| disease | Acute Glomerulonephritis after Streptococcal Infection |
| alias | Poststreptococcal Acute Glomerulonephritis |
Poststreptococcal acute glomerulonephritis is more common in children and adolescents, and occasionally seen in the elderly. The incidence rate is higher in males than in females, approximately 2-3:1.
bubble_chart Etiology
This disease is caused by infection with type A hemolytic streptococci, and the reasons are as follows: ① The disease often occurs after streptococcal infections such as tonsillitis, pharyngitis, scarlet fever, erysipelas, and pyoderma. The onset season coincides with the epidemic season of streptococcal infections. For example, cases caused by upper respiratory tract infections are more common in winter and spring, while those caused by skin suppurative diseases are more common in summer and autumn. ② The titer of anti-streptolysin O antibody (ASO antibody) in the patient's blood is elevated. ③ During the epidemic season, controlling streptococcal infections with antibiotics can reduce the incidence of acute glomerulonephritis. ④ The M protein antigen of the streptococcal cell wall is found in the glomeruli.
The strains of hemolytic streptococci associated with glomerulonephritis often vary with the epidemic situation. There are so-called "nephritogenic streptococci," with type 12 of group A being the most common, followed by types 1, 4, 18, 25, 41, 49, etc., while types 2, 49, 55, 57, and 60 are often associated with pyoderma and glomerulonephritis. The occurrence of acute glomerulonephritis and the severity of the lesions are not related to the severity of the streptococcal infection. Individuals who have had glomerulonephritis after streptococcal infection develop type-specific, permanent, and protective immunity to the M protein, so recurrence is rare.
bubble_chart PathogenesisIt is currently believed that this disease is caused by an immune response following infection, for the following reasons.
1. Acute glomerulonephritis after streptococcal infection generally does not occur at the peak of the streptococcal infection but develops 1 week or 2–3 weeks after the onset of infection, which aligns with the typical incubation period of an immune response.
2. In the early stages of acute glomerulonephritis, a significant decrease in serum total complement concentration (CH50) can be observed. Measurements of individual complement levels reveal reductions in all components, with C3 and C5 showing more pronounced declines later, indicating the presence of an immune response. The complement system may be activated through both the classical and alternative pathways. Circulating immune complexes are often positive.
3. Lange et al., using fluorescent antibody techniques, found streptococcal antigens in the glomerular mesangial cells and on the glomerular basement membrane. Electron microscopy revealed dense, lumpy hump-like deposits between the glomerular basement membrane and the epithelial cell foot processes, containing immune complexes and complement. IgG and C3 were observed as granular deposits on the patient's glomeruli. The presence of complement deposits, polymorphonuclear leukocytes, and mononuclear cell infiltration in the glomeruli suggests that these three types of inflammatory mediators further promote disease progression. Macrophage proliferation also plays a significant role in the development of the lesions.
bubble_chart Pathological Changes
The pathological changes of acute glomerulonephritis vary depending on the course and severity of the disease. In mild cases, renal biopsy reveals only congestion of glomerular capillaries, grade I proliferation of endothelial and mesangial cells, insignificant immune complex deposition on the glomerular basement membrane, and no dense deposits under electron microscopy. In typical cases, light microscopy shows diffuse proliferation and swelling of glomerular capillary endothelial cells, leading to varying degrees of capillary lumen obstruction. Mesangial cells also proliferate and swell, accompanied by infiltration of neutrophils, eosinophils, and monocytes, fibrin deposition, and impaired blood flow in the glomerular capillaries, causing ischemia and reduced glomerular filtration rate. These changes are most pronounced around 7–10 days. In a few severe cases, the epithelial cells of the glomerular capsule also proliferate, forming crescents, and the capsular space may contain abundant red blood cells. Macrophage proliferation can also form crescents. The glomerular basement membrane is generally normal, but electron microscopy reveals high-density "hump-like" deposits on the epithelial side of the basement membrane, as well as irregular deposits on the inner side. The basement membrane density may be uneven, with some areas thinning or rupturing, and fusion of epithelial cell foot processes. Immunofluorescence shows the presence of C3 and IgG in the "humps" and granular deposits along the capillaries. Renal tubular cells exhibit cloudy swelling, with red blood cell and white blood cell casts in the lumen, and renal interstitial edema.
