Acute glomerulonephritis in pregnancy
Introduction
Introduction to pregnancy with acute glomerulonephritis Patients with clinical symptoms of acute glomerulonephritis (acuteglomerulonephritis) actually include acute glomerular disorders caused by multiple causes, many of which are caused by bacterial, viral, and protozoal infections. This section discusses acute infections. Glomerulonephritis, acute glomerulonephritis caused by streptococcal infection and acute glomerulonephritis caused by non-streptococcal infection. basic knowledge The proportion of the disease: the proportion of the disease in a specific pregnancy group is 3% Susceptible population: pregnant women Mode of infection: non-infectious Complications: heart failure, hypertensive encephalopathy, acute renal failure
Cause
Pregnancy with acute glomerulonephritis
(1) Causes of the disease
The cause of acute nephritis in pregnant women is the same as that of non-pregnant women. The incidence of acute nephritis is mostly caused by the immune response caused by streptococcal infection. It belongs to an immune complex type nephritis from the pathogenesis, and some patients are infected by other bacteria (such as pneumonia). Caused by bacteria caused by bacteria such as cocci, staphylococcus, meningococcus, or viral infections (such as mumps virus, measles virus, etc.).
(two) pathogenesis
1. Physiological changes in the kidney during pregnancy
(1) Renal blood flow and renal plasma flow: blood flow in the kidney encounters resistance in two main parts, namely the glomerular glomerular arteries (also called the small arteries) and the bulging arteries (also known as the ball) Small arteries), the pressure difference between the aorta and the arterioles of the ball is about 4.6 kPa (35 mmHg), that is, from 13.3 kPa (100 mmHg) to 8.7 kPa (65 mmHg), while the microvasculature of the ball and the capillaries around the tubules There is a similar decline between 8.7 kPa (65 mmHg) and 2 kPa (15 mmHg). The renal cortical blood flow accounts for 80% to 90% of the total blood flow of the kidney, while the renal medulla accounts for 10% to 20%. Under stress, the renal blood flow in the renal cortex can be diverted in order to regulate the discharge of sodium. In the case of hemorrhage and shock, the vasoconstriction of the arterioles through the ball increases the resistance of the renal blood vessels, so that more blood The life center is supplied, and the arteriolar resistance decreases to maintain glomerular filtration pressure. From the early pregnancy, the renal plasma flow rate continues to increase to full term, and the whole pregnancy increases by about 25%.
(2) glomerular filtration rate: at the second month of pregnancy, the glomerular filtration rate increased, up to 50%, continued to decline after 37 to 38 weeks of pregnancy, postpartum return to pre-pregnancy levels .
(3) Postural position and renal function during pregnancy: When the normal steric position is normal, the extracellular fluid moves to the lower limbs to stimulate the sympathetic nervous system, which increases the peripheral vascular resistance and maintains the blood volume. The central blood volume is increased by the sympathetic tone and the increase of circulating catecholamines. Relatively decline, when the kidney enters the ball artery of the balllet to release the renin, which causes angiotensin to rise, stimulates the secretion of aldosterone, promotes the reabsorption of sodium by the renal tubule, thus reducing the excretion of sodium and water, Assali et al. It is believed that pregnant women are more sensitive to the reaction of straight steric position, which reduces the urinary flow and glomerular filtration rate. Pritchard et al. found that the supine position of pregnant women caused a significant decrease in water and sodium excretion through the control of the lateral and non-pregnant women. Baird et al. The study found that the supine position of pregnant women in the third trimester significantly reduced the excretion of the right kidney, suggesting the danger of mechanical compression of the uterus. Therefore, the role of the position of the pregnant woman should be considered when estimating the renal function. When the pregnant woman should diuresis and sodium excretion in the third trimester, the patient Should be taken laterally.
(4) creatinine and urea nitrogen: serum creatinine and blood urea nitrogen levels reflect glomerular filtration rate, no significant changes in the production of urea and creatinine during pregnancy, but due to increased glomerular filtration rate during pregnancy, Serum creatinine and blood urea nitrogen levels can be decreased, normal serum creatinine value is (53.0 ± 12.4) mol / L [(0.6 ± 0.14) mg / dl] during non-pregnancy, and decreased to (40.7 ± 11.5) mol during pregnancy. /L[(0.46±0.13) mg/dl], blood urea nitrogen also has a similar decrease, the normal value is (4.6±1.1) mmol/L [(13±3) mg/dl] during non-pregnancy, during pregnancy (2.9 ± 0.5) mmol / L [(8.2 ± 1.3) mg / dl], so the normal value in non-pregnancy, after pregnancy, prompted renal insufficiency.
