Acute tubulointerstitial nephritis

　　Acute tubulointerstitial nephritis is an allergic toxicity to drug treatment. Only a few drugs (in more than 80 related drugs) are associated with most cases, and the identification of drug-related etiology is important because severe renal damage can often be prevented or reversed. Sarcoidosis, legionellosis (a systemic disease with pneumonia as the main manifestation caused by legionella), leptospirosis, streptococcal and viral infections, and certain traditional Chinese herbal medicines may also be related.

　　Acute tubulointerstitial nephritis generally has a good prognosis, and renal damage can usually be restored after stopping the related drugs. However, for chronic persistent interstitial renal damage, the prognosis is poor, and it can lead to chronic renal insufficiency.

　　Acute tubulointerstitial nephritis presents with various symptoms, but the typical manifestation is acute renal failure associated with medication or infection, which is transient and may be accompanied by oliguria. Fever is present in most cases, and may be accompanied by rash. White blood cells, red blood cells, and white blood cell casts are often found in the urine sediment, but sometimes no abnormalities are present. In 75% of cases, there may be sex-eosinophils in both blood and urine, and proteinuria is usually small in amount. Nonsteroidal anti-inflammatory drug-induced diseases are characterized by a lack of fever, rash, and eosinophilia, but often there is nephrotic-range proteinuria associated with glomerular微小病变（also seen in ampicillin, rifampin, interferon, or ranitidine). Many patients present with signs of tubular dysfunction, such as polyuria (defects in concentration), reduced volume (defects in Na conservation), hyperkalemia (defects in K excretion), and metabolic acidosis (defects in acid excretion).

　　There is no effective preventive measure for acute tubulointerstitial nephritis. For drug-induced cases, attention should be paid to medication safety. Have regular meals, avoid overexertion, and maintain a regular lifestyle.

　　Renal biopsy is the only method to diagnose acute tubulointerstitial nephritis. The earliest manifestation is interstitial edema, followed by typical interstitial lymphocytes, plasma cells, eosinophils, and a small amount of neutrophils. In severe cases, inflammatory cells can invade the intercellular spaces between the cells lining the tubular basement membrane (tubulitis). In other specimens, granuloma reactions secondary to methicillin, sulfonamides, mycobacteria, and fungi may be seen.

　　Patients with acute tubulointerstitial nephritis should rest in bed, drink plenty of water, and consume more than 2500 milliliters of water per day to increase urine output and promote the rapid excretion of bacteria, toxins, and inflammatory secretions. Patients can eat acidic foods or take a large amount of vitamin C to acidify the urine. The diet should be light and easy to digest, and should provide abundant nutrition, including sufficient calories, a sufficient amount of high-quality protein, and vitamins.

　　The treatment of acute tubulointerstitial nephritis mainly involves treating acute rheumatic fever, tracking and observing renal changes, and paying attention to differential diagnosis. Since the disease is short-term and self-limiting, no special treatment is required, and it generally improves or returns to normal with the improvement of rheumatic fever. If hematuria is significant, refer to the treatment of IgA nephritis.