The lesions primarily affect the glomeruli, causing hematuria, proteinuria, and reduced glomerular filtration rate, leading to sodium and water retention. Tubular function remains largely normal, manifesting as edema, hypertension, and in severe cases, left heart failure and hypertensive encephalopathy.
bubble_chart Clinical Manifestations
One to three weeks before the onset of this disease, there is often a history of upper respiratory tract inflammation, such as tonsillitis, pharyngitis, and skin infections like erysipelas or pyoderma, which are streptococcal infections. The latter has a longer incubation period, typically 2 to 4 weeks, followed by a sudden onset, though some cases may develop symptoms just days after infection. The most common manifestations are edema, hematuria, and proteinuria. In children, the condition is sometimes discovered only when symptoms such as headache, nausea, vomiting, spasms, shortness of breath, or palpitations appear. The severity varies widely: mild cases may be asymptomatic, with only slight abnormalities in routine urine tests, and are diagnosed as having typical acute glomerulonephritis only upon renal biopsy—a condition some refer to as "subclinical acute glomerulonephritis." About 3–5% of cases are severe, presenting with anuria or even progressing to acute renal failure, classified as severe acute glomerulonephritis. If this type is primarily characterized by acute vascular inflammation and cellular infiltration, most patients can still recover.
(1) Edema: Seen in about 70–90% of cases, varying in severity. It is often noticeable as eyelid edema upon waking in the morning, likely due to the supine position and the looseness of the tissue in that area. Edema is also more pronounced in the lower limbs and scrotum. In severe cases, serous membrane cavity effusion may occur, most commonly in the pleural cavity. The primary cause of edema is the pathological changes in the glomerular capillaries and external vascular compression, which reduce renal blood flow and impair filtration. Coupled with the relatively normal function of the renal tubules, this leads to increased fluid reabsorption. Additionally, excessive intake of sodium and water during oliguria often exacerbates edema. The retention of sodium and water expands extracellular and intravascular volume. In some cases, edema is related to heart failure. Generally, edema begins to subside after 1–2 weeks, but in severe cases, it may last longer, up to 3–4 weeks.
(2) Hypertension: Seen in 70–90% of patients, with varying severity. It is usually grade I or grade II, with adults typically showing readings around 20.0–24.0/12.0–13.3 kPa (150–180/90–100 mmHg), often fluctuating, possibly due to the degree of vascular spasm. A few cases are more severe and may develop into hypertensive crisis. The duration of hypertension does not always align with that of edema; in most cases, blood pressure tends to normalize within about 2 weeks, with children recovering faster than adults. Sometimes, hypertension may persist for a long time, serving as a precursor to chronicity.
The cause of hypertension in acute glomerulonephritis was previously thought to be excessive renin secretion due to renal ischemia during glomerulonephritis. However, measurements of renin levels in acute glomerulonephritis patients often show normal or low values. Therefore, it is increasingly believed that reduced glomerular filtration rate leading to sodium and water retention, increased blood volume, and vascular spasm may be the primary causes of hypertension.
(3) Urinary abnormalities:
1. Oliguria or anuria: Urine output decreases during edema, typically around 400–700 ml per day, lasting 1–2 weeks before gradually increasing. During oliguria, urine specific gravity may rise slightly. During the stage of convalescence, daily urine output may exceed 2000 ml. In a few severe cases, urine output drops significantly to less than 300 ml or even anuria.
2. Hematuria: Present in almost every case but varying in severity. In severe cases, it manifests as gross hematuria, often appearing as a turbid coffee-bean color. This is likely due to red blood cells passing through damaged glomeruli and/or peritubular capillary walls into the nephron. Gross hematuria does not last long, usually converting to microscopic hematuria within days, which may persist for a long time but generally resolves within 6 months, though some cases may take up to 2 years to fully recover.
3. Proteinuria The positive rate reaches over 95%, often presenting as mild to moderate proteinuria, with severe cases being relatively rare. Proteinuria may result from the loss of the anionic layer in the capillary wall, indicating an absence of charge selectivity, or from an increase in the pore size of glomerular capillaries, allowing large plasma proteins to be filtered through the glomerular membrane fistula disease. Generally, 2–3 weeks after the onset of illness, proteinuria reduces to trace or minimal levels, and in most cases disappears within 2–3 months, though it may persist longer in adult patients. Persistent proteinuria suggests a tendency toward chronic progression.