(5) Uric acid clearance rate: In normal pregnancy, the increase in glomerular filtration rate leads to an increase in uric acid clearance, so serum uric acid concentration drops to 178.5 to 208.2 mol/L [(3.0 to 3.5) mg/dl].
2. The current reason for the immune response after infection is as follows:
(1) Acute glomerulonephritis after streptococcal infection generally does not occur at the peak of streptococcal infection, but occurs at the onset of 1 week or 2 to 3 weeks, in line with the appearance of general immune response.
(2) In the early stage of acute glomerulonephritis, the total serum complement concentration (CH50) can be significantly reduced. The complement values are measured and the concentration is decreased. However, the C3 and CH50 decrease are more obvious. In the presence of an immune response, complement may be activated by both classical and bypass pathways, and the circulating immune complex is often positive.
(3) Lange et al. used fluorescent antibody method to find streptococcal antigen in mesangial cells and glomerular basement membrane. Under electron microscope, there was a gap between glomerular basement membrane and epithelial cell foot process. The dense lump-like hump is present, containing immune complexes and complement. The IgG and C3 on the glomeruli of the patient are granular, and there is complement deposition in the glomeruli, and polymorphonuclear leukocytes and monocytes infiltrate. These three types of inflammatory mediators further promote the development of lesions. Macrophage proliferation also plays an important role in the development of lesions. NF-B nuclear transcription factor plays a key role in the cells of the immune system, and NF-B regulates kidneys. Many inflammatory cytokines and cell adhesion molecule genes are transcribed in the pathogenesis of glomerulonephritis.
(4) Cosimo Stambe et al. used immunostaining to find that P-P38 increased 10-fold in glomerular innate cells of patients with glomerulonephritis after infection, which was helpful for neutrophil infiltration.
3. The pathological changes of acute glomerulonephritis vary with the course of the disease and the severity of the lesion.
Light renal biopsy only showed glomerular capillary congestion, endothelial cells and mesangial cells slightly proliferated, immune complex deposition on the glomerular basement membrane was not significant, no dense sediment under electron microscope, typical cases in optical microscopy It can be seen that diffuse glomerular capillary endothelial cells proliferate, swell, and cause capillary luminal occlusion, and mesangial cells also proliferate and swell, with neutral and eosinophils, monocyte infiltration, fibrin Deposition, glomerular capillary blood flow is blocked, causing ischemia, reducing glomerular filtration rate, the above changes are generally most obvious in 7 ~ 10 days, a small number of serious cases of glomerular balloon epithelial cells also proliferated, the formation In the crescentic body, there may be a large number of red blood cells in the cystic cavity. The proliferation of macrophages can also form a crescent, and the glomerular basement membrane is generally normal, but under the electron microscope, the epithelial side of the basement membrane has a "hump"-like height. Density deposits, there may also be irregular deposits on the inside of the basement membrane, the density of the basement membrane is sometimes uneven, some of them may be thin and thin, and the epithelial cells may have a fusion phenomenon. IgG and C3-ray visible in the "hump" in the present and showed granular deposition along the capillary, cloudy swelling of tubular cells, red blood cells and white blood cells in the lumen tube, renal interstitial edema.
Most patients recover faster, the above changes can disappear completely in a short period of time, a small number of patients with glomerular capillary pedicle stromal cell proliferation and sediment disappearance will take several months or longer, a small number of patients continue to develop lesions, glomeruli The proliferation of capsular epithelial cells is more obvious, and it can adhere to the glomerular capillary plexus, forming a crescentic body locally. Macrophage proliferation can also form a crescent, gradually turning into chronic, in severe cases, into the small arterioles. Glomerular necrosis and thrombosis can occur in glomerular capillaries, or epithelial cells and macrophages can proliferate significantly, which can be converted into crescentic nephritis, which causes renal failure in the short term.
