Recently, some patients have seen articles on the internet about adefovir causing kidney damage and are very concerned, especially those who have taken and are taking adefovir against hepatitis B virus. Adefovir is a nucleoside reverse transcriptase inhibitor (NRTI) whose main mechanisms of action include: (1) competition for deoxynucleoside triphosphate substrates; and (2) termination of viral DNA strand lengthening. The drug was first developed for combination therapy of AIDS (trade name Preveon, dose 60-120 mg/d), but the Food anddrug administration (FDA) denied the application in 1999 because of significant kidney damage when taken at therapeutic doses. Gilead later restarted studies of the drug for the treatment of hepatitis B. It was approved by the FDA in September 2002 under the trade name Hepsera for the treatment of hepatitis B. The following year, the drug was also approved in Europe. The following year it was also approved in Europe, and in China, after phase II/III clinical trials, the Chinese Drug Administration (CFDA) approved the drug for marketing in China in 2005, and millions of people are currently taking it in China. I. Clinical performance A large number of studies have illustrated that adefovir is safe for renal function at a dosage of 10 mg/d, and a number of previous foreign and domestic large clinical trials have shown that this dosage is effective and safe for hepatitis B treatment. However, with the increased use of adefovir for hepatitis B treatment, reports of related renal damage have gradually increased. I have also found several cases of adefovir-induced renal damage and low phosphorus osteochondrosis in patients in clinical practice. Their clinical manifestations are also mainly symptoms related to tubular damage, including: (1) mild renal function abnormalities (elevated creatinine), decreased blood uric acid, phosphorus and potassium, corresponding elevated 24-hour urine sodium, phosphorus and potassium, and may present with renal glycosuria and proteinuria, combined with renal tubular acidosis. (2) Some patients have complex proximal tubular dysfunction, i.e. Fanconi syndrome, which manifests as renal glycosuria, total amino acid urine, and elevated urinary phosphate. (3) Severe cases may be combined with acute renal failure. II. Mechanism of occurrence Adefovir is excreted in its original form through the kidney by a combination of glomerular filtration and active tubular secretion. There are many studies on adefovir-associated renal damage, and it is currently believed that the occurrence of nephrotoxicity may be related to active uptake by the organic anion transporter (HOAT1) on the basolateral side of the proximal tubule and rate-limiting secretion mediated by multidrug resistance-associated protein 2/4 (MRP2/4) on the luminal membrane side. Adefovir-induced renal damage is characterized by 3 features: dose dependence, time dependence and reversibility. Domestic scholars have conducted a literature review study showing that the renal damage associated with 10 mg/d doses of adefovir is from Asian populations. Consider the possible causes: it may be related to HOAT1 gene polymorphism, higher incidence of hepatitis B, and relatively lower body weight in Asian populations. III. How to monitor and treat Patients taking adefovir, especially those with a history of renal disease and elderly patients, should be strictly aware of its adverse effects on renal function. Clinically, based on the patient’s history of hepatitis B and medication history, combined with their related renal injury manifestations: such as progressive worsening of nocturia, secondary bone pain, osteoporosis, auxiliary tests suggesting impaired tubular function and decreased blood phosphorus, the possibility of this diagnosis needs to be considered after excluding other rheumatic diseases such as arthritis, multiple myeloma, etc. Treatment is also relatively easy, stop taking adefovir and switch to other antiviral drugs such as entecavir, and apply symptomatic treatment such as phosphorus supplementation and anti-osteoporosis to achieve significant relief. Regular monitoring of blood creatinine, electrolytes and liver function and viral replication is required. In conclusion, adefovir should remain relatively safe for most patients in the treatment of hepatitis B. The mechanism of its nephrotoxicity in Asian populations still needs further research to clarify. For this disease there is no clear diagnostic criteria, it is recommended to monitor renal function and electrolytes every 3 months during the drug administration for proper prevention and treatment.