4. Urinary Sediment In the early stage, in addition to a large number of red blood cells, white blood cells are also often increased, and epithelial cells as well as various casts are commonly seen. Among the casts, hyaline casts and granular casts are the most frequent. The appearance of red blood cell casts indicates disease activity.
5. The levels of fibrin degradation products (FDP) and C3 in the urine are often elevated, especially during the diuretic phase.
(IV) Other Symptoms Children often have fever, sometimes as high as 39°C, accompanied by fear of cold. Adults often experience lumbar soreness and lumbago, and a few patients may have frequent urination and urgency. Patients may also exhibit symptoms such as nausea, vomiting, anorexia, epistaxis, headache, and fatigue.
(V) Fundus Examination The fundus of most patients is normal, but a few may show small stirred pulse spasms and grade I optic disc edema, which are closely related to elevated blood pressure. If manifestations such as hemorrhage or exudation are present, it is highly likely to be an acute exacerbation of chronic glomerulonephritis.
(VI) Blood Tests The red blood cell count shows grade I reduction, possibly due to blood dilution after water retention. White blood cells may increase during the initial stage [first stage] of the disease, and the percentage of eosinophils may also rise, along with an accelerated erythrocyte sedimentation rate. In most cases, blood non-protein nitrogen and urea nitrogen levels are normal, though a few may be slightly elevated, while creatinine is generally normal. Both rise in cases of anuria. Plasma total protein and cholesterol measurements are mostly normal, though electrophoresis may reveal a slight decrease in albumin levels. In 70–90% of patients, serum anti-streptolysin O (ASO) antibody titers are elevated, but normal levels do not rule out the possibility of streptococcal infection. Other antibodies, including anti-deoxyribonuclease antibodies, anti-streptokinase antibodies, anti-hyaluronidase antibodies, and DPNase antibodies, may also be elevated. In the early stages of the disease, serum total complement concentration (CH50) and C3 may be significantly reduced, recovering later as the condition improves. Additionally, there may be transient frigidity globulinemia and positive circulating immune complexes. C-reactive protein and wind-dampness-like factors are mostly normal or negative.
(VII) Renal Function Tests The findings vary. Most patients exhibit varying degrees of renal insufficiency, with changes in glomerular filtration rate being the most pronounced. Both endogenous creatinine clearance and inulin clearance are reduced, while renal blood flow is mostly normal. Tubular function is also altered. This may be due to the reduction in filtration area caused by the infiltration of inflammatory cells into the glomerular capillaries, or it may result from an increase in reversible local vasoactive substances that contract membrane cells, such as angiotensin II and leukotrienes, leading to a decrease in effective filtration area and consequently reduced perfusion of glomerular capillaries.
In glomerulonephritis, the following severe conditions may sometimes occur, mostly in children who do not rest adequately or receive improper treatment after onset. In recent years, with improved medical conditions, such symptoms have become rare. However, clinicians must have sufficient understanding of the pathophysiology, diagnosis, and management of these severe conditions.
1. Heart Failure Heart failure occurs due to a decrease in the glomerular filtration rate, leading to reduced excretion of water and sodium. However, tubular reabsorption does not decrease proportionally and remains relatively increased, resulting in water and sodium retention in the body. Additionally, renal ischemia may increase renin secretion, causing secondary hyperaldosteronism, which exacerbates sodium retention and expands plasma volume. Some authors used chromium-labeled red blood cells to measure the blood volume in 10 typical cases of acute glomerulonephritis, finding an average blood volume of 79 ml/kg and plasma volume of 51 ml/kg. During the convalescence stage, these values returned to 63 ml/kg and 37 ml/kg, respectively. Hypertension is also a contributing factor, as increased resistance to left ventricular output places additional burden on the heart. Myocardial pathology may also play a role. Autopsy data from this condition show that some cases exhibit myocardial interstitial edema and/or serous myocarditis, though the lesions are mild, with no significant myocardial cell necrosis or interstitial inflammatory infiltration. The onset may be gradual or sudden, typically occurring within the first 1–2 weeks after the onset of acute glomerulonephritis. The severity and progression vary. Generally, patients present with