The lesion is mainly in the glomerulus, causing hematuria, proteinuria, glomerular filtration rate, leading to sodium, water retention, and renal tubular function is basically normal, manifested as edema, high blood pressure, severe left heart failure and high Blood pressure encephalopathy.
Prevention
Pregnancy with acute glomerulonephritis prevention
Enhance physical fitness, improve body defense function, maintain environmental sanitation, reduce upper respiratory tract infection, angina, tonsillitis and other diseases, pay attention to clean, reduce the occurrence of pyoderma, active treatment in the occurrence of the above diseases, and use clearing chronic Infected foci such as repeated tonsillitis, sinusitis, etc., in the case of Streptococcus mutans infection, antibiotics can be used to prevent the onset of the disease, the incidence of acute glomerulonephritis has decreased in recent years.
Complication
Pregnancy with complications of acute glomerulonephritis Complications, heart failure, hypertensive encephalopathy, acute renal failure
Heart failure
Often occurring in the first to second weeks after the onset of acute glomerulonephritis, the onset is rapid, varying in severity, a few serious cases can be acute pulmonary edema and sudden onset, and other manifestations of acute glomerulonephritis may be complete It is concealed that the cause of acute pulmonary edema is related to the low pulmonary artery resistance, low pressure and large flow in the normal pulmonary circulation, and also related to the loose structure of the lung tissue, negative pressure in the thoracic cavity, etc., and the whole body is hyperemia in acute glomerulonephritis. The blood volume increases, and the reserve capacity of the pulmonary circulation for capacity expansion is much smaller than that of the systemic circulation. Animal experiments show that the normal atrial protein pressure requires only 1.33 kPa (10 mmHg) to cause pulmonary edema. X-ray examination finds early There may be an increase in heart shadow, even if the clinical symptoms are not obvious, X-ray examination also proves that this change, sometimes a small amount of chest and pericardial effusion, heart failure is often critical, but after active rescue and better diuretic effect Can be quickly improved, the enlarged heart can be fully restored to normal, only the ECG T wave change sometimes takes several weeks to recover.
2. Hypertensive encephalopathy
Hypertensive encephalopathy refers to a syndrome in which neurological symptoms such as headache, vomiting, convulsions, and coma are the main manifestations of sudden increase in blood pressure. The pathogenesis is generally considered to be based on systemic hypertension. Regulatory disorder, resulting in hypoxia and varying degrees of cerebral edema, mostly associated with severe hypertension, sometimes blood pressure can suddenly rise and the incidence, not necessarily parallel with the severity of edema, clinically before and after the onset of cerebrovascular Contrast-enhanced examination can confirm significant arterial spasm. There are significant arterial spasms in the fundus examination. The degree of clinical hypertension is not completely parallel with the presence or absence of brain symptoms. It can be considered that systemic hypertension is in the attack of this disease. Although it plays an important role, it is not the only factor. Cerebral edema is a secondary change rather than a basic cause. Once cerebral edema is formed, the cerebral hypoxia is aggravated and a vicious circle can be formed. In addition, acute glomerulonephritis is already present. There is water, sodium retention, and cerebral edema is easier to form.
Hypertensive encephalopathy occurs in the early stage of acute glomerulonephritis. Generally, in the first 1-2 weeks, on average, on the 5th day, the onset is more urgent, convulsions occur, and the blood pressure of the patient before coma is sharply increased, complaining of headache, nausea, Vomiting, and varying degrees of consciousness change, drowsiness, irritability, etc. Some patients also have visual impairment, including temporary darkness, no signs of localization in the nervous system examination, shallow reflection and tendon reflexes can be weakened or disappeared, Can be positive, and can appear pathological reflex, some patients with severe cerebral palsy may have signs of cerebral palsy, such as pupillary changes, respiratory rhythm disorders, etc., fundus examination in addition to common extensive or local retinal arteriospasm, sometimes visible retinal hemorrhage, exudation And optic disc edema, EEG examination showed transient focal dysfunction or bilateral synchronous cusp slow wave, sometimes rhythm is poor, in many cases, two abnormalities exist simultaneously, cerebrospinal fluid examination appearance is clear, pressure and protein are normal or Slightly increased, occasionally a small number of red blood cells or white blood cells.
