Glomerulonephritis in children

Causes and classification

In most clinical situations, the exact cause of the disease remains unclear—such forms are referred to as idiopathic. If a trigger is identified, glomerulonephritis (GN) is classified as secondary. It may develop against the background of systemic lupus erythematosus, vasculitis, chronic viral hepatitis (B or C), or Crohn's disease.

Among established infectious factors, bacteria (especially streptococci), viruses (CMV, HIV, enteroviruses, herpes), and even parasites (malarial plasmodium) are the leaders. Inflammation can be triggered by medications (NSAIDs, gold salts), toxins, and non-infectious triggers such as vaccination or severe hypothermia, which provoke an allergic reaction in the presence of sensitization.

Based on the clinical course, the process is divided into acute, rapidly progressive, and chronic. However, the gold standard of modern nephrology is the morphological classification based on the results of a lifetime renal biopsy. It is grounded in the assessment of the presence and degree of cellular proliferation in the tissues.

Mechanisms of immune-mediated glomerular damage

Glomerulonephritis is triggered as an immune response to a foreign antigen. There are two main scenarios for the destruction of the renal filter:

1. Immune complex mechanism. Antigen-antibody complexes form in the bloodstream or directly within the glomerulus (in situ). They activate the complement system. This results in a massive release of chemotactic factors that attract leukocytes and platelets. A membrane attack complex (MAC) is formed, which directly punctures the glomerular basement membrane (GBM) while simultaneously activating the coagulation and kinin systems.
2. Antibody-mediated (cytotoxic) mechanism. The body begins producing antibodies against its own renal tissues: basement membrane glycoproteins, podocyte antigens, or mesangial cell antigens. Depositing on glomerular structures, these antibodies trigger the inflammatory cascade.

In response to injury, blood cells migrate into the glomeruli. A massive secretion of cytokines (TNFα, IL-1), growth factors, and enzymes begins. Prolonged inflammation forces the resident renal cells to divide uncontrollably (proliferation) and synthesize excessive extracellular matrix, ultimately leading to the replacement of functional tissue with a scar—glomerulosclerosis.

Non-immune factors in chronification

In addition to immune aggression, the progression of renal failure is driven by secondary factors:

• Hemodynamic shock. Due to systemic hypertension and attempts by surviving nephrons to shoulder a double workload, pressure rises inside the glomeruli. The filter is stretched, and plasma macromolecules become trapped in the tissues, locally activating the renin-angiotensin-aldosterone system (RAAS). Angiotensin II acts as a stimulant for cell proliferation.
• Toxicity of proteinuria. Proteins that have "broken through" the damaged filter are reabsorbed by the proximal tubular epithelium. The epithelium becomes overloaded and begins secreting chemokines and endothelin, provoking secondary inflammation and fibrosis in the tubulointerstitial tissue.
• Hyperlipidemia. Excess lipids are toxic to the capillary endothelium. Their lipid peroxidation products cause mesangial cells to synthesize collagen, accelerating glomerular destruction.

Principles of inpatient treatment

Children with acute glomerulonephritis are treated strictly in an inpatient setting. Therapy is based on several foundational lines:

• Strict diet and fluid management. Fluid intake is calculated based on the previous day's diuresis plus insensible losses. A salt-free diet is prescribed during the edema and hypertension phase. Protein is strictly restricted (0.5–1.0 g/kg/day), and potassium-rich foods are excluded, maintaining energy balance through fats and carbohydrates.
• Antibacterial support. Indicated in active streptococcal infection. Penicillins (amoxicillin) are prescribed for 7–10 days; in case of intolerance, macrolides or cephalosporins are used.
• Symptomatic control. Loop diuretics (furosemide) are used to relieve edema. For persistent hypertension, calcium channel blockers or beta-blockers are used.
• Hemostasis correction. Antiplatelet agents are used to improve microcirculation, and in nephrotic syndrome (when the risk of thrombosis is high), anticoagulants are used.

Class and exam questions

What else to study on this topic

• Clinical presentation of nephrotic and nephritic syndromes
• Specifics of immunosuppressive therapy (glucocorticoids and cytostatics)
• Indications for renal replacement therapy (dialysis) in acute kidney injury
• Differential diagnosis with IgA nephropathy and hereditary nephritis
• Morphological picture of fibroplastic glomerulonephritis

Other topics in "Chapter 8. Kidney and Urinary Tract Diseases"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.