oliguria, worsening edema, and gradually develop cough, shortness of breath, and dyspnea, making it difficult to lie flat. Examination may reveal rales or wheezing at the lung bases, an enlarged cardiac border, tachycardia, muffled first heart sound, and gallop rhythm. Other findings include hepatomegaly and jugular vein distension. In severe cases, acute pulmonary edema may manifest abruptly, overshadowing other symptoms of acute glomerulonephritis. The mechanism of acute pulmonary edema is related to the low resistance (only 1/8 of systemic circulation) and low pressure (only 1/8 of systemic pressure) in the pulmonary circulation, despite its high flow rate. Although pulmonary vessels are small, their blood flow is nearly equal to systemic circulation. Additionally, the loose structure of lung tissue and the negative pressure in the thoracic cavity facilitate fluid leakage from pulmonary capillaries. However, under normal conditions, the plasma colloid osmotic pressure (3.33–4.27 kPa, or 25–32 mmHg) far exceeds the pulmonary capillary pressure (0.667–1.47 kPa, or 5–11 mmHg), preventing pulmonary edema. In acute glomerulonephritis, systemic congestion and increased blood volume occur, but the pulmonary circulation has much less capacity to accommodate volume expansion compared to systemic circulation. In children, an increase of 100–200 ml in blood volume can raise pulmonary capillary pressure enough to cause pulmonary edema. Animal studies show that with normal plasma protein levels, a left atrial pressure of just 1.33 kPa (10 mmHg) can induce pulmonary edema. Chest X-rays may reveal early cardiac enlargement, even in clinically asymptomatic cases, and occasionally small amounts of pleural or pericardial effusion. Although heart failure is often critical, prompt treatment with effective diuresis can lead to rapid improvement, with the enlarged heart returning to normal. However, ECG T-wave changes may take weeks to resolve.
2. Hypertensive Encephalopathy
Hypertensive encephalopathy refers to a syndrome characterized by neurological symptoms such as headache, vomiting, spasm, and unconsciousness due to a sharp increase in blood pressure. The pathogenesis is generally believed to involve dysregulation of cerebral resistance vessels under systemic hypertension, leading to hypoxia and varying degrees of cerebral edema. It is often associated with severe hypertension, and sometimes the condition can be triggered by a sudden rise in blood pressure, which may not necessarily correlate with the severity of edema. Clinically, significant vasospasm is observed in cerebral angiography before and after the onset, and fundus examination reveals marked vasospasm during episodes. The degree of clinical hypertension does not always parallel the presence or severity of neurological symptoms, suggesting that while systemic hypertension plays a crucial role, it is not the sole factor. Cerebral edema is a secondary change rather than the primary cause. Once cerebral edema develops, it exacerbates cerebral hypoxia, creating a vicious cycle. Additionally, acute glomerulonephritis often involves water and sodium retention, further predisposing to cerebral edema.
Clinical manifestations: Hypertensive encephalopathy typically occurs early in the course of acute glomerulonephritis, usually within the first 1–2 weeks, with an average onset on the fifth day. The onset is abrupt, with a sharp rise in blood pressure preceding symptoms such as headache, nausea, vomiting, and varying degrees of altered consciousness, including drowsiness and dysphoria. Some patients may experience visual disturbances, including temporary blindness. Neurological examinations often reveal no focal signs, but superficial and tendon reflexes may be diminished or absent, ankle clonus may be positive, and pathological reflexes may appear. Severe cases may exhibit signs of brain herniation, such as pupillary changes or irregular breathing patterns. Fundus examination commonly shows widespread or localized retinal arteriolar spasms, and occasionally retinal hemorrhages, exudates, or papilledema. EEG may display transient focal disturbances or bilateral synchronous sharp and slow waves, sometimes with poor rhythmicity, and many cases exhibit both abnormalities. Cerebrospinal fluid is typically clear, with normal or slightly elevated pressure and protein levels, and occasionally a few red or white blood cells.
Most patients recover with appropriate emergency treatment. However, severe cases, especially those with status epilepticus, may suffer permanent neurological damage due to prolonged cerebral hypoxia, even if life-saving treatment is administered.
3. Acute Renal Failure In severe cases, blood urea nitrogen may rise by 10 mg/dL daily, serum creatinine may increase by 0.5 mg/dL daily, and serum creatinine levels may exceed 3.5 mg/dL, indicating acute renal failure.
