Aktuelle Rheumatologie 2012; 37(05): 306-312
DOI: 10.1055/s-0032-1323681
Übersichtsarbeit
© Georg Thieme Verlag KG Stuttgart · New York

Die tubulointerstitielle Nephritis

Tubulointerstitial Nephritis
F. Strutz
1   Fachbereich Nephrologie, Stiftung Deutsche Klinik für Diagnostik, Wiesbaden
› Institutsangaben
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Publikationsverlauf

Publikationsdatum:
27. September 2012 (online)

Zusammenfassung

Die tubulointerstitielle Nephritis ist eine häufige Ursache für einen akuten Anstieg der Retentionswerte und sollte daher auch von Rheumatologen in ihren Grundzügen gekannt werden. Sie ist gekennzeichnet durch eine im Tubulointerstitium der Niere ablaufende Inflammation. Es kann eine akute von einer chronischen Form unterschieden werden. Bei der akuten Form der tubulointerstitiellen Nephritis findet sich die medikamentös induzierte Form am häufigsten, wobei Antibiotika, nicht-steroidale Antiphlogistika und Protonenpumpenhemmer besonders häufig induzierende Medikamente darstellen, also Medikamente, die auch bzw. gerade von Rheumatologen häufig eingesetzt werden. Diagnostisch hilft insbesondere eine sorgfältige Anamnese weiter. Eosinophilie, Eosinophilurie, Proteinurie, Hämaturie kommen häufig, aber nicht immer vor. Die klassiche Trias ist dagegen selten. Dies gilt natürlich noch mehr für die nicht-allergischen Erkrankungsformen. Eine definitive Diagnose aller Formen der interstitiellen Nephritis ist weiterhin nur mittels Nierenbiopsie möglich. Dies gilt auch für die in den letzten Jahren zunehmend beschriebene IgG4-Form, die einige charakteristische histologische Veränderungen aufweist. Die wichtigste therapeutische Maßnahme bei der allergischen Form besteht in der Beendigung der induzierenden Medikation. Möglicherweise ist auch eine frühzeitig eingeleitete Glukokortikoidtherapie eine zusätzliche Therapieoption. Auch bei den systemischen Entzündungen inklusive der IgG4-assoziierten Nephritis sind Glukokortikoide therapeutisch in den meisten Fällen sehr gut wirksam. Bei schweren Fällen (Verdoppelung des Kreatininwertes, ausgeprägte Proteinurie, Oligurie oder Anurie, Gewichtszunahme) sollte immer ein Nephrologe zur weiteren Diagnostik und Therapie hinzugezogen werden.

Abstract

Tubulointerstitial nephritis is a common cause of acute increases in creatinine and BUN values and should thus be known by the rheumatologist, at least in general terms. It is characterised by an inflammatory reaction within the tubulointerstitial space of the kidney. A chronic form must be distinguished from an acute form of the disease. In regard to the acute form of tubulointerstitial nephritis, the drug-induced variant is the most common form of the disease. Antibiotics, non-steroidal anti-inflammatory drugs and proton pump inhibitors are among the most common drugs inducing interstitial nephritis, these are drugs often used by rheumatologists. Diagnosis is usually made by carefully evaluating the medical history of the patient. Eosinophilia, eosinophiluria, proteinuria, and haematuria are common, but are not found in all cases. The classical triad is uncommon. This is even more common in the non-allergic variants of the disease. A definite diagnosis of tubulointerstitial nephritis can only be made by kidney biopsy. This is also true for the IgG4-associated form of interstitial nephritis which has a number of particular histological changes not common to other forms of the disease. In regard to therapy, the most important measure for the drug-induced variant is the cessation of the inducing drug. In addition, early application of glucocorticoids may hasten resolution of the interstitial inflammation. In addition, glucocorticoids may be very helpful in the therapy for the interstitial inflammation in those forms that are associated with systemic disease including IgG4-associated nephritis. A nephrologist should always be consulted in severe cases (robust increases of creatinine value, robust proteinurie, oliguria or anuria, increases in body weight) for further diagnosis and therapy.

 
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