Painkillers may cause acute renal failure.

Xiao, a 53-year-old teacher, suspected gout and bought painkillers himself. Two days later, she developed edema and was diagnosed with acute renal failure. The report has aroused widespread concern in society, and various media have reprinted it to remind the public of the safety of drug use. Why do painkillers cause acute renal failure? How can we avoid such incidents?

What is a painkiller?

Pain is a protective response, which warns us to stay away from harmful dangers. Pain is also a bad feeling, accompanied by negative emotional reactions such as disgust and anxiety; Severe pain is even unbearable. Because pain triggers the stress response of the human body, it may also cause other injuries. Therefore, besides the endogenous pain control mechanism of human body can increase the tolerance to pain, people often need the help of drugs to relieve pain for moderate or above pain.

Clinically, all drugs acting on various aspects of endogenous regulation mechanisms such as pain stimulation, signal formation and transmission, pain formation and airway pain relief are collectively referred to as analgesics.

Classification of painkillers

There are two kinds of commonly used painkillers. One is narcotic painkiller, which is very painful. These drugs work by simulating or acting on the endogenous inhibition system of pain, such as opium, morphine and demerol. This kind of painkiller mainly acts on the central nervous system and is dependent on anesthesia and physiology. Therefore, the clinical use of narcotic drugs mandated by law is greatly restricted.

The other is anti-inflammatory painkillers. Both exogenous substances and various injuries will cause inflammatory reactions. During the reaction, various inflammatory mediators can stimulate pain through peripheral or central channels. By inhibiting or eliminating inflammatory reaction, substances that inhibit the production and function of inflammatory mediators can also relieve pain. These drugs are called anti-inflammatory and analgesic drugs.

According to the different chemical structures, anti-inflammatory and analgesic drugs can be divided into two categories. One is adrenocortical hormone, also known as glucocorticoid, which is the most effective anti-inflammatory and analgesic drug to inhibit inflammatory reaction and relieve pain through endogenous analgesic system. Because these drugs are steroid hormones, they are also called steroid anti-inflammatory and analgesic drugs.

Accordingly, other drugs with anti-inflammatory and analgesic effects without steroid ring structure are collectively called non-steroidal anti-inflammatory drugs (NSAIDs). Non-steroidal anti-inflammatory drugs are the most widely used drugs in clinic, commonly known as painkillers.

According to the chemical structure, NSAIDs can be divided into many types. For example, formic acid, also known as salicylic acid, stands for aspirin; Acetic acid: The representative drugs are diclofenac and indomethacin. Propionic acid: The representative drugs are ibuprofen and naproxen. Xikang: Piroxicam, Meloxicam, etc. Sibu: Celecoxib, rofecoxib, etc. Pyrazolone include metamizone, aminopyrine, phenylbutazone and oxyphenylbutazone. Others, such as nimesulide.

In addition, smooth muscle spasmolytic drugs can relieve smooth muscle spasmodic pain, skeletal muscle relaxants can relieve muscle tension pain, and anti-anxiety drugs and sedatives can relieve some pain. However, these categories are not classic painkillers.

Anti-inflammatory and analgesic mechanism of non-steroidal anti-inflammatory drugs

Prostaglandin (PG) is an important inflammatory mediator, which mediates pain and fever in inflammatory reaction. Prostaglandin is converted from a lipid substance called arachidonic acid existing on the cell membrane. Cyclooxygenase (COX) is the key enzyme in this transformation process. Non-steroidal anti-inflammatory drugs play an anti-inflammatory, analgesic and antipyretic role by inhibiting COX and reducing PG production.

In addition, NSAIDs can also inhibit the activity of phosphodiesterase, stabilize the lysosomal membrane by inhibiting phosphodiesterase (ADR), and reduce the release of lysosomes, thus inhibiting the inflammatory reaction.

Toxic mechanism of non-steroidal anti-inflammatory drugs

In 1990s, COX- 1 and COX-2 were found to be two isoenzymes of COX. COX- 1 is a structural enzyme, which exists in normal tissues such as blood vessels, stomach and kidney, and mainly mediates the formation of physiological prostaglandin. COX-2 is an inducible enzyme, which is produced in large quantities under the stimulation of inflammatory cytokines. It mainly exists in the inflammatory site and acts as an inflammatory mediator to promote the synthesis of prostaglandin.

Prostaglandins in normal tissues have many important physiological functions: dilating arteries, regulating renal blood flow and increasing renal filtration rate; Promote sodium excretion and lower blood pressure; Inhibit gastric acid secretion; Contraction of uterine muscle fibers and dissolution of corpus luteum; Tracheal smooth muscle relaxation; Nasal mucosa vasoconstriction; Inhibit platelet aggregation, etc.

NSAIDs inhibit the synthesis of prostaglandin in inflammatory tissues and play an anti-inflammatory role. At the same time, non-selective inhibition of prostaglandin synthesis in normal tissues leads to a series of side effects, especially in gastrointestinal tract and kidney.

NSAIDs acute renal injury

Acute renal injury caused by non-steroidal anti-inflammatory drugs is one of the common adverse drug reactions in clinic. Most of them can recover after stopping taking drugs, and a few can cause serious kidney injury or even death.