Acute interstitial nephritis (AIN) is an immune-mediated kidney injury. We studied its clinicopathological features, the role of corticosteroids, the outcomes, and the predictors of poor outcomes in biopsy-proven AIN. This was a 5-year retrospective, single-center observational cohort study of patients with biopsy-proven AIN. Of 2890 native renal biopsies, 61 (2.1%) had the features of AIN. The most common etiology was drug intake (27 patients), followed by infection-related AIN (14 patients), autoimmune conditions (six patients), malignancy (four patients), others (five patients), and unknown causes (four patients). Patients with autoimmune diseases were younger (
P
= 0.02), had a higher frequency of anemia (
P
= 0.004), and features of chronicity (
P
= 0.006). Hematuria (
P
= 0.004) and eosinophils (
P
= 0.05), and crystals in the tubules were mostly seen in drug-induced AIN. There was a significant difference in the recovery of patients receiving steroids within 1 week and 1 week after presentation. The predictors of poor outcomes were serum creatinine [hazard ratio (HR) = 1.4,
P
= 0.04)], an autoimmune etiology (HR = 3.2,
P
= 0.05), interstitial fibrosis or tubular atrophy (HR = 1.4,
P
= 0.04), and delayed treatment with corticosteroids (HR = 0.01,
P
= 0.04). Infections and ayurvedic medicines are important causes of AIN in India. The triad of eosinophils in the interstitium, oxalate crystals in the tubular epithelium, and red blood cells in the tubular lumen suggest drug-induced AIN. The initial time period is crucial, and we advocate using corticosteroids even before biopsy reports are available.