Acute Tubulointerstitial Nephritis

Abstract

Acute interstitial nephritis (AIN) is an important cause of acute kidney injury (AKI). The presence of AKI due to AIN is thought to be as high as 10–27% with approximately 23–58% of patients requiring acute dialysis. However, this is likely to be an underestimate as often most cases that are highly suspicious for AIN are treated empirically without a renal biopsy, especially in the elderly and those where a renal biopsy may be contraindicated. The pathophysiology of the condition is poorly understood but is likely related to an immunologically mediated hypersensitivity reaction. The commonest cause of AIN is drugs (70–75%), autoimmune and systemic disease (10–20%), infections (4–10%) and idiopathic (5–10%). The clinical presentation often associated with AIN includes the classical triad of a maculopapular rash, eosinophilia/eosinophiluria and fever. However, these findings are seen in only one-third of AIN cases. Definitive diagnosis of AIN is made from a renal biopsy which reveals interstitial inflammation with lymphocyte predominance with normal glomeruli and vessels. The immunofluorescence is typically negative in AIN. The treatment of AIN includes treating the underlying cause if known. In AIN caused by drugs, often discontinuation of the offending drug may help resolve the AKI. However, several studies have supported the use of corticosteroid therapy to aid renal recovery in AIN. Steroid-sparing agents, e.g. mycophenolate and cyclosporine, have been used in isolated cases with success. The long-term outlook for AKI due to AIN is generally good, but up to 44% of patients with AIN will require ongoing renal replacement therapy.