〔Disease Course〕
The course of acute glomerulonephritis varies widely, ranging from a few days to over a year, with most cases resolving within 4–8 weeks. Adults tend to have a longer course than children. Edema and hypertension usually subside first, while proteinuria and hematuria may persist for several months to a year. The prognosis of acute glomerulonephritis is generally favorable, with clinical recovery rates approaching 100% in follow-ups 10 years after streptococcal infection outbreaks. Sporadic cases show slightly lower recovery rates, but the prognosis remains excellent in children, reaching around 90%. Adult recovery rates are lower, ranging from 50–70%. Baldwin’s 10-year follow-up in adults revealed persistent proteinuria in nearly 40% of patients and an increased number of sclerotic glomeruli. Symptoms of acute glomerulonephritis may fluctuate in severity, and the extent of hematuria or proteinuria does not clearly correlate with recovery chances.
Previously, it was believed that proteinuria and microscopic hematuria persisting for 6 months to over a year indicated progression to chronic glomerulonephritis. However, recent renal biopsy and clinical data show that urinary abnormalities and active histological findings may gradually resolve within 2–3 years of follow-up. Therefore, the distinction between acute and chronic glomerulonephritis should be based on a comprehensive analysis of clinical data and disease progression rather than solely on duration.
According to follow-up data, residual lesions may still be present in the kidneys when the clinical manifestations of acute glomerulonephritis disappear. Over time, exudation and proliferative sexually transmitted disease changes gradually subside, but glomerular fibrosis sometimes occurs. In some patients, routine urine tests still reveal common bletilla tuber and red blood cells, while biopsy shows that diffuse inflammatory sexually transmitted disease changes in the kidneys have largely disappeared, with only focal sexually transmitted disease changes remaining—a condition referred to as "healing with defects." In some patients, as follow-up time increases, biopsies reveal a trend of increasing glomerular fibrosis. In such cases, continued follow-up observation is advisable to monitor for the possibility of progression to chronic glomerulonephritis.
〔Acute Glomerulonephritis in the Elderly〕
Elderly patients with acute glomerulonephritis confirmed by renal biopsy or autopsy exhibit the following characteristics: ①Most patients have an insidious onset, often lacking a clear history of preceding infection, and present with significant edema or azotemia. ②Pathologically, the glomeruli show proliferative and exudative changes, with crescent formation observed in 20–40% of glomeruli and abundant polymorphonuclear neutrophils in the renal tubules. ③Hypertension and azotemia are common, with significantly higher rates of azotemia and anemia compared to younger age groups. ④Heart failure is frequently observed. ⑤Half of the cases present with anuria or prolonged oliguria. ⑥Approximately one-fifth of patients develop nephrotic syndrome, a higher incidence than in children or adults with nephritis, and may exhibit severe pyuria resembling acute pyelonephritis. ⑦The mortality rate is high, often due to acute complications from infections or other systemic conditions leading to general debilitation, rather than progressive renal disease. Among survivors followed for 5 years, 30–40% exhibit grade I elevation in serum creatinine and blood urea nitrogen, and follow-up renal biopsies reveal incomplete histological resolution. At Zhongshan Hospital, from 1981 to 1994, among 750 cases of renal biopsy-confirmed parenchymal kidney diseases, including 581 cases of primary parenchymal kidney diseases, 11 elderly patients (aged ≥60) with acute glomerulonephritis were treated with anticoagulants and hormones. Complete remission was achieved in 28.6%, partial remission in 57.1%, and mortality was 14.3%, yielding an overall remission rate of 85.7%.
Typical cases present with symptoms such as edema, hematuria, and proteinuria following streptococcal infections in the pharyngeal isthmus, skin, etc., and diagnosis is usually straightforward. The diagnosis of acute poststreptococcal glomerulonephritis generally requires at least two of the following three criteria: ① Detection of nephritogenic M-protein type β-hemolytic group A streptococci at the site of pharyngeal or skin lesions; ② A positive immune response to streptococcal extracellular enzymes—anti-streptolysin O (ASO), anti-streptokinase (ASK), anti-deoxyribonuclease B (ADNAase B), anti-nicotinamide adenine dinucleotidase (ANADase), or anti-hyaluronidase (AH). ASO levels typically rise after pharyngeal infections, while AH, ADNAase, and ANADase responses are positive following skin infections; ③ A transient decrease in serum C3 concentration, which returns to normal within 8 weeks after the onset of nephritic symptoms. For cases with atypical symptoms, thorough examination is necessary, particularly repeated urinalysis, to confirm the diagnosis.
bubble_chart Treatment Measures
Most cases of acute glomerulonephritis can heal spontaneously, so excessive medication is unnecessary for mild cases. The following measures can be taken.
