Acute renal failure during pregnancy

　　The factors causing acute renal failure during pregnancy include various causes of hypovolemia, renal vascular spasm, and microvascular hemolysis, occasionally due to toxic damage, the main ones are described as follows.

　　1. Hypovolemia with massive blood loss is seen in placenta previa, early placental abruption, stillbirth, and postpartum hemorrhage; severe dehydration is seen in severe pregnancy-induced vomiting.

　　2. Renal vascular spasm is often part of systemic vascular spasm, which can be secondary to hypovolemia; endotoxin stimulation or specific manifestations of certain obstetric complications such as severe hypertension during pregnancy.

　　3. Microvascular hemolysis is caused by hemolysis, hemoglobinuria, and the formation of fibrin thrombi in the glomerular capillaries associated with acute renal failure, which is seen in acute fatty liver of pregnancy, HELLP syndrome, and other conditions.

　　4. Other complications occasionally occur in blood type mismatched transfusions, amniotic fluid embolism, and rarely due to obstruction of acute renal failure caused by compression of the ureter by a large uterus.

　　There are many complications of acute renal failure during pregnancy, common ones include the following:

　　1. Infection is one of the most common and serious complications, often seen in severe trauma, burns, and other causes of hypermetabolic acute renal failure.

　　2. Cardiovascular system complications, including arrhythmia, heart failure, pericarditis, hypertension, etc.

　　3. Neurological complications, including headache, drowsiness, muscle twitching, coma, epilepsy, etc., are related to the retention of toxins in the body, water intoxication, electrolyte disorder, and acid-base balance disorder.

　　6. There is a possibility of spontaneous abortion.

　　According to the different stages of acute renal failure during pregnancy, the common symptoms are also different. The specific introduction is as follows:

　　1. Oliguria stage

　　In the early stage of acute renal failure during pregnancy, the clinical manifestations are often masked by the symptoms of the primary disease, such as persistent shock caused by different reasons, hemolytic reaction, toxic symptoms, etc., which enter the oliguria stage after several hours or 1 to 2 days. The prognosis is poor for those with oliguria exceeding one month, and renal insufficiency is difficult to recover. Edema, hypertension, heart failure, electrolyte disorder, metabolic acidosis, azotemia, infection, anemia with bleeding tendency, decreased hemoglobin, pale complexion and nail beds, subcutaneous ecchymosis, hematoma at the injection site, gastrointestinal bleeding, and other symptoms may occur.

　　2. Polyuria phase

　　Patients in the polyuria phase may have polyuria, electrolyte imbalance, azotemia, and often have low fever, which is highly susceptible to infection. Therefore, intensive monitoring should be strengthened.

　　3. Recovery phase

　　After the oliguria and polyuria phases, the tissue is extensively damaged, and during the recovery period, symptoms such as weakness, anemia, weight loss, and muscle atrophy are common. Sometimes, symptoms of peripheral neuritis may occur. It often takes 3 to 6 months, or even up to a year, to fully recover.

　　To reduce the incidence of acute renal failure during pregnancy, it is recommended that pregnant women pay attention to the following preventive measures:

　　1. Prevent the occurrence of the primary disease, understand the indications, contraindications, and usage of nephrotoxic drugs; strictly implement operational procedures for blood collection, blood matching, and blood transfusion to prevent acute renal failure caused by incompatibility of blood types. These measures fundamentally prevent the occurrence of acute renal failure syndrome.

　　2. Actively rescue critically ill patients and control the diseases that induce acute renal failure early. For example, placental abruption, obstetric hemorrhagic shock, amniotic fluid embolism, and severe pregnancy-induced hypertension syndrome are all diseases that are highly likely to lead to acute renal failure. Therefore, when these diseases occur, they should be actively treated, the primary disease focus should be removed, and pregnancy should be terminated in a timely manner to prevent or alleviate shock and disseminated intravascular coagulation, and to control the induction of acute renal failure.

