Abstract

Acute tubulointerstitial nephritis was formerly only observed during the early phase of infections. With the emergence of antibiotics this disease became a rarity. In contrast the importance of drug-associated acute tubulointerstitial nephritis grew in importance and is now the most common form and expression of a hyperergic reaction of the kidneys. Acute tubulointerstitial nephritis occurs as a third form in cases of systemic autoimmune diseases, e.g., in idiopathic tubulointerstitial nephritis or within the scope of Sjögrens syndrome with distal tubular acidosis. The common symptoms of the drug-induced form are fever, side pain, microhematuria or macrohematuria and a mostly sharp increase in creatinine levels but to a greatly differing extent. Histologically, there is interstitial edema and interstitial lymphocyte-rich infiltration with tubulitis. The symptoms can be subclinical or even non-existent. In most case remission occurs, sometimes only partial remission or transformation to chronic interstitial nephritis. Risk factors are for example delayed diagnosis, recurrent episodes and the accompanying use of analgesics. The more acute and intense the clinical symptoms are, the earlier the diagnosis and therefore the better the prognosis. A temporary steroid treatment can promote regression.

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