(1) Rest Rest is important for preventing symptom exacerbation and promoting disease recovery. Opinions vary on whether patients with significant edema and hypertension should be completely bedridden, but if mild activity worsens symptoms or urine test abnormalities, bed rest is still advisable. Avoid exposure to cold and dampness to prevent renal arteriolar spasm caused by cold, which could aggravate renal ischemia.
(2) Diet During the initial stage of the disease, dietary control is crucial. In principle, a low-salt diet with restricted fluid intake is recommended, as most patients have edema and hypertension. If blood pressure is very high and edema is severe, a salt-free diet should be adopted, with daily fluid intake limited to 1,000 ml. For patients with anuria, management should follow acute renal failure protocols. Daily protein intake for adults should be 30–40 g or calculated as 0.6 g/(kg·d) to avoid increasing the kidneys' burden.
(3) Infection Control Active treatment should be administered for any lingering precursor infections, such as pharyngitis, tonsillitis, pyoderma, sinusitis, or otitis media. Since precursor infections can sometimes be hidden and difficult to detect, even in cases of acute glomerulonephritis without an identifiable infection, a 10–14-day course of penicillin (or lincomycin/erythromycin for those allergic) is generally recommended to prevent further antigen invasion and avoid recurrent or prolonged glomerulonephritis. Antibiotics harmful to the kidneys should be avoided.
(4) Chinese Medicine Treatment Most treatments follow the principles of ventilating the lung and disinhibiting water, clearing heat, and removing toxins. However, close attention should be paid to modern medical research trends. Some literature reports that Chinese medicinals such as Stephania Tetrandra, Magnolia Bark, and Dutohmanspipe Fruit can cause renal interstitial inflammation and fibrosis, so their use is best avoided. Some Chinese herbal medicines contain nonsteroidal anti-inflammatory agents like mefenamic acid, which should also be used cautiously as they may induce acute renal failure.
(5) Symptomatic Treatment
1. Edema and Oliguria Mild cases may not require diuretics. For significant edema, furosemide (20–40 mg, three times daily) can be used. Severe cases with acute nephritic syndrome may require intravenous injection of 80–200 mg furosemide in 20 ml of 5% glucose solution once or twice daily. Alternatively, 80–100 mg furosemide can be added to 250 ml of 20% mannitol for intravenous drip once daily, often producing significant diuretic effects.
2. Hypertension and Hypertensive Encephalopathy Grade I hypertension can generally be managed with stricter fluid and salt control and diuretics. For moderate to severe (Grade III) cases, oral reserpine (0.25 mg, two to three times daily) may be used. If blood pressure rises sharply, 1 mg reserpine can be administered intramuscularly. For extremely high blood pressure, severe headache, or impending hypertensive encephalopathy, intravenous diazoxide (3–5 mg/kg) can rapidly dilate blood vessels and lower blood pressure. Alternatives include phentolamine (Regitine) or sodium nitroprusside. Currently, angiotensin-converting enzyme inhibitors (e.g., captopril, enalapril, benazepril) are preferred, as they reduce both systemic and glomerular hypertension, potentially improving or delaying the progression of mild to moderate (Grade II) renal insufficiency caused by various diseases. Calcium channel blockers can also be used, though their impact on renal function remains debated. Griffin suggests that while calcium channel blockers reduce systemic hypertension, they offer no protective effect on glomeruli. The harmful effects of nifedipine on pressure transmission and glomerular injury have been confirmed.
In the event of hypertensive encephalopathy, in addition to rapid blood pressure reduction, administer diazepam 10mg intravenously for spasms, which may be repeated if necessary. Phenytoin sodium or paraldehyde injections may also be used. Previously, magnesium sulfate injections were employed to lower blood pressure, but the effect was not particularly significant. If renal function is impaired, injection may lead to hypermagnesemia, affecting consciousness and respiration, thus careful consideration is warranted.
