Acute Glomerulonephritis in children

Acute Glomerulonephritis in Children Submitted to Muktarali kyzy begimai by Riya Patil of Group 32 1. Introduction Acute glomerulonephritis (AGN) is a clinical syndrome characterized by the sudden onset of hematuria, proteinuria, hypertension, and varying degrees of renal dysfunction. It primarily results from inflammation of the glomeruli, the filtering units of the kidney. In children, AGN is a significant cause of acute kidney injury and can result in serious complications if not promptly recognized and managed. The condition is most commonly post-infectious, especially following a streptococcal infection, but may also arise from a variety of other causes, including autoimmune and systemic diseases. The incidence of AGN in children varies globally, influenced by socioeconomic conditions, healthcare access, and infection rates. Early detection, appropriate investigation, and prompt treatment are crucial in ensuring favorable outcomes and preventing long-term renal damage. This article provides a comprehensive overview of acute glomerulonephritis in children, discussing its epidemiology, pathogenesis, clinical features, diagnostic approach, management, and prognosis. 2. Epidemiology Acute glomerulonephritis is more common in children between the ages of 5 and 12 years, with a slight male predominance. Post-streptococcal glomerulonephritis (PSGN) is the most frequent form seen in this age group, particularly in developing countries where streptococcal infections are more prevalent due to overcrowding and limited healthcare access. The incidence of PSGN has declined in developed countries due to improved hygiene and prompt treatment of streptococcal infections. However, other causes of AGN, such as Henoch-Schönlein purpura nephritis and lupus nephritis, remain significant contributors. Seasonal variations are also observed, with a higher incidence of PSGN during colder months, correlating with the increased prevalence of streptococcal infections. 3. Etiology and Risk Factors The etiology of acute glomerulonephritis in children can be broadly categorized into infectious and non-infectious causes: Infectious Causes: - Post-streptococcal (most common) - Other bacterial infections (e.g., staphylococcus, pneumococcus) - Viral infections (e.g., hepatitis B and C, HIV, Epstein-Barr virus) - Parasitic infections (e.g., malaria, schistosomiasis) Non-infectious Causes: - IgA nephropathy - Henoch-Schönlein purpura (now called IgA vasculitis) - Systemic lupus erythematosus - Membranoproliferative glomerulonephritis - Vasculitides (e.g., granulomatosis with polyangiitis) Risk Factors: - Recent history of sore throat or skin infection - Poor socioeconomic conditions - Inadequate treatment of streptococcal infections - Family history of autoimmune diseases - Certain genetic predispositions 4. Pathophysiology The pathophysiology of AGN involves immune-mediated injury to the glomeruli. In post-infectious GN, for instance, streptococcal antigens form immune complexes that deposit in the glomerular basement membrane, triggering complement activation and recruitment of inflammatory cells. This results in glomerular inflammation, proliferation of mesangial and endothelial cells, and damage to the capillary walls, causing leakage of red blood cells and protein into the urine. In diseases like lupus nephritis, autoantibodies target native antigens in the kidney, while in IgA nephropathy and IgA vasculitis, there is deposition of IgA-containing immune complexes. The precise mechanisms may vary, but all forms of AGN share the common endpoint of glomerular inflammation and injury. 5. Clinical Features The clinical presentation of AGN can range from asymptomatic microscopic hematuria to full-blown nephritic syndrome. Common features include: - Hematuria (often cola- or tea-colored urine) - Proteinuria (usually sub-nephrotic) - Edema (especially periorbital and lower extremities) - Hypertension - Oliguria or decreased urine output - General malaise, fatigue, and irritability In severe cases, children may present with signs of acute kidney injury, such as elevated creatinine, fluid overload, and uremic symptoms (e.g., nausea, vomiting, confusion). 6. Diagnosis A thorough history and physical examination are critical. The diagnosis is supported by laboratory and imaging studies: Laboratory Tests: - Urinalysis: hematuria, proteinuria, red blood cell casts - Blood tests: elevated BUN and creatinine, low complement (C3) levels (especially in PSGN) - Antistreptolysin O (ASO) titer or anti-DNase B: evidence of recent streptococcal infection - Complete blood count: may show anemia or leukocytosis - Autoimmune panel: ANA, anti-dsDNA, ANCA (for suspected lupus or vasculitis) Imaging: - Renal ultrasound: may show enlarged kidneys with increased echogenicity Renal Biopsy: - Reserved for atypical cases, rapidly progressive disease, or suspicion of systemic disease - Helps determine exact histopathology and guide treatment 7. Differential Diagnosis The differential diagnosis for AGN includes: - Nephrotic syndrome (primarily proteinuria and edema without hematuria or hypertension) - Hemolytic uremic syndrome - Acute interstitial nephritis - Urinary tract infection - Structural anomalies of the urinary tract 8. Complications Although many children recover fully from AGN, complications can occur: - Acute kidney injury - Hypertensive encephalopathy - Pulmonary edema - Electrolyte imbalances (e.g., hyperkalemia) - Chronic kidney disease (especially with recurrent or severe episodes) - End-stage renal disease (rare but serious) 9. Management and Treatment Management is largely supportive, with treatment tailored to the underlying cause. *General Measures:* - Bed rest during the acute phase - Salt and fluid restriction to manage edema and hypertension - Antihypertensive therapy (e.g., calcium channel blockers, ACE inhibitors) - Diuretics for fluid overload - Antibiotics if an ongoing infection is present (e.g., penicillin for streptococcal infection) *Specific Therapies:* - Corticosteroids: for cases with IgA nephropathy, lupus nephritis, or vasculitis - Immunosuppressive agents (cyclophosphamide, mycophenolate mofetil) for severe autoimmune GN - Plasma exchange in rapidly progressive GN or severe vasculitis - Dialysis in cases of severe acute kidney injury 13. Case Studies or Examples L *Case 1: Post-Streptococcal GN* A 7-year-old boy presents with dark-colored urine, facial swelling, and elevated blood pressure. He had a sore throat 2 weeks prior. Investigations show low C3, elevated ASO titer, and hematuria with red cell casts. He is managed with fluid restriction, antihypertensives, and close monitoring. He recovers completely within 4 weeks. Case 2: Lupus Nephritis A 12-year-old girl presents with fatigue, joint pain, and facial rash. Urinalysis reveals hematuria and proteinuria. ANA and anti-dsDNA are positive. Renal biopsy shows Class IV lupus nephritis. She is treated with corticosteroids and mycophenolate mofetil, with good response. Conclusion Acute glomerulonephritis in children remains an important pediatric condition requiring timely diagnosis and management. While most cases resolve without complications, a subset may progress to chronic kidney disease or require long-term follow-up. Improved understanding of the underlying pathophysiology and advances in treatment have significantly enhanced outcomes. Continued research and public health measures are essential to further reduce the burden of this condition, especially in resource-limited settings. Reference https://my.clevelandclinic.org/health/diseases/16167-glomerulonephritis-gn https://emedicine.medscape.com/article/239278-overview https://www.kidney.org/kidney-topics/glomerulonephritis https://en.wikipedia.org/wiki/Glomerulonephritis https://www.mayoclinic.org/diseases-conditions/glomerulonephritis/symptoms-causes/syc-20355705