Acute renal damage (AKI), once known as acute renal failure, is a clinical syndrome of severe reduction of kidney function in a short period of time due to multiple causes. Not only does it seriously affect the health of the patient, but it can also cause a series of complications and even endanger life. Knowledge of acute kidney damage is of great importance for early detection, timely treatment and improved patient prognosis. I. Causes of acute kidney damage The causes of acute kidney damage are complex and can be broadly classified into pre-renal, renal and post-renal. Prenal factors are mainly caused by insufficient renal blood infusion, which is common in cases of reduced effective circulatory blood capacity, such as extensive haemorrhage, severe dehydration and heart failure. When the body is in a state of shock, the kidneys are not provided with sufficient blood, and there is a significant decline in the rate of renal balls filtering, leading to acute kidney damage. The kidney factor refers to the damage caused by the disease of the kidney itself, of which acute kidney tube failure is most common, mostly caused by adrenal ischaemic, renal toxic substances (e.g., drugs, film-making agents, heavy metals, etc.). In addition, nephrocyte diseases, internal and renal vascular diseases may cause acute kidney damage. For example, certain self-immuno-immuno-inflammatory diseases cause nephro-nephrenia, or drug-inflammatory inflammation. Post-renal factors, such as urinary blockages, prostate growth and tumour oppression, can hinder normal urine discharges, leading to higher internal pressure within the kidney, which in turn affects the kidney function. II. Symptoms of acute kidney damage Symptoms of acute kidney damage varied at different stages. During the initial period, the patient may have only symptoms of a pregenital disease, such as severe post-traumatic pain, excessive haemorrhage leading to headache, etc., and changes in kidney function may not yet be apparent. Utility is a more typical stage of acute kidney damage, and patients usually have less urine (24 hours with less than 400 ml) or less than 100 ml, accompanied by an oedema, which can be seen as oedema, edema to the lower limbs and even edema to the whole body, as a result of renal drainage disorders and fluid retention in the body. In addition, there may be signs of digestive systems such as nausea, vomiting and appetite, due to the accumulation of toxins in the body, which affects the gastrointestinal function. As the condition evolves, patients may experience cardiovascular system symptoms such as hypertension, heart failure and cardiac disorders, as well as other systems such as respiratory difficulties and cognitive disorders. The urinary period is characterized by a gradual increase in the amount of urine, which can reach 3000 – 5000 ml per day, and even more, at a time when the oedema of patients is gradually decreasing, but due to the high number of urinations, hydrolytic disorders such as low potassium haemorrhage, sodium haemorrhage and sodium haemorrhage may occur, requiring close monitoring and timely adjustment. At the time of recovery, the patient ‘ s urine has gradually returned to normal and the kidney function has improved, but full recovery may take months or even longer, and some patients may leave behind different levels of kidney damage. III. Diagnosis of acute kidney damage The diagnosis of acute kidney damage is based on patient ‘ s history, symptoms, signs and relevant laboratory examinations. Detailed inquiries into the patient ‘ s recent trauma, surgery, infection, history of medication, etc. are essential to identify the cause of the disease. During the medical examination, care is taken to observe the vital signs of the patient, the edema, the signs of urinary obstruction, etc. In terms of laboratory examinations, serocelline acetic anhydride and urea nitrogen are commonly used as indicators for the assessment of kidney function, and in cases of acute kidney damage, serocal acetic anhydride and urea nitrogen tend to rise rapidly in a short period of time. In addition, urine tests, including urine routines, urine permeation pressure and sodium urine, are required to determine the functioning of the kidney tube. For example, in cases of pre-renal acute kidney damage, urine penetration pressure is usually high and sodium is low, while in cases of kidney acute kidney damage, urine penetration pressure may decrease and sodium is elevated. Video-testing, such as ultrasound, CT etc., helps to detect morphological anomalies in kidneys and urinary blockages. In cases where the cause of the disease is unknown, a renal examination may also be required to determine the pathology of the kidney and to guide the treatment. Treatment for acute kidney damage The principles of treatment for acute kidney damage are the removal of causes, the maintenance of internal environmental stability, the prevention and treatment of complications and the promotion of renal function rehabilitation. For acute kidney damage caused by pre-renal factors, the key is to supplement blood capacity, to correct the state of shock, and to restore renal blood injections through rapid infusion of liquids such as saline, plasma, erythrocyte, etc. At the same time, active treatment is required for primary diseases, such as control of heart failure, bleeding, etc. The treatment for acute kidney damage is more complex, and for acute kidney tube failure, the use of drugs or other renal toxicity substances that may cause kidney damage is first discontinued. During urination, the intake of liquids is strictly controlled, and the principle of “to measure” is followed to prevent complications such as heart failure and pulmonary oedema due to excess fluids. At the same time, dietary adjustments are needed to limit the intake of protein, potassium, phosphorus, etc., in order to reduce the kidney burden. Complications such as potassium haematosis and metabolic acid poisoning are treated in a timely manner, such as the use of calcium to counter the toxic effects of potassium haematosis on the heart and the use of sodium carbonate to correct metabolic acid poisoning. During urinary periods, care is taken to supplement moisture and electrolyte to prevent hydrolytic disorders. Treatment for post-renal acute kidney damage is mainly to remove urinary road barriers, such as the removal of stones from surgery and the treatment of prostate growth, so as to restore the flow of the urinary path. Renal substitution treatment, such as blood dialysis, peritoneal dialysis, etc., may be required for seriously ill patients to remove toxins and excess water from the body, maintain internal environmental stability and create conditions for renal function restoration. V. Prevention of acute kidney damage The key to preventing acute kidney damage lies in the active treatment of primary diseases and the avoidance of risk factors that may lead to kidney damage. In the use of drugs, especially those with potential renal toxicity (e.g. amino-clucose antibiotics, inflammatory drugs, etc.), the renal function changes are closely monitored by rigorous control of the adaptive certificate and dose. For patients requiring a photographic examination, the kidney function should be fully assessed and appropriate waterization measures should be taken before and after the examination to reduce the damage to the kidneys caused by the agent. In cases where there is a risk of a lack of effective cyclic blood capacity, such as the elderly, diabetics, cardiovascular diseases, etc., water should be replenished in a timely manner to avoid dehydration and shock. In addition, regular medical examinations, monitoring of kidney function indicators and early detection and treatment of possible kidney diseases are important measures to prevent acute kidney damage. Acute kidney damage is a serious clinical syndrome, with complex causes, diverse symptoms, diagnosis and treatment. By in-depth knowledge of their causes, symptoms, diagnosis and treatment, as well as by actively taking preventive measures, we are better able to cope with the disease, improve its treatment and quality of life and reduce its morbidity and mortality. Both health-care workers and the general population should focus on the prevention and treatment of acute kidney damage and work to maintain kidney health.
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