1, penicillins: almost all kinds of penicillins have caused this disease, but dimethoxypenicillin is the most. In recent years, there seems to be an increasing trend in the literature for amoxicillin (hydroxybenzyl penicillin) and oxypiperazine penicillin to cause the disease. The incubation period is usually 2 weeks, but can range from 2 days to several weeks. It is more common in children and the dose of the drug is not related to the onset of the disease. In addition to acute allergic interstitial nephritis, some cases present with renal sodium loss, hyperchloremic acidosis and hyperkalemia. The pathogenesis is related to the binding of penicillin semi-antigen to the tubular basement membrane, resulting in the formation of anti-tubular basement membrane antibodies. A few weeks after stopping the drug, the kidney function can be expected to recover, a few cases need dialysis treatment. 2, cephalosporins: the use of this class of drugs alone is not very high nephrotoxicity, but the combined use of aminoglycoside antibiotics can cause acute tubular necrosis and acute interstitial nephritis. 3, aminoglycosides: to cause non-oliguric acute renal failure as the main clinical features, often accompanied by renal loss of potassium and magnesium, can appear hypokalemia and hypomagnesemia. Usually there is an increase in blood creatinine after a few days of medication, generally not serious, so it is easy to be ignored; individual severe oliguric type of acute renal failure requires dialysis treatment. Acute tubular necrosis caused by this class of drugs is common, while acute interstitial nephritis is relatively rare. Neomycin is the most nephrotoxic drug in this class, followed by gentamicin and butamycin, tobramycin and etanercept, and streptomycin is the least. The severity of the disease is often proportional to the dose and duration of treatment, and the nephrotoxic effect increases significantly with the combination of other nephrotoxic drugs, cephalosporins, pre-existing renal insufficiency, advanced age, insufficient extracellular fluid volume, pre-existing liver disease and potassium deficiency. Discontinuation of drugs, appropriate supportive treatment and dialysis treatment if necessary, can often achieve satisfactory results. 4, tetracyclines: this class of drugs, except for doxycycline and dimethylaminotetracycline, should not be used because of the obvious accumulation effect in renal failure. This class of drugs can inhibit protein synthesis and cause nitrogen retention, which is more prominent when the original renal insufficiency. Desmethylgentamicin has a dose-related nephrogenic effect, so it can be used in hyponatremia with inappropriate antidiuretic hormone secretion syndrome, but can trigger acute renal failure if used in hyponatremia in cirrhosis. Although the latter is often reversible, its use should be avoided. Acute interstitial nephritis caused by expired tetracycline is often characterized by Fanconi syndrome. 5, anti-tuberculosis drugs: commonly used anti-tuberculosis drugs can cause acute interstitial nephritis, but rifampin is the most. Intermittent use or reuse after discontinuation, sometimes even another dose of rifampin, can cause acute interstitial nephritis. Clinically, it often presents as acute renal failure of the fever, chills, lumbago, anuria or oliguria type. More specifically, it is often associated with temporary hypercalcemia, the cause of which is unknown. Renal function can be restored after discontinuation of the drug, but sometimes quite slowly. Corticosteroids are not helpful for recovery. 6. Amphotericin B: One or several types of renal damage often occur after receiving more than 2 g of this product. Distal tubular impairment is the earliest, and distal tubular acidosis, nephrogenic uremia and nephrogenic potassium loss may occur; glomerular filtration rate is often normal; complete recovery is often possible with discontinuation of the drug at this time. The drug can cause ischemic renal damage due to renal vasoconstriction, which can lead to progressive and only partially recovered acute renal failure. Loss of sodium can aggravate the damage, sodium supplementation has a certain preventive effect. 7, sulfonamides: antibacterial sulfonamides and diuretic sulfonamides can cause acute interstitial nephritis. Combination of drugs, such as the use of cotrimoxazole or dihydrothiazide cooperation aminoglutethimide and the occurrence of the disease has a close relationship. Typical manifestations often occur within a few days of drug use, but those with acute interstitial nephritis caused by existing sulfonamides can have symptoms resurfacing within hours. The clinical manifestations are similar to those caused by penicillin, but the rash is less common, and dialysis is required in severe cases. Recovery is often possible after discontinuation of the drug, and corticosteroids are beneficial. For those who have renal disease, eosinophilia and/or significant decrease in renal function during treatment, as well as other signs and symptoms of allergic reactions, should be highly alert. 8, non-steroidal anti-inflammatory drugs: anti-inflammatory pain and other drugs can reduce prostaglandin synthesis, in the existing sodium deficiency, the effective circulation of blood volume, the elderly and pre-existing renal disease, prone to acute tubular necrosis due to inadequate renal perfusion, to oliguric type is more common. The risk is particularly high when combined with aminoglutethimide. Acute interstitial nephritis is commonly caused by fenoprofen, pramipexole, neproxen and other drugs. Large amounts of proteinuria are a distinctive feature, and nephrotic syndrome may occur; cytopenia, rash, and eosinophilia are not uncommon. In renal pathology, except for acute interstitial nephritis, it may be accompanied by fusion of glomerular epithelial cell peduncles. The onset of the disease may be days to months after drug administration. Recovery remains slow after timely discontinuation of the drug, often for months or years, and therefore dialysis treatment is often required. The effects of corticosteroids are uncertain, so they should not be used for more than 2 weeks. These drugs can also cause glomerulonephritis, systemic vasculitis, chronic interstitial nephritis, and renal papillary necrosis. In addition, this class of drugs has caused sodium and water retention, can aggravate the original heart failure and hypertension, but also can cause type IV renal tubular acidosis, all need to take into account. 9. Allopurinol: This product causes acute interstitial nephritis, which often develops around 3 weeks after the drug is administered. In addition to acute allergic interstitial nephritis, most of them have epidermal exfoliative maculopapular rash and acute liver function injury. The mortality rate is as high as 20%, and the common causes of death are severe systemic allergic reactions, sepsis, gastrointestinal bleeding, and acute hepatic and renal failure. The vast majority of cases occur at conventional therapeutic doses and are therefore thought to be related to allergic reactions. In many cases, there is pre-existing renal insufficiency, so the allergen is suspected to be allopurinol and its metabolites. Treatment includes discontinuation of the drug and supportive therapy as necessary, with dialysis if needed. The efficacy of corticosteroids is uncertain. Use with caution, especially after the application of diuretics, and reduce the dose in case of renal insufficiency. 10, histamine receptor antagonists and proton pump inhibitors: the first reported in this class of drugs is cimetidine, now involves almost all histamine receptor antagonists, omeprazole and other proton pump inhibitors have also been reported to cause acute interstitial nephritis. Clinically, it may be associated with polymyositis, and increased serum creatinine is then also associated with inhibition of creatinine secretion by the renal tubules by this product. Because T lymphocytes have histamine H2 receptors, cytotoxic and suppressive T lymphocytes are increased in the kidney and blood, so it is believed that the cell-mediated immune response is involved in the pathogenesis of the disease, which often recovers rapidly after discontinuation of the drug. 11, converting enzyme inhibitors: this product caused by nephrotoxicity is mainly affect the renal vasodilation, change the hemodynamics, causing acute tubular necrosis, especially when the double kidney or isolated renal artery stenosis. Some drugs have been shown to cause membranous nephropathy. Acute interstitial nephritis is also not uncommon. It often improves or recovers with timely discontinuation of the drug, but can often recur with reuse of the drug.