Renal failure can be divided into acute and chronic conditions. The progression of acute renal failure is rapid, usually due to insufficient blood supply to the kidneys (such as trauma or burns), functional damage caused by blockage of the kidneys due to certain factors, or damage caused by toxins, leading to the occurrence of acute renal failure. The main cause of chronic kidney failure is long-term kidney disease, which gradually decreases in kidney function over time and causes the occurrence of kidney failure.
Drug induced acute renal failure can be very serious, even life-threatening, and prevention should be the primary principle. One type of drug-induced acute renal failure is unrelated to dosage and belongs to allergic constitution, while the other type is closely related to drug dosage and course of treatment. Before its occurrence, there are often some susceptible factors or potential factors that already exist in certain populations. If nephrotoxic drugs are used or overused on this basis, acute renal failure can easily occur. Therefore, in clinical practice, the prevention of drug-induced acute renal failure can be approached from the following aspects:
① Before taking medication, a detailed medical history and drug allergy history should be consulted, and drugs with previous allergic symptoms should be prohibited;
② Strictly control the use of nephrotoxic drugs: the elderly, children, diabetes, hypertension, hypercoagulability and hypovolemia patients should be cautious when using drugs. These patients are prone to drug-induced acute renal failure. Dehydrated patients should replenish their fluids before taking medication. Patients with cardiac insufficiency and liver disease should consider the dosage of medication due to renal perfusion issues and decreased detoxification ability of the liver; Patients with kidney disease should avoid using non steroidal anti-inflammatory drugs as much as possible; Even for the normal population, it is necessary to strictly control the dosage and course of nephrotoxic drugs when there is a need for medication such as a cold;
③ Avoid co use of nephrotoxic drugs: if cephalosporins are not suitable for combined use with aminoglycosides. Aminoglycosides should not be used in combination with diuretics as much as possible;
④ The renal toxicity of contrast media is only inferior to aminoglycosides. The predisposing factors are: excessive dose of contrast media or repeated contrast media, old age, dehydration, insufficient renal perfusion or renal damage, diabetes, hypertension or multiple myeloma. Therefore, patients with the above diseases should try not to do contrast examinations, and then supplement sufficient liquid before receiving iodine contrast media;
⑤ Before tumor chemotherapy, allopurinol should be taken in advance to reduce the formation and excretion of uric acid;
⑥ Liquid supplementation should be done before and during chemotherapy (such as cisplatin) to reduce the incidence of nephrotoxicity;
⑦ Some drugs that are prone to forming crystals in urine should be treated with both alkaline urine and hydration to avoid renal tubular obstruction;
⑧ It is not advisable to use 6-aminocaproic acid for the treatment of nephrogenic bleeding to avoid causing obstruction of blood clots in the ureter. Even if using this drug for other hemorrhagic diseases, close observation is also advisable;
⑨ If necessary, drug blood concentration monitoring should be carried out: if the peak plasma concentration of gentamicin exceeds 12mg/L, renal toxicity significantly increases. Measuring the concentration of cyclosporin also helps to adjust its dosage in a timely manner to avoid ARF caused by toxoplasmosis;
⑩ When using drugs that may cause acute renal failure, especially those with direct renal toxicity damage, it is advisable to monitor them, such as measuring urinary lysozyme, B-N-acetylglucosamine transferase, B2 microglobulin, and other sensitive indicators that reflect renal tubular damage, in order to detect renal damage early and stop taking drugs as soon as possible to avoid acute renal failure. For drugs that mediate acute renal failure through hemodynamics, such as angiotensin converting enzyme inhibitors, blood urea nitrogen, creatinine, and even CFR can be measured to observe whether they cause reversible renal damage. Early renal damage returns to normal after discontinuation of medication.
Some people believe that acute renal failure in hospitalized patients is partly iatrogenic and mostly drug-induced, which deserves attention.
If kidney damage is still in the early stage, it can be controlled through medication and diet, but there is no hope of recovery for end-stage renal failure. For chronic kidney failure, there are only two ways to treat it: kidney washing therapy or kidney transplantation. Kidney transplantation refers to the process of transplanting the kidney of an organ donor into the body of a transplant recipient through surgery. A family member, spouse, close friend, or person who has died of brain damage and signed their consent to donate organs during their lifetime. Of course, the most matched kidney usually comes from the siblings of the recipient, as their genetic compatibility is the most likely.
Kidney transplantation is currently the best method for treating kidney failure, as the kidney transplanted into the patient's body can almost completely replace the function of the already failed kidney, allowing the patient to live a normal life. Unfortunately, not every patient with renal failure has the opportunity to receive a kidney transplant. This is because there may not be suitable kidneys or relatives willing to donate kidneys, or because the number of organ donors after brain death is much lower than the number of those in need. It takes a long time for patients to wait for a suitable kidney for kidney transplantation, as the donor's kidney must match the patient's body. At this point, the patient must undergo regular kidney washing treatment to maintain life until a new kidney can be obtained through transplantation surgery.