　　3. Rapidly correct functional oliguria Once functional oliguria is caused by pathogenic factors, rapid measures should be taken to restore it to normal, thereby reducing the incidence of organic oliguria.

　　The examination of acute renal failure during pregnancy can be handled according to the normal acute renal failure. Common examination items include the following:

　　1. Urine examination

　　Urine volume: The urine is acidic, and if the 24-hour urine volume is less than 400 ml, observing the urine volume per hour is the best method to discover acute renal failure early. Therefore, it is advisable to place a catheter early to calculate the urine volume; if the patient cooperates, it is recommended to urinate once per hour to avoid the risk of infection from indwelling catheters.

　　Urine specific gravity: In the early stage, the specific gravity can be normal or increased, and then it decreases and stabilizes at about 1.012. If the urine specific gravity is higher than 1.020, it often indicates dehydration.

　　Urine constituents: In functional oliguria, there are usually only transparent or fine-grained casts. During acute tubular necrosis, there are large amounts of epithelial cell casts, degenerative cell casts, coarse-grained casts, and a large number of renal tubular epithelial cells. During renal cortex necrosis, there may be hematuria, hemoglobinuria, pigment casts, and necrotic epithelial cell casts.

　　Urine sodium concentration: During the oliguria phase, tubular damage reduces the ability to reabsorb sodium salts, resulting in increased urine sodium and a concentration usually between 30 to 60 mmol/L.

　　2. Routine blood examination

　　The total white blood cell count can reach about 20×10^9/L, with neutrophils accounting for 80% to 95%; the degree of anemia depends on the presence of bleeding, hemolysis, and the extent of nitrogen retention. The hematocrit usually decreases to 20% to 25%. When there is disseminated intravascular coagulation, the platelet count decreases.

　　3. Blood Chemistry

　　Blood biochemical tests show increased levels of blood urea nitrogen, creatinine, and serum potassium concentration, and decreased levels of serum sodium, chloride, calcium, and carbon dioxide binding power. In acute tubular necrosis, the ability of renal tubules to absorb water decreases, and the ratio of urine urea to blood urea is often below 15, and the ratio of urine creatinine to blood creatinine decreases to below 20.

　　4. Urine-Plasma Osmotic Pressure Ratio

　　This ratio reflects the concentrating and diluting ability of renal tubules. When renal tubules are damaged, due to poor concentrating function, the ratio is often below 1.15.

　　5. Diuresis Test

　　If there is no significant increase in urine output even after blood volume is replenished, diuresis test can be performed to differentiate. First, inject 100-125ml of 20% mannitol intravenously, and the urine output per hour should not exceed 40ml, indicating renal failure; if mannitol is ineffective, replace it with intravenous injection of 40-60mg of furosemide, and if the urine output per hour exceeds 40ml, it still indicates good renal function.

　　There are no special dietary requirements for patients with acute renal failure during pregnancy, and general normal diet is sufficient. It is important to ensure a rich and balanced diet, and meet the needs of calories, proteins, and vitamins required for normal human metabolism. Appropriately increase the intake of vegetables and fruits.

　　Acute renal failure during pregnancy should first be treated for the primary disease, then prevent and treat complications such as infection, and finally, timely treatment of acute renal failure is also needed. The following is a specific introduction to the treatment of this disease:

　　I. Treatment of Oliguria Phase

　　1. Strictly control fluid intake;

　　2. Pay attention to dietary structure;

　　3. Correct electrolyte imbalance;

　　4. Correct metabolic acidosis;

　　5. Prevent and treat infection;

　　6. Treat hypertension and heart failure;

　　7. Use dialysis therapy.

　　II. Treatment during Polyuria and Recovery Phase

　　The polyuria phase indicates that the condition is improving, but due to the incomplete recovery of renal tubular function, patients still have serious water and electrolyte imbalances and azotemia, and the body's weakness is also prone to infection. Therefore, it is still necessary to treat it as oliguria phase at the beginning and not to relax various precautions.