Diagnosing Acute Glomerulonephritis in Children: A Comprehensive Approach
Acute glomerulonephritis (AGN) is a common kidney disorder in pediatric populations, often arising after a bacterial or viral infection. Early and accurate diagnosis is essential to prevent complications such as hypertension, fluid overload, or long-term renal damage. The diagnostic process involves a combination of clinical evaluation, laboratory testing, and careful differential analysis to determine both the presence and underlying cause of the condition.
Physical Examination: Identifying Key Clinical Signs
One of the first steps in diagnosing acute glomerulonephritis in children is a thorough physical examination. Physicians pay close attention to signs of edema, particularly around the face, periorbital area, and lower extremities. Swelling may be subtle but is often more noticeable in the morning due to fluid redistribution during sleep.
Blood pressure measurement is critical, as many children with AGN develop hypertension due to fluid retention and activation of the renin-angiotensin system. Elevated heart rate and signs of circulatory congestion—such as rapid breathing, jugular venous distension, or crackles in the lungs—may also indicate fluid overload, requiring prompt medical intervention.
Laboratory Testing: Assessing Kidney Function and Damage
Comprehensive laboratory tests are essential for evaluating the extent of kidney involvement. Urinalysis typically reveals hallmark signs of glomerular injury, including hematuria (blood in urine), which may present as cola-colored or tea-colored urine, and proteinuria (excess protein in urine).
The degree of proteinuria is quantified through a 24-hour urine collection or spot urine protein-to-creatinine ratio. Determining whether the proteinuria is glomerular (indicating damage to the filtration barrier) or tubular (suggesting impaired reabsorption) helps guide further diagnostic and treatment decisions. Blood tests, including serum creatinine and blood urea nitrogen (BUN), provide insight into overall kidney function and help stage the severity of renal impairment.
Identifying the Underlying Cause: Post-Infectious vs. Other Forms
While post-infectious glomerulonephritis—commonly following streptococcal infections like pharyngitis or impetigo—is the most frequent cause in children, it's vital to rule out other potential etiologies. Some cases initially diagnosed as acute may actually represent an early presentation of chronic glomerulonephritis or secondary forms triggered by systemic diseases.
To differentiate, clinicians assess specific serological markers. Antistreptolysin O (ASO) titers help confirm recent streptococcal infection. Complement levels, especially C3 and C4, are often measured; low C3 with normal or slightly reduced C4 is typical in post-streptococcal GN, while abnormalities in both may suggest alternative diagnoses such as lupus nephritis or membranoproliferative glomerulonephritis.
Differential Diagnosis: Ruling Out Systemic Conditions
In atypical presentations, further investigation is necessary to exclude secondary causes. For example, systemic lupus erythematosus (SLE) can manifest as lupus nephritis, particularly in older female children. In such cases, testing for antinuclear antibodies (ANA), anti-dsDNA, and additional complement components (C1q) becomes crucial.
Similarly, Henoch-Schönlein purpura (HSP)—a vasculitic condition—can lead to purpuric rash, joint pain, abdominal symptoms, and renal involvement. Physical examination for palpable purpura on the lower limbs and assessment of IgA levels support this diagnosis.
Viral etiologies, such as hepatitis B virus (HBV), must also be considered, especially in endemic regions or high-risk patients. Hepatitis B surface antigen (HBsAg) and other viral markers should be included in the workup when clinically suspected.
Tailoring Diagnosis for Optimal Outcomes
A precise diagnosis of acute glomerulonephritis in children requires integrating clinical findings with targeted lab investigations. Beyond confirming the diagnosis, identifying the root cause ensures appropriate management—whether it's supportive care for post-infectious cases or immunosuppressive therapy for autoimmune-related forms.
Early detection, careful monitoring, and individualized treatment plans significantly improve prognosis and reduce the risk of progression to chronic kidney disease. Pediatricians and nephrologists must remain vigilant, especially in cases with atypical features, to ensure every child receives timely and effective care.