3. Acute renal failure
In severe cases, blood urea nitrogen increased by 3.6mmol/L per day, serum creatinine increased by 44.2mol/L per day, and serum creatinine could be >309.4moL/L. Acute renal failure occurred.
Symptom
Pregnancy with acute glomerular neuritis symptoms Common symptoms Edema, hematuria, low back pain with frequent urination, urine... Hypertension, fatigue, nausea, pregnancy, toxemia
Acute nephritis in pregnancy is more common in early pregnancy and younger pregnant women. It often occurs in tonsillitis, sinusitis, scarlet fever and rickets 10 to 20 days after high blood pressure, edema and hematuria, patients complain of fatigue, headache nausea and vomiting, can be further combined Acute pulmonary edema, acute renal failure or hypertensive encephalopathy.
Examine
Examination of pregnancy with acute glomerulonephritis
The specific gravity of urine is increased, mostly at 1.022~1.032, when the edema is less than 400~700ml, a few people are less than 300ml, and the urine volume can reach 2000ml during recovery. The urine sediment contains many red blood cells, transparent, granule or red blood cell cast. Anti-"O" titer >300U Todd, renal function test performance is different, most patients have varying degrees of renal insufficiency, the most obvious change in renal function filtration rate, endogenous creatinine clearance and inulin clearance The rate is reduced, these phenomena are easy to be confused with pregnancy-induced hypertension and pre-eclampsia, but the hematuria and cast type are rare in patients with pregnancy-induced hypertension and no complications.
Fundus examination: Most patients have normal fundus, and a small number of small arteriospasm and mild optic disc edema may be associated with elevated blood pressure. If there is bleeding, exudation, etc., it is likely to be an acute attack of chronic glomerulonephritis.
Diagnosis
Diagnosis and differential diagnosis of pregnancy complicated with acute glomerulonephritis
diagnosis
Typical cases in the pharyngeal isthmus, skin and other streptococcal infections after edema, hematuria, proteinuria and other symptoms, the diagnosis is more difficult, the diagnosis of acute glomerulonephritis after streptococcal infection is at least two of the following three characteristics Based on:
1 The M protein type -hemolytic streptococcus group A which can cause nephritis is detected in the pharyngeal or skin lesions.
2 Immune response to Streptococcal extracellular enzymes - anti-streptolysin "O" (ASO), anti-streptokinase (ASK), anti-DNase B (ADNAaseB), anti-CoA enzyme (ANADase), anti- The hyaluronidase (AH) is positive for one or more, ASO is increased after pharyngeal infection, and AH, ADNAase and ANADase are positive after skin infection.
The serum concentration of 3C3 decreased temporarily, and the symptoms of renal inflammation returned to normal within 8 weeks after the onset of symptoms. The symptoms were not obvious and should be examined in detail. In particular, the urine routine should be checked repeatedly to confirm the diagnosis.
Differential diagnosis
The disease should be identified with the following diseases.
1. Other glomerulonephritis manifested by acute nephritis syndrome
Whether it is primary or secondary glomerulonephritis, it can induce activity after upper respiratory tract infection, symptoms of acute nephritis syndrome should be identified with glomerulonephritis after streptococcal infection, after non-streptococcal infection Glomerulonephritis including endocarditis after infection, shunt nephritis, sepsis, pneumococcal pneumonia, typhoid fever, secondary syphilis, meningococcalemia, glomerulonephritis after viral and parasitic infection, secondary Including multi-system diseases: systemic lupus erythematosus, vasculitis, allergic purpura, etc., non-primary glomerular diseases characterized by acute nephritic syndrome mainly include thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, Arteriosclerotic embolic nephropathy and acute allergic interstitial nephritis, secondary system often have other systemic symptoms, kidney biopsy can be done when it is difficult, may be helpful for diagnosis.
2. A small number of streptococcal infection after glomerulonephritis
It is characterized by nephrotic syndrome and should be differentiated from other nephrotic syndromes.
3. Rapid progressive glomerulonephritis
The onset of acute glomerulonephritis is often similar to acute glomerulonephritis. However, the treatment and prognosis are different. Therefore, patients with severe symptoms and rapid deterioration of the disease should be highly vigilant. When necessary, a renal biopsy should be performed to confirm the diagnosis.
