Acute glomerulonephritis (AGN), commonly referred to as acute nephritis, is a prevalent urinary system disease in children. It encompasses various glomerular diseases with diverse etiologies, characterized by sudden onset and presenting symptoms such as hematuria, proteinuria, edema, hypertension, and reduced glomerular filtration rate. In pediatrics, post-streptococcal acute glomerulonephritis is the most common type. This condition has a favorable prognosis, often following a self-limiting course lasting from 6 months to 1 year. It is an immune complex-mediated nephritis caused by nephritogenic strains of group A β-hemolytic streptococci. Pathologically, it manifests as diffuse endocapillary proliferative changes, with features including proliferation of glomerular endothelial and mesangial cells, infiltration of neutrophils, and subepithelial deposits (humps) during the acute phase. The primary pathophysiological alterations stem from glomerular inflammation leading to narrowed glomerular capillary lumens, decreased glomerular filtration rate, sodium and water retention, and expanded extracellular fluid volume.

bubble_chart Diagnosis

Typical cases

1. History, symptoms, and signs: More common in school-aged children. Acute onset. A history of respiratory or skin infection 1–3 weeks before onset. Initial manifestations include edema (starting as morning eyelid swelling, which can progress to generalized non-pitting edema in severe cases), gross hematuria (appearing as meat-washing water-like, brown, or dark tea-colored urine) in half of the cases, and a certain degree of reduced urine output. Additionally, symptoms such as lack of strength, headache, dizziness, nausea, vomiting, abdominal pain, and dull lower back pain may occur. Physical examination reveals edema (non-pitting) and elevated blood pressure.
2. Laboratory tests: Urinalysis may show gross or microscopic hematuria, with glomerular hematuria changes (i.e., polymorphic, severely deformed red blood cells) observed in red blood cell morphology. Red blood cell casts may be seen in the urine sediment, and sometimes white blood cells, renal tubular epithelial cells, or granular casts are also present. Urine protein is generally + to ++. Peripheral blood tests often show grade I anemia, and the white blood cell count varies depending on whether the primary streptococcal infection is still present. Erythrocyte sedimentation rate (ESR) is often elevated. Bacteriological and serological tests for streptococcal infection include throat or skin lesion cultures, with elevated anti-streptolysin O (ASO) titers. Blood complement tests show a significant decrease in total complement and C3 within 6–8 weeks of acute onset. Renal function tests often indicate varying degrees of decreased glomerular filtration rate, transient azotemia, and grade I elevation in blood urea nitrogen and creatinine.

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Severe cases: During the acute phase, severe manifestations mainly include:

1. Severe circulatory congestion, progressing to heart failure and pulmonary edema, primarily due to water and sodium retention and expanded blood volume. The child may exhibit dysphoria, shortness of breath, orthopnea, moist rales at the lung bases, tachycardia, gallop rhythm, cardiomegaly, abdominal pain, and hepatomegaly.
2. Hypertensive encephalopathy: Manifested as severe headache, vomiting, visual disturbances, or even seizures and unconsciousness, caused by a rapid rise in blood pressure, cerebrovascular spasm, and cerebral edema.
3. Acute renal failure: Oliguria, severe azotemia, electrolyte imbalances (hyperkalemia, hyponatremia, hyperphosphatemia, hypocalcemia), water retention, and metabolic acidosis.

Atypical cases include the following:

1. Subclinical cases: A history of streptococcal infection without clear clinical symptoms or signs, or even normal urinalysis. Diagnosis is suspected based on clinical epidemiological history and dynamic changes in blood complement levels, with confirmation relying on renal biopsy.
2. Extranephritic symptoms: Children with nephritis may show minimal or only transient mild urinary abnormalities but exhibit edema, elevated blood pressure, or even hypertensive encephalopathy and severe circulatory congestion. Repeated urinalysis and blood complement tests are necessary to aid diagnosis.

