Abstract
Jegliche Vesikopathie des Kindesalters dreht sich von Anfang an um gestörte Speicherung und um gestörte Entleerung, bedingt entweder obstruktiv, permanent wie temporär, oder refluxiv oder neurogen. Molekulargenese und Morphogenese bedingen einander. Frühembryonaler Beginn der Obstruktion verändert den Detrusor dysplastisch und veranlaßt mittels vorzeitigem Verschluß des Urachus aszendierend urorenale Dysplasie. Spätembryonaler Beginn der Obstruktion gestaltet den Detrusor hyperkollagenisierend mittels Faser- und Nuxusverarmung hypopiastisch und induziert aszendierend hypoplastische Uronephropathie. Vorzeitige Erschöpfung des Dehnungspotentials bedingt Residualharn. Refluxive Vesikopathie, aus trigonaler Dysmorphic und Desorganisation, verhält sich zur obstruktiven Vesikopathie vorausgehend und koinzidental, ist nicht obstruktiv verursacht. Fehlerhafte Knospenanlage hat viel Anteil. Neurogene Vesikopathie, später erscheinend, form- und funktionslädierend, gleicht sich beiden an, der obstruktiven wie der refluxiven Komponente. Zusätzlich bringt Neurogenität verschieden hohe Grade der Harninkontinenz erschwerend hinzu, Blasendivertikel sind ein Sonderfall der obstruktiven Vesikopathie. Kollagenisiertheit des krankhaften Detrusors erschwert jede Art von operativer Harnleitereinpflanzung. Bakterielle Urethrozystitis, mit und ohne Pyelonephritis, überkommt jede Form der kongenitalen Vesikopathie. Extremform der chronisch erkrankten und reduzierten Harnblase ist die Endstadien-Schrumpfblase. Enuresis ist Ausdruck einer neuroregelativen Funktionsstörung einer verspäteten Maturation.
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Sigel, A. (2001). Krankheitslehre der Harnblase des Kindesalters. In: Sigel, A., Ringert, RH. (eds) Kinderurologie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-08080-1_4
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