Klinische Wochenschrift

, Volume 63, Issue 18, pp 978–987 | Cite as

Medikamentöse Behandlung der chronisch verlaufenden Glomerulonephritiden: Contra

  • K. Andrassy
  • R. Waldherr
  • E. Ritz
Zum Geleit

Zusammenfassung

Das Thema der therapeutischen Beeinflussung der entzündlichen Pathomechanismen bei chronisch-idiopathischer Glomerulonephritis bedarf einiger kritischer Anmerkungen. Eine ätiologische Behandlung ist nur in Ausnahmefällen möglich (infektiöse Tropenkrankheiten, infizierter ventrikuloatrialer Shunt etc.). Einer erfolgreichen Beeinflussung der Pathomechanismen, welche die glomeruläre Entzündung auslösen und unterhalten, steht unsere Unkenntnis über die im einzelnen verantwortlichen Schritte entgegen. Neuere Untersuchungen legen Schlüsselrollen für die terminale Komponente des Komplementsystems, Produkte des Lipoxygenaseabbauweges der Arachidonsäure sowie Sauerstoffradikale nahe, welche therapeutisch nicht oder nur beschränkt beeinflußbar sind. Ferner beruht die Progredienz glomerulärer Entzündungen in die Niereninsuffizienz in der Regel auf fortschreitender Sklerosierung von Glomerulus, Gefäßen und Interstitium und nicht auf zunehmenden aktiv entzündlichen glomerulären Läsionen. Beispielhaft wurden bei der Sichtung der veröffentlichten kontrollierten Therapiestudien die Untersuchungen bei extramembranöser und membranoproliferativer Glomerulonephritis herausgegriffen. Hierbei wurde eine im Ausmaß nur beschränkte, und nicht in allen Studien gesicherte, Beeinflussung der Nierenfunktion gefunden, der andererseits erhebliche Nebenwirkungen gegenüberstehen. Eine abschließende Wertung kommt zu dem Urteil, daß eine medikamentöse Beeinflussung der entzündlichen Pathomechanismen fragwürdig ist, daß jedoch ein therapeutischer Nihilismus nicht angezeigt ist angesichts der Beeinflußbarkeit unspezifischer Schädigungsmechanismen (antihypertensive Behandlung, diätetische Intervention).

Schlüsselwörter

Glomerulonephritis Extramembranöse Glomerulonephritis Membranoproliferative Glomerulonephritis Lupus erythematodes Steroide Plättchenhemmer 

Drug treatment of chronic glomerulonephritides: Contra

Summary

It is controversial whether the pathomechanisms involved in chronic idiopathic glomerulonephritis are susceptible to therapeutic intervention. Etiological therapy, i.e. elimintion of the responsible antigen, is possible only in exceptional cases, e.g. tropical diseases, infected ventriculoatrial shunt etc. Antiinflammatory therapy directed against pathomechanisms initiating or maintaining glomerular inflammation has an uncertain theoretical foundation because of lack of knowledge relating to the exact steps mediating tissue injury. Recent studies suggest keyroles for terminal components of complement system, products of lipoxygenase pathway of arachidonic acid and oxygen radicals — all of which are not readily influenced by available therapeutic modulaties. Finally, progression of glomerular inflammation to renal failure is usually not the cause of cumulative acute inflammatory glomerular lesions but rather the consequence of progressive sclerosis of glomeruli, arterioles and interstitium. As examples of controlled intervention trials, studies on extramembranous and membranoproliferative glomerulonephritis are discussed. The studies show limited and not always statistically significant influence on renal function, however, at the expense of considerable side effects. It is concluded that it is highly questionable whether inflammatory pathomechanisms are influenced by currently available drugs. However, therapeutic nihilism is not appropriate given modalities to influence mechanisms of nonspecific damage, e.g. by antihypertensive medication or dietary intervention.

Key words

Glomerulonephritis Extramembraneous glomerulonephritis Membranoproliferative glomerulonephritis Lupus erythematosus Steroids Antiplatelet agents 

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Copyright information

© Springer-Verlag GmbH & Co. KG 1985

Authors and Affiliations

  • K. Andrassy
    • 1
  • R. Waldherr
    • 2
  • E. Ritz
    • 1
  1. 1.Medinische Klinik der Universität HeidelbergGermany
  2. 2.Pathologisches Institut der Universität HeidelbergGermany

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