With the progress of modern medicine and the widespread use of interventional therapy in cardiovascular diseases, the incidence of drug-induced kidney injury is increasing year by year. According to relevant data, acute kidney injury caused by drugs up to 28.9%, patients over 60 years of age accounted for 51%, combined with underlying diseases of chronic kidney disease is the most common, accounting for about 20%. In addition to causing acute renal failure, drug-related kidney injury can also cause acute interstitial nephritis, acute nephritis syndrome, nephrotic syndrome, acute obstructive nephropathy, chronic kidney damage, etc. If early detection and timely treatment, it can be reversed. Otherwise, it can progress to chronic renal failure, and serious cases require long-term dialysis treatment, causing serious harm to patients. 1.What are the drugs that cause kidney damage? There are thousands of drugs that cause kidney injury, as follows: (1) aminoglycosides, such as gentamicin, kanamycin, streptomycin, butamycin, etc.; (2) contrast agents, such as panadol, etc.; (3) painkillers and non-steroidal drugs, such as paracetamol, aspirin, indomethacin, pautazone, ibuprofen, etc.; (4) aristolochic acid drugs, such as Chinese medicine Guanmutong, Han (5) Anti-cancer drugs, such as cisplatin, mitomycin, methotrexate, etc.; (6) Antifungal drugs, such as amphotericin B, etc.; (7) Sulfonamides, such as sulfadiazine, sulfamethoxazole, etc.; (8) Immunosuppressive drugs, such as cyclosporine A, cyclophosphamide, etc.; (9) Anti-tuberculosis drugs, such as rifampin, etc.; (10) Penicillins, such as methylpenicillin, benzyl (11) Cephalosporins, such as cephalexin, cefadroxil, cefazolin, cefradine, etc.; (12) Antihypertensive drugs, such as converting enzyme inhibitors, etc.; (13) Biological products, such as interleukin 2, interferon, penicillamine and allopurinol, etc.; (14) Anti-thyroid drugs, such as propylthiouracil, etc.; (15) Hypolipidemic drugs, such as statins (15) lipid-lowering drugs, such as statins, etc. The most common drugs in clinical practice are antibiotics, contrast agents and painkillers. 2, the causes and mechanisms of drug-related kidney injury (1) direct nephrotoxicity. Some drugs and their metabolites are excreted by the kidneys, which can directly cause nephrotoxicity. The renal tubules, especially the proximal tubules, due to its concentration and reabsorption function, so that it is exposed to high concentrations of toxins, vulnerable to drug toxicity. Some drugs can cause tubular cytotoxic reactions by impairing mitochondrial function, interfering with tubular transport, enhancing oxidative stress or generating free radicals, resulting in tubular epithelial cell necrosis. The extent of such damage is dose dependent. (2) Drugs cause renal ischemic injury by affecting renal vascular and hemodynamic changes. Such as non-steroidal drugs, converting enzyme inhibitor drugs and immunosuppressants such as cyclosporine A and tacrolimus. (3) Immunoinflammatory response. Drugs can act as semi-antigens and deposit in the glomerular and tubular basement membranes, thus activating complement to cause immune injury and leading to acute interstitial nephritis. The injured renal intrinsic cells, including necrotic tubular epithelial cells, can produce new antigens, resulting in the production of autoantibodies and aggravating the injury. For example, penicillin-induced kidney injury. Such injury is not related to the drug dose and time of use. (4) Some drugs themselves or metabolites are easy to form crystals in the kidney tissue, deposited in the distal tubular lumen, blocking the urinary flow, stimulating interstitial reaction, causing obstructive nephropathy, such as sulfonamide antibiotics caused by kidney injury. (5) Metabolic disorders. Anti-tumor drugs can cause tumor cell lysis syndrome with deposition of uric acid and calcium and phosphorus crystals, which manifests as hyperuricemia and hypercalcemia, leading to kidney injury. Vitamin D causes disorders of calcium and phosphorus metabolism can cause interstitial nephritis and renal calcification, and diuretics can cause water-electrolyte disorders, which can lead to kidney injury. (6) Rhabdomyolysis. Some drugs can induce rhabdomyolysis through direct toxic effects on myocytes, or indirect damage to myocytes, resulting in the release of myoglobin and creatine kinase into the blood, myoglobin through direct toxic effects and blockage of renal tubules, resulting in acute renal failure. Such as lipid-lowering drugs of statins. (7) Thrombotic microangiopathy. Thrombotic microangiopathy of organ damage, often associated with platelet thrombosis in the microcirculation, the mechanism of immune-mediated and direct endothelial toxicity, commonly used drugs such as antiplatelet drugs. 