi.org/10.1007/s11560-015-0028-z
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DOI: https://doi.org/10.1007/s11560-015-0028-z