Tubulointerstitial nephritis can be divided into chronic tubulointerstitial nephritis and acute tubulointerstitial nephritis, infectious acute tubulointerstitial nephritis. Then, which drugs can cause tubulointerstitial nephritis? The following is an introduction to what are the drugs that cause tubulointerstitial nephritis. 1, penicillin: almost all kinds of penicillin have caused this disease, but to dimethoate benzylpenicillin for the most. In recent years, it seems that amoxicillin (hydroxyamphetamine benzylpenicillin) and oxpiperazine penicillin also have a tendency to increase in the literature. 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 medication is not associated with 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 renal tubular basement membrane, resulting in the formation of anti-renal tubular basement membrane antibodies. A few weeks after stopping the drug, 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-hyponatremic 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 drug use, which is generally not serious, so it is easy to be neglected; individual severe oliguric acute renal failure requires dialysis treatment. This class of drugs cause acute tubular necrosis is common, acute interstitial nephritis is relatively rare. The nephrotoxicity of this class of drugs is most common with neomycin, followed by gentamicin and butamidocanamycin, tobramycin and ethylcissomycin, and streptomycin is the least severe. The severity of the disease is often proportional to the dosage and duration of treatment, and the nephrotoxic effects are significantly increased by 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 the drug, appropriate supportive therapy and dialysis treatment, if necessary, can often obtain satisfactory results. 4, tetracycline class: this class of drugs in addition to prednisone and dimethylamine tetracycline, because in renal failure, there is obvious accumulation effect and should not be applied. This class of drugs can inhibit protein synthesis, causing nitrogen retention, more prominent in the original renal insufficiency. Nortriptyline has a dose-related nephrogenic uremic effect and can be used for hyponatremia with the syndrome of inappropriate secretion of antidiuretic hormone, but if used for hyponatremia in cirrhosis, it can trigger acute renal failure. Although the latter is often a reversible course, it should be avoided. Acute interstitial nephritis caused by expired tetracycline, often characterized by Fanconi syndrome. 5, anti-tuberculosis drugs: commonly used anti-tuberculosis drugs can cause acute interstitial nephritis, but rifampicin is the most. Intermittent use or use again after stopping the drug, sometimes even a dose of rifampicin, can cause acute interstitial nephritis. Clinical manifestations are often fever, chills, back pain, anuria or oliguria type acute renal failure. More specifically, it is often accompanied by temporary hypercalcemia, the cause of which is not known. Renal function recovers after discontinuation of the drug, but sometimes quite slowly. Corticosteroids are not helpful for recovery. 6, amphotericin B: receiving more than 2 grams of this product often appear one or several kinds of renal damage. Distal tubular function damage appears earliest, can appear distal tubular acidosis, renal dysuria and renal loss of potassium; glomerular filtration rate is often normal; at this time stopping the drug can often be completely recovered. This drug can cause renal vasoconstriction caused by ischemic renal damage, progressive and only partially recoverable acute renal failure can occur. 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. Combined use of drugs, such as the use of cotrimoxazole or dihydrothiazide cooperation amphotericin has a close relationship with the occurrence of this disease. Typical manifestations often occur within a few days of drug use, but those with existing sulfonamide-induced acute interstitial nephritis can have symptoms reappear within a few hours. Clinical manifestations are similar to those caused by penicillin, but the rash is less common, and severe cases also require dialysis. Recovery is often possible after discontinuation of the drug, and corticosteroid drugs are beneficial. For those who have renal disease, eosinophilia and / or renal function decreased significantly in the treatment, as well as other signs and symptoms of allergic reactions, should be highly vigilant. 8, non-steroidal anti-inflammatory drugs: anti-inflammatory pain and other drugs can make prostaglandin synthesis is reduced, in the existing sodium deficiency, effective circulating blood volume is insufficient, the elderly and the original renal disease, prone to acute tubular necrosis due to renal insufficiency of perfusion, with oliguria as the most common. The risk is particularly high in combination with amphotericin. Acute interstitial nephritis is commonly caused by fenoprofen, probenecid, and nepsilon. Massive proteinuria is a distinctive feature, and nephrotic syndrome may occur; cyturia, rash, and eosinophilia are uncommon. In nephropathology, except for acute interstitial nephritis, it may be accompanied by fusion of glomerular epithelial cell peduncles. The onset of the disease can be days to months after drug administration. Recovery remains slow after prompt discontinuation of the drug, often for months or years, so dialysis is often required. Corticosteroids have uncertain effects and should not be used for more than 2 weeks. This class of drugs can also cause glomerulonephritis, systemic vasculitis, chronic interstitial nephritis and renal papillary necrosis and other damage. In addition, this class of drugs have caused sodium and water retention, can aggravate the original heart failure and hypertension, but also can trigger type IV renal tubular acidosis, all need to take into account. 9, allopurinol: this product causes acute interstitial nephritis often in the drug about 3 weeks onset. In addition to acute allergic interstitial nephritis performance, the vast majority of epidermal exfoliative maculopapular rash, acute liver function impairment. 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 routine therapeutic doses and are therefore thought to be related to anaphylactic reactions. Many cases have pre-existing renal insufficiency, so the allergen is suspected to be allopurinol and its metabolites. Treatment consists of discontinuation of the drug and necessary supportive therapy, with dialysis if needed. The efficacy of corticosteroid drugs is not certain. Use this drug with caution, especially after the application of diuretics, and in renal insufficiency to reduce the amount of preventive significance. 10, histamine receptor antagonists and proton pump inhibitors: the first reported in this class of drugs is cimetidine, now almost involving all the histamine receptor antagonists, omeprazole and other proton pump inhibitors have caused acute interstitial nephritis reported. Clinically, it can be accompanied by polymyositis, and increased serum creatinine is also associated with the inhibition of tubular creatinine secretion by the product. Because T lymphocytes have histamine H2 receptor, cytotoxicity and inhibitory T lymphocytes increase in the kidney and blood, so it is believed that the cell-mediated immune response is involved in the pathogenesis of this disease, the disease is often rapidly recovered after stopping the drug. 11, converting enzyme inhibitors: the nephrotoxicity caused by this product is mainly to affect the renal vasodilatation, change the hemodynamics, causing acute tubular necrosis, especially when the double kidney or isolated renal artery stenosis. Some drugs proved to cause membranous nephropathy. It is not uncommon to cause acute interstitial nephritis. Timely discontinuation of the drug can often be improved or recovered, and reuse of the drug can often recur.