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DOI: 10.1055/s-0038-1629361
Akute Niereninsuffizienz im Neugeborenenalter
Acute kidney injury in the neonatePublication History
Eingereicht am:16 September 2013
angenommen am:23 September 2013
Publication Date:
31 January 2018 (online)

Zusammenfassung
Eine akute Niereninsuffzienz (AKI) im Neugeborenenalter stellt eine Herausforderung an den Neonatologen dar. Häufig kann in der Neonatalzeit nicht eindeutig zwischen einer akuten und chronischen Niereninsuffizienz unterschieden werden, auch können Überlappungen bestehen. Ein Volumenmangelschock, z. B. aufgrund einer Sepsis stellt einen zeitlich definierten Beginn einer akuten prärenalen Niereninsuffizienz dar. Die bereits intrauterin terminierte Nie reninsuffizienz, bedingt z. B. durch eine genetische Anlagestö-rung der Nieren, wird durch die Geburt erstmals manifest. Hier besteht also eine bereits chronische, anlagebedingte Insuffizienz neben einer akuten Insuffizienz durch die Abnabelung. Durch eine ausgeprägte postrenale Abflussstörung kann es bereits intrauterin zu einer Fehlentwicklung des Nierenparenchyms mit Nephronenverlust kommen. Durch die
Geburt ist das Neugeborene erstmals auf seine eigene Nierenfunktion angewiesen. Eine zusätzliche Belastung des Systems, z. B. durch arterielle Hypotonie, kann dann das labile Gleichgewicht zerstören. Während prä- und postrenale Niereninsuffizienzen meist rasch diagnostiziert und therapiert werden können, ist die Ursache der renalen Niereninsuffizienz kausal schwieriger zu diagnostizieren und oft nur symptomatisch zu behandeln. Auch eine Dialysebehandlung mit evtl. späterer Transplantation muss als Behandlungsoption erwogen werden. Frühgeborene sind besonders gefährdet.
Summary
Acute kidney injury (AKI) of the neonate is a serious challenge to the neonatologist. Distinction between acute kidney injury and chronic renal insufficiency in the neonatal period is not always possible, and overlaps of the two entities may occur. Hypoperfusion and hypovolemia secondary due to sepsis are often the triggering event of subsequent acute prerenal insufficiency. In most cases, the time of onset can be determined. Genetic conditions interfering with normal renal development predispose the neonate to chronic renal insufficiency that may present as acute kidney injury at the time of birth. Further severe postrenal obstruction in utero can result in dysplastic development of the fetal renal parenchyma with nephron loss. After birth, when the neonate depends solely on its own kidney function, additional stressors like systemic arterial hypotension can modify the fragile balance. While pre- and postrenal insufficiencies are relatively easy to diagnose and treat, the etiology of renal insufficiency is often difficult to determine. In many cases, the underlying disease can only be treated symptomatically. Dialysis and, finally, kidney transplant have to be considered. Preterm neonates are at higher risk for acute kidney injury with an overall higher rate of long-term morbidities.
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