Acute renal insufficiency

　　One, pre-renal azotemia

　　1, The reasons for decreased vascular content include hemorrhage, gastrointestinal loss, dehydration, excessive diuresis, and others.

　　2, The situation of systemic vascular resistance sepsis, allergic reaction, anesthesia, the use of drugs to reduce the afterload of the heart. Angiotensin-converting enzyme inhibitors, non-steroidal anti-inflammatory drugs, adrenaline, norepinephrine, anesthetics, and cyclosporine can all cause a decrease in glomerular filtration function.

　　3, Insufficient cardiac output leading to insufficient effective circulating volume, cardiac shock, congestive heart failure, pulmonary embolism, pericardial tamponade, and other causes lead to decreased renal blood perfusion.

　　Two, post-renal azotemia

　　Including urethral obstruction, bladder dysfunction or obstruction, ureteral or renal pelvis obstruction. Benign prostatic hyperplasia, bladder, prostate, or cervical cancer, retroperitoneal fibrosis, or neurogenic bladder can all lead to urinary tract obstruction.

　　Uncommon causes include bilateral ureteral calculi, urethral calculi, and renal papillary necrosis. In patients with solitary kidneys, unilateral urinary tract obstruction can cause post-renal azotemia.

　　Three, renal parenchymal

　　1, Glomerulonephritis, post-infection glomerulonephritis after severe infection, and nephrotic syndrome with ARF.

　　2, The pathological manifestations of acute interstitial nephritis are interstitial inflammation with edema and tubular damage. It is mainly caused by drugs, other causes include infectious diseases, immune diseases, or idiopathic diseases.

　　3, The etiology of acute tubular necrosis is ischemia and poisoning.

　　4, Renal vascular disease is relatively rare.

　　Four, the occurrence of chronic renal insufficiency based on

　　Chronic glomerulonephritis complicated with acute interstitial nephritis, diabetic nephropathy complicated with contrast nephropathy, and various glomerulonephritis causing prerenal azotemia after the use of ACE inhibitors.

　　1, Cardiovascular system complications include hypertension, arrhythmia, heart failure, pericarditis, and others.

　　2, Metabolic acidosis and electrolyte disorder may lead to hyponatremia, severe acidosis, and hyperkalemia. One of the most dangerous complications of acute renal failure is severe acidosis.

　　3. Gastrointestinal complications: Manifested as hematemesis, melena, anorexia, abdominal distension, nausea, vomiting, etc., and bleeding is mostly due to stress ulcers or erosion of the gastrointestinal mucosa.

　　4. Hematological complications: Due to the rapid decline in renal function, it can lead to a decrease in erythropoietin, thus causing anemia, but most cases are not severe. However, in a small number of patients, the reduction in coagulation factors may lead to a tendency to bleed.

　　5. Infection: It is one of the most serious and common complications, often seen in acute renal failure of hypermetabolic type caused by burns, trauma, etc.

　　6. Neurological complications: May manifest as coma, epilepsy, headache, drowsiness, muscle spasms, etc. Neurological complications and acid-base imbalance, retention of toxins in the body, electrolyte disorders, and water intoxication are closely related.

　　1. Pre-renal azotemia may present with oliguria and increased blood urea nitrogen.

　　2. Post-renal azotemia may present with sudden anuria or intermittent anuria.

　　3. Renal parenchymal disease can present differently depending on the affected site.

　　(1) RPCN has an acute nephritic syndrome.

　　(2) Typical oliguric phase, polyuric phase, and recovery phase of oliguric ATN.

　　(3) Drug-induced AIN often has a history of medication use, and a few have a history of allergy. It presents with interstitial tubular dysfunction, such as anemia, hypokalemia, normal blood glucose with positive urine glucose, and acidosis that is not parallel to the decline in renal function.

　　(4) Renal vascular ARF with malignant hypertension, unilateral or bilateral large vessel lesions.

　　1. First, treat the primary disease, such as hypertension, diabetes, etc., to prevent the exacerbation of renal artery and glomerular sclerosis.

　　2. Actively control infection, especially urinary and respiratory tract infections, and prevent secondary infection.

　　3. Actively correct water and electrolyte balance and acid-base balance disorders.

　　4. Diuresis and correction of heart failure.

　　5. In terms of diet, consume a high-calorie, high-quality low-protein, low-phosphorus diet supplemented with essential amino acids, appropriate vitamins, minerals, and trace elements.

　　6. Avoid catching cold, dampness, and overexertion, prevent colds, and do not use drugs that damage the kidneys.

　　7. Adequate and effective dialysis.

　　8. Comprehensive treatment for complications is required, including correcting anemia, preventing gastrointestinal bleeding, and anticoagulation therapy for those with hypercoagulable states. For patients with progressive disease, it is advisable to switch to hemodialysis therapy as soon as possible.

　　1. Routine blood test

　　Significant anemia, with normal cellular anemia, normal or increased white blood cell count. Thrombocytopenia, and accelerated erythrocyte sedimentation rate.

　　2. Urinalysis for renal insufficiency

　　There are differences in the initial disease, but the common points are:

　　1. The urine osmolality is reduced, usually below 450 mOsm per kilogram, with a specific gravity of less than 1.018, and in severe cases, it is fixed between 1.010 and 1.012. During the urine concentration and dilution test, the amount of nocturnal urine is greater than that of the daytime, and the specific gravity of each urine sample is over 1.020, with the difference between the highest and lowest specific gravity less than 0.008;

　　2. Urine output decreases, usually below 1000ml per day;

　　3. Urinary protein levels increase, and in the late stage, due to the vast majority of glomeruli being destroyed, urinary protein levels反而 decrease;

　　4. Urine Sediment Examination, the number of white blood cells in the urine sediment increases (commonly full of the field in the acute phase, and 5/field in the chronic phase), and sometimes white blood cell casts can be produced.

　　5. Urine Bacterial Examination: This method of nephritis examination is relatively simple. When there are a large number of bacteria in the urine, Gram staining examination can be performed on the urine sediment smear, and 90% of the bacteria can be found. The results of the examination have a high positive rate.

　　3. X-ray Examination

　　When X-ray examination is performed, if the patient's nephritis recurs repeatedly or the patient's condition has developed to a state that is difficult to control, X-ray examination should be used for nephritis at this time, including abdominal X-ray, intravenous pyelography, and micturition cystogram. The purpose is to exclude the presence of stones, congenital malformations of the urinary system, nephroptosis, and other lesions.

　　For patients with acute renal failure, avoid spicy, salty, and high-protein foods. Diet should be high in calories, high-quality low-protein, low-phosphorus, with essential amino acids, appropriate vitamins, minerals, and trace elements.

　　1. The treatment of pre-renal azotemia should first find the cause.

　　2. When ARF is suspected to be caused by post-renal obstruction, a catheter should be placed in the bladder. The residual urine volume in the bladder can increase, or a large amount of urine retained due to obstruction can be drained.

　　3. For severe acute poststreptococcal glomerulonephritis after renal实质性 disease, treatment should be primarily supportive and symptomatic, and dialysis may be applied when necessary; for nephrotic syndrome complicated with ARF, hormone treatment for nephrotic syndrome should be actively applied, and dialysis therapy may be supplemented when necessary. The key to treatment is to discontinue sensitizing drugs, and corticosteroid treatment may be necessary when necessary. The treatment of mild ATN is mainly supportive and symptomatic conservative treatment. Malignant hypertension should be gradually and actively reduced. Early renal artery or renal vein thrombosis or embolism and other large vascular diseases of the kidney should be treated with thrombolytic and anticoagulant therapy accordingly.