Renal interstitial damage has different clinical manifestations due to its different etiology and is nonspecific. The main prominent manifestation is oliguric or non-oliguric acute renal insufficiency, which may be accompanied by non-specific manifestations such as fatigue and weakness, fever and arthralgia. Loss of renal tubular function may present with hypospecific and hypoosmolar urine, tubular proteinuria, and disturbances in water, electrolyte, and acid-base balance, with some patients presenting with Fanconi syndrome. History of infection or drug application, clinical manifestations, and some laboratory and imaging tests help in the diagnosis, but renal pathology remains the gold standard for diagnosing interstitial nephritis. Acute interstitial nephritis should be considered in the clinical presentation of unexplained acute renal insufficiency. Chronic interstitial nephritis should be considered if the following clinical features are present: ① the presence of triggers leading to chronic interstitial nephritis, such as long-term use of painkillers, chronic urinary obstruction, etc., or a family history of chronic interstitial nephritis; ② clinical manifestations of tubular dysfunction, such as nausea, polyuria, nocturia, renal tubular acidosis, etc., or renal insufficiency without hypertension, hyperuricemia, etc.; ③ urinalysis shows serious Impaired tubular function. A small amount of small molecule proteinuria (<2.0 g/24 hours), urinary RBP, lysozyme, urinary β2-microglobulin, and NAG are elevated, and glycosuria and aminoaciduria may be present. Chronic interstitial nephritis requires further etiologic clarification based on history and clinicopathologic features.