Tubulointerstitial nephritis can be divided into chronic tubulointerstitial nephritis and acute tubulointerstitial nephritis, infectious acute tubulointerstitial nephritis. So, which drugs can cause tubulointerstitial nephritis? The following are some of the drugs that cause tubulointerstitial nephritis.1. Penicillin: Almost all kinds of penicillin have caused this disease, but dimethoxyphenicillin is the most. In recent years, there seems to be an increasing trend in the literature for those caused by amoxicillin (hydroxybenzyl penicillin) and oxypiperazine penicillin. 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. 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. After several weeks of discontinuation, renal 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, hypokalemia and hypomagnesemia can occur. 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 when other nephrotoxic drugs, cephalosporins, pre-existing renal insufficiency, advanced age, insufficient extracellular fluid volume, pre-existing liver disease and potassium deficiency are combined. The drug can be discontinued, appropriate supportive treatment and dialysis treatment if necessary, often to obtain 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. The 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 in 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 uropathy and nephrogenic potassium loss may occur; glomerular filtration rate is often normal; complete recovery is often achieved by stopping 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. The 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. The patient should be highly alert to the presence of eosinophilia and/or a significant decrease in renal function, as well as other signs and symptoms of allergic reactions. 8. non-steroidal anti-inflammatory drugs: drugs such as anti-inflammatory pain can reduce the synthesis of prostaglandins, which can lead to acute tubular necrosis due to insufficient renal perfusion in people with sodium deficiency, insufficient effective circulating blood volume, the elderly and pre-existing renal disease. The most common type is oliguric. The risk is particularly high when combined with aminoglutethimide. Acute interstitial nephritis is commonly caused by fenoprofen, proneurofen and neproxen. Large amounts of proteinuria are the distinctive feature, and nephrotic syndrome may occur; cyturia, rash, and eosinophilia are not uncommon. Renal pathology may be accompanied by glomerular epithelial cell peduncle fusion in addition to acute interstitial nephritis. The onset of the disease can be several days to months after drug administration. Recovery remains slow after timely discontinuation, often for months or years, so 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 often in about 3 weeks of drug onset. In addition to acute allergic interstitial nephritis, the majority 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. It is important to use this drug with caution, especially after the application of diuretics, and to reduce the dose in renal insufficiency. 10. Histamine receptor antagonists and proton pump inhibitors: The first drug in this class was reported as cimetidine, and now almost all histamine receptor antagonists are involved, and proton pump inhibitors such as omeprazole have 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 diseased kidneys and blood, so it is believed that cell-mediated immune response is involved in the pathogenesis of the disease, which often recovers rapidly after discontinuation of the drug.11, angiotensin-converting enzyme inhibitors: the nephrotoxicity caused by this product mainly affects renal vasodilation, altering hemodynamics and causing acute tubular necrosis, especially in both kidneys or isolated When the renal artery stenosis. Some drugs have been shown to cause membranous nephropathy. Acute interstitial nephritis is also not uncommon. It often improves or recovers when the drug is discontinued in time, but can often recur when the drug is reintroduced.