Antihypertensive Therapie bei Diabetes mellitus View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2001

AUTHORS

U. O. Wenzel , F. Thaiss , R. A. K. Stahl

ABSTRACT

Brenner und Mitarbeiter aus Boston haben Mitte der 80er Jahre im Tiermodell gezeigt, dass eine antihypertensive Therapie die Entwicklung der diabetischen Nephropathie hemmt und dass ACE-Hemmer konventionellen Antihypertensiva überlegen sind (Anderson et al. 1985, 1992, 1986, 1989; Zatz et al. 1986). Dass hoher Blutdruck das Fortschreiten der diabetischen Nephropathie beschleunigt, wurde von Berkmann aber schon vor mehr als 20 Jahren berichtet. Er fand bei einem Patienten mit einseitiger Nierenarterienstenose die typische noduläre diabetische Glomerulosklerose nur in der dem hohen Blutdruck ausgesetzten Niere, nicht aber in der durch die Nierenarterienstenose vor der Hypertonie geschützten ischämischen Niere (Berkmann u. Rifkin 1973). Fast 50 Jahre nach der Beschreibung der diabetischen Veränderungen an der menschlichen Niere durch Kimmelstiel und Wilson zeigten die ersten systematischen Untersuchungen an Patienten von Mogensen, dass eine antihypertensive Therapie bei Patienten mit Typ 1-Diabetes und Nephropathie die Albuminurie senkte und den Filtratverlust verlangsamte (Kimmelstiel u. Wilson 1936; Mogensen 1982). Parving und Mitarbeiter haben den Nutzen einer antihypertensiven Therapie dann in mehreren Arbeiten bei Patienten mit Typ 1-Diabetes und Nephropathie bestätigt (Parving 1991; Parving et al. 1983, 1991, 1996b). Die grundlegenden Arbeiten von Parving und Mitarbeitern über die antihypertensive Therapie bei Diabetes wurden zunächst mit Diuretika, β-Blockern, Vasodilatoren und zentral wirkenden Antihypertensiva durchgeführt (Parving et al. 1987). Diese Therapie reduzierte den monatlichen Verlust der glomerulären Filtrationsrate (GFR) von 1 ml/min auf 0,3 ml/min. Klinisch bedeutet das, dass die terminale Niereninsuffizienz damit nicht nach 7, sondern erst nach 15–20 Jahren erreicht wird. More... »

PAGES

191-206

Book

TITLE

Klinische Diabetologie

ISBN

978-3-642-64016-2
978-3-642-59539-4

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-642-59539-4_13

DOI

http://dx.doi.org/10.1007/978-3-642-59539-4_13

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1022932772


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130 schema:description Brenner und Mitarbeiter aus Boston haben Mitte der 80er Jahre im Tiermodell gezeigt, dass eine antihypertensive Therapie die Entwicklung der diabetischen Nephropathie hemmt und dass ACE-Hemmer konventionellen Antihypertensiva überlegen sind (Anderson et al. 1985, 1992, 1986, 1989; Zatz et al. 1986). Dass hoher Blutdruck das Fortschreiten der diabetischen Nephropathie beschleunigt, wurde von Berkmann aber schon vor mehr als 20 Jahren berichtet. Er fand bei einem Patienten mit einseitiger Nierenarterienstenose die typische noduläre diabetische Glomerulosklerose nur in der dem hohen Blutdruck ausgesetzten Niere, nicht aber in der durch die Nierenarterienstenose vor der Hypertonie geschützten ischämischen Niere (Berkmann u. Rifkin 1973). Fast 50 Jahre nach der Beschreibung der diabetischen Veränderungen an der menschlichen Niere durch Kimmelstiel und Wilson zeigten die ersten systematischen Untersuchungen an Patienten von Mogensen, dass eine antihypertensive Therapie bei Patienten mit Typ 1-Diabetes und Nephropathie die Albuminurie senkte und den Filtratverlust verlangsamte (Kimmelstiel u. Wilson 1936; Mogensen 1982). Parving und Mitarbeiter haben den Nutzen einer antihypertensiven Therapie dann in mehreren Arbeiten bei Patienten mit Typ 1-Diabetes und Nephropathie bestätigt (Parving 1991; Parving et al. 1983, 1991, 1996b). Die grundlegenden Arbeiten von Parving und Mitarbeitern über die antihypertensive Therapie bei Diabetes wurden zunächst mit Diuretika, β-Blockern, Vasodilatoren und zentral wirkenden Antihypertensiva durchgeführt (Parving et al. 1987). Diese Therapie reduzierte den monatlichen Verlust der glomerulären Filtrationsrate (GFR) von 1 ml/min auf 0,3 ml/min. Klinisch bedeutet das, dass die terminale Niereninsuffizienz damit nicht nach 7, sondern erst nach 15–20 Jahren erreicht wird.
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