3, the clinical manifestations of drug-related kidney injury (1) acute renal tubular necrosis. Drug nephrotoxicity caused by acute tubular necrosis, acute renal failure is mostly non-oliguric type, manifested as a rapid increase in blood creatinine, urea nitrogen, creatinine clearance rate decreased, urine specific gravity and urine osmolality decreased, metabolic acidosis and electrolyte disorders. In severe cases, the disease is often unrecoverable and gradually evolves into chronic renal failure, or worse, requires long-term dialysis to maintain life. Aminoglycoside antibiotics cause the most, followed by cephalosporin antibiotics and amphotericin B class. (2) Acute interstitial nephritis. The clinical manifestations are: ① systemic allergic reactions: mainly drug fever, drug rash, generalized lymph node enlargement, joint pain, blood eosinophils, blood IgE elevation; ② renal allergic reactions, manifested as aseptic leukocyturia; renal tubular function damage can lead to acute renal failure. At this time, if the drug can be timely discontinued or the application of hormones and desensitizing drugs, the renal function can be restored to normal. Often caused by penicillins and cephalosporins. (3) Acute nephritis syndrome or nephrotic syndrome. The immune response caused by drugs leads to glomerulonephritis, with clinical manifestations of proteinuria, hematuria, elevated blood pressure and edema, and in a few cases, high edema and nephrotic syndrome manifestations. Commonly steroids, reserpine, penicillamine and biological products caused by kidney damage. (4) Chronic kidney damage. Long-term use of analgesics, calcium antagonists or lithium may lead to chronic kidney damage. 4, drug-related kidney damage how to determine? Drug-related kidney damage may be restored if it can be detected early and treated early. Therefore, the use of drugs must be closely observed, once there is little or no urine, hematuria, unexplained edema, lumbar swelling and pain, unexplained increase in blood creatinine should be highly suspicious of the possibility of drug-induced kidney damage, must immediately discontinue the suspected drugs, can be judged according to the following two points: (1) the history of drug use that may produce kidney damage, including the specific drug type, dosage course, the interval between the use of drugs and the occurrence of kidney damage, after discontinuation of drugs renal recovery. (2) Early laboratory tests for drug-related kidney injury include: urine β2 microglobulin, urine microalbumin, transferrin, NAG enzyme, protein/creatinine ratio, endogenous creatinine clearance, serum CystatinC, NGAL, and renal injury molecule-1. Serum CystatinC is highly sensitive in the diagnosis of drug-related kidney injury. Urine microalbumin mainly reflects the glomerular filtration function, γ-glutamyl transferase for tubular injury indicators, the combination of the two tests is conducive to the early detection of kidney injury and determine whether it is glomerular or tubular injury and the degree of drug-related kidney injury is a more ideal screening index. 5, drug-related kidney injury prevention and control measures (1) close observation of clinical manifestations, close monitoring of urinary enzymes, urine protein, urine microalbumin, blood creatinine and CystatinC and other indicators of change, once identified as drug-related kidney injury, immediately stop or replace the drug to prevent further aggravation of kidney damage, except aristolochic acid nephropathy, most early kidney damage can be reversed. (2) Promote drug excretion, protect renal function, support therapy, correct electrolyte and acid-base balance imbalance, and renal replacement therapy should be performed in patients with severe acute renal failure. (3) Early judgment and timely treatment of drug-related kidney injury is the key to improve the prognosis. Some preventive measures can reduce the incidence of drug-related kidney injury, such as sulfonamides in the formation of crystals in the urine during the drug period need to drink more water and alkalinization of urine; the use of amphotericin B, cyclosporine A can be used simultaneously with calcium antagonists to reduce its impact on the kidney; such as allergy-induced interstitial nephritis can be short-term application of adrenocorticotropic hormone and prohibit the use of allergenic drugs and derivatives of the drug. 6, kidney disease patients how to use drugs correctly? (1) Patients with underlying renal disease are prohibited from taking aminoglycosides, such as gentamicin, kanamycin, streptomycin and the Chinese medicine Guanmutong. (2)When using drugs in patients with kidney disease, the metabolic pathway of the drug should be clarified, and the drug excreted by the kidneys should be reduced in dose and prolonged according to the degree of kidney function damage. (3) In patients older than 60 years old, diabetic patients, patients with glomerular filtration rate <60 ml/min, and patients with decreased renal reserve capacity should pay attention to dose reduction. (4) When consuming converting enzyme inhibitors in elderly patients, it is necessary to know whether there is stenosis of renal artery or whether there is stenosis of renal artery when using converting enzyme inhibitors with elevated blood creatinine, and to use converting enzyme inhibitors with caution when learning creatinine >265umol/l. (5) Contrast agents should be used with caution when there is underlying renal disease. If renal insufficiency combined with acute myocardial infarction requires intervention, coronary angiography should be done first after hemodialysis, and then hemodialysis and hydration therapy after angiography. (6) Patients with primary nephrotic syndrome presenting with elevated blood creatinine should try not to use cyclosporine A, tretinoin and other kidney-damaging drugs. (7) Drug allergy history must be inquired before drug use, and the indications of drugs, side effects must be strictly grasped to avoid abuse. Pay attention to the dosage and therapeutic course in drug application, and when multiple drugs are used in combination, pay attention to the related effects of drugs. (8) Try to use equivalent and less nephrotoxic drugs in patients with existing damage to renal function.