3. Acute Heart Failure Water and salt retention are the main predisposing factors, leading to high-output heart failure. The primary treatment focuses on reducing circulating blood volume, and intravenous injection of furosemide can be administered for rapid diuresis. If pulmonary edema is significant, sedatives, pethidine, or morphine (use with caution in children) may be injected, along with slow intravenous injection or drip of phentolamine (5–10 mg) to dilate blood vessels and reduce cardiac load. Sodium nitroprusside can also be used. Other measures may refer to "cardiac insufficiency." Although digitalis is commonly used in heart failure, it is not a primary intervention. For severe heart failure unresponsive to general treatments, isolated ultrafiltration therapy may be considered.
For patients with acute glomerulonephritis, if proteinuria and microscopic hematuria resolve slowly or show a persistent tendency, potential infection foci (e.g., tonsillitis) should be investigated and addressed. These measures are generally undertaken when glomerulonephritis is relatively stable and infections have been controlled for at least 3 months. Prior to removal, penicillin injections should be administered.
The short-term and long-term prognosis of acute poststreptococcal glomerulonephritis (APSGN) in children is generally excellent, with very few deaths resulting from complications of renal failure. Almost all patients experience spontaneous resolution of clinical symptoms within weeks of onset, while urinary sediment abnormalities and proteinuria gradually disappear over the following months. In a small number of cases, urinary abnormalities may persist for several years before normalizing. Long-term follow-up of children with APSGN and no prior history of chronic glomerular disease rarely shows progression to chronic kidney disease. In rare instances, APSGN may develop into crescentic glomerulonephritis, accompanied by a rapidly progressive and malignant course. Persistent heavy proteinuria and/or abnormal GFR over the long term suggest a poor prognosis. Some authors report that sporadic cases of APSGN in children have a worse long-term prognosis, with some children slowly progressing to progressive glomerulosclerosis, reduced GFR, and hypertension after acute symptoms resolve. The prognosis of acute poststreptococcal glomerulonephritis in adults is worse than in children. These patients may exhibit persistent proteinuria and/or hematuria, or develop chronic progressive glomerulosclerosis, leading to hypertension and renal failure. Therefore, adults with APSGN who still have proteinuria and/or hematuria six months after onset should undergo early renal biopsy to clarify pathological changes and receive aggressive treatment. Of course, the prognosis of acute glomerulonephritis in the elderly is even poorer. However, if diagnosed and treated promptly—including renal biopsy for definitive diagnosis, low-dose corticosteroids, and low-molecular-weight heparin and/or urokinase for those with hypercoagulability—the condition may still improve, and most patients can recover.
Strengthen the constitution, improve the body's defense mechanisms, and maintain environmental hygiene to reduce upper respiratory infections, pharyngitis, tonsillitis, and other diseases. Pay attention to cleanliness to minimize the occurrence of pyoderma. When these diseases occur, active treatment should be pursued, and chronic infection sites such as recurrent tonsillitis and sinusitis should be addressed. For children in group living environments during streptococcal infection outbreaks, antibiotics can be used for prevention to reduce incidence. In recent years, the incidence of acute glomerulonephritis has declined compared to previous levels.
This disease should be differentiated from the following conditions.
(I) Acute nephritis syndrome manifested by other glomerulonephritis Whether primary or secondary glomerulonephritis, upper respiratory tract infections can induce its activity, presenting symptoms of acute nephritis syndrome, which should be differentiated from post-streptococcal glomerulonephritis. Non-streptococcal post-infectious glomerulonephritis includes post-infectious endocarditis, shunt nephritis, sepsis, pneumococcal pneumonia, cold-damage disease, intermediate stage [second stage] syphilis, meningococcemia, and glomerulonephritis following viral and Chinese Taxillus Herb infections. Secondary cases include multisystem diseases: systemic lupus erythematosus, vasculitis, Henoch-Schönlein purpura, etc. Non-glomerular diseases that may present features of acute nephritis syndrome mainly include thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, stirred pulse sclerosing embolic nephropathy, and acute allergic interstitial nephritis. Secondary cases often present with other systemic symptoms, and when in doubt, a renal biopsy may be performed, which could aid in diagnosis.
(II) A minority of post-streptococcal glomerulonephritis presents as nephrotic syndrome and should be differentiated from other nephrotic syndromes.
(III) Rapidly progressive glomerulonephritis The onset of rapidly progressive glomerulonephritis is often similar to acute glomerulonephritis, but the treatment and prognosis differ significantly. Therefore, heightened vigilance is required for patients with severe symptoms and rapid deterioration, and a renal biopsy may be necessary to confirm the diagnosis when indicated.