bubble_chart Treatment Measures

1. General Treatment: Bed rest is required for 1-2 weeks after onset, and activity can be gradually resumed once hypertension and gross hematuria disappear. Heavy physical activity should be avoided within 3 months. For patients with edema and high blood pressure, salt and protein intake should be restricted in the diet. To completely eliminate streptococcal infection, penicillin is generally administered for 7-10 days.
2. Diuretics: If edema, hypertension, and oliguria persist despite controlling water and salt intake, diuretics should be administered. Hydrochlorothiazide is commonly used at a dosage of 1-2 mg/kg per day, divided into 2-3 oral doses. When the glomerular filtration rate (GFR) <25 ml/( min? m2)時上藥常無效而需強力速效的拌利尿劑，如呋喃苯胺酸(速尿)口服或注射，每次1～2mg/kg,或用布美他尼(丁尿胺或丁苯氧酸），成人劑量0.5～1.0mg/次，兒童酌減。
3. Antihypertensive Drugs: If blood pressure remains high despite rest, salt restriction, and diuretics, antihypertensive drugs are necessary. In pediatrics, reserpine can still be used, with an initial dose of 0.07 mg/kg (maximum not exceeding 2.0 mg), administered intramuscularly or orally, followed by 0.03 mg/kg per day divided into 2-3 oral doses. Hydralazine can also be combined at an oral dose of 0.5-1.0 mg/kg three times daily. In recent years, calcium channel blockers such as nifedipine (heart pain relief) at 0.25 mg/(kg·d) or angiotensin-converting enzyme inhibitors like captopril, starting at 0.3 mg/(kg·d), have also been used.
4. Hypertensive Encephalopathy: Emergency treatment is required. The key is rapid blood pressure reduction. Sodium nitroprusside can be administered intravenously, with 5-10 mg added to 100 ml of 5% glucose solution (each ml containing 50-100 μg), starting at a rate of 1 μg/kg per minute, adjusted based on blood pressure. This agent acts rapidly, taking effect within half a minute, but its effects also disappear quickly after discontinuation. Therefore, blood pressure changes must be closely monitored. This agent should be freshly prepared, and the infusion bottle should be shielded from light. Diazoxide can also be used for blood pressure reduction, administered intravenously at 3-5 mg/kg, taking effect in 1-2 minutes and lasting 4-12 hours. For patients with convulsions, in addition to blood pressure reduction, oxygen supply, anticonvulsant therapy, and symptomatic treatment should be promptly provided.
5. For severe circulatory congestion, aggressive diuresis should be pursued, and sodium nitroprusside can be administered intravenously to reduce cardiac preload and afterload. Digitalis drugs are generally not used for circulatory congestion symptoms. However, for cases of true heart failure, fast-acting cardiotonic agents such as cedilanid should be selected, and the dose should be small to avoid cumulative toxicity. For patients unresponsive to conservative drug therapy, dialysis can be performed to rapidly achieve dehydration and restore blood volume.
6. Acute Renal Insufficiency (see relevant chapter).
7. Dialysis Therapy: Suitable for acute renal failure and cases of high blood volume unresponsive to conservative treatment.

bubble_chart Differentiation

1. Attention should be paid to avoid misdiagnosing atypical cases as fistula disease, and those with prominent manifestations such as circulatory congestion or hypertensive encephalopathy should not be misdiagnosed.
2. It should be distinguished from certain primary glomerular diseases that present with acute nephritic syndrome at a certain stage of the disease course. Examples include IgA nephropathy (often presenting with hematuria 1–2 days after respiratory infection, usually without significant edema or hypertension, and normal complement levels) and membranoproliferative glomerulonephritis, among others. A biopsy may be necessary for differentiation. The initial stage of rapidly progressive glomerulonephritis often resembles acute nephritis, but renal function progressively deteriorates over weeks or months, with oliguria progressing to uremia and a poor prognosis.
3. It should also be distinguished from systemic diseases involving the kidneys, such as systemic lupus erythematosus, vasculitis, Henoch-Schönlein purpura, hemolytic-uremic syndrome, and hereditary nephritis.
4. During the course of chronic nephritis, acute exacerbations triggered by factors such as infection, urinary tract obstruction, or medication use should also be differentiated from acute nephritis.
5. It should be distinguished from post-infectious nephritis caused by non-streptococcal pathogens.
6. In a few children with acute nephritis, proteinuria may be significant, even reaching nephrotic levels, making it difficult to distinguish from nephritic-type nephrotic syndrome. In such cases, close clinical follow-up or even renal biopsy may be required for differentiation.