Why Glomerulonephritis Is Classified as an Immune-Mediated Inflammation
When most people think of inflammation, they often associate it with infections caused by pathogens such as bacteria or viruses—conditions that typically require antibiotic or antiviral treatments. However, glomerulonephritis, whether in its acute or chronic form, is fundamentally different. It is not the result of a direct infection within the kidney but rather an immune-mediated inflammatory condition. This means the body's own immune system mistakenly targets the glomeruli—the tiny filtering units in the kidneys—leading to tissue damage and impaired kidney function.
Understanding Immune Complex Deposition in the Kidneys
The root cause of glomerulonephritis lies in the formation and deposition of antigen-antibody complexes. When antigens—foreign or self-produced substances—are detected by the immune system, antibodies are generated to neutralize them. These immune complexes can circulate through the bloodstream and eventually become trapped in the delicate structures of the glomeruli, particularly in the mesangial areas or along the basement membranes.
Once deposited, these complexes trigger a cascade of immune responses, including the activation of complement proteins and recruitment of inflammatory cells. This leads to swelling, cellular damage, and disruption of the filtration barrier. As a result, key clinical signs emerge: proteinuria (excess protein in urine), hematuria (blood in urine), and elevated serum creatinine levels—hallmarks of declining kidney function.
Types of Antigens Involved in Glomerular Damage
Antigens involved in this process are broadly categorized into two types: endogenous (internal) and exogenous (external). Endogenous antigens originate from the body itself—such as nuclear components like DNA, which may be released during cell death or autoimmune conditions like systemic lupus erythematosus (SLE). Exogenous antigens come from outside sources, including bacterial proteins (e.g., streptococcal antigens post-infection), viral particles, or fungal elements.
Regardless of origin, when these antigens bind with antibodies, they form immune complexes that deposit in the glomeruli. Over time, this accumulation causes structural damage and chronic inflammation, progressively impairing renal function if left unchecked.
Why Antibiotics Are Not the Solution
Given that glomerulonephritis stems from immune dysregulation rather than active infection, treatment does not rely on antimicrobial agents. Administering antibiotics would be ineffective and potentially harmful due to unnecessary exposure and risk of resistance.
Instead, the cornerstone of therapy involves modulating the overactive immune response. Clinicians typically prescribe corticosteroids and other immunosuppressive drugs—such as cyclophosphamide, mycophenolate mofetil, or rituximab—depending on the underlying cause and severity of disease. These medications help reduce inflammation, minimize immune complex formation, and protect the kidneys from further injury.
Long-Term Management and Prognosis
Early diagnosis and targeted immunosuppressive therapy are crucial for preserving kidney health and preventing progression to end-stage renal disease. Patients often require ongoing monitoring of urine protein levels, blood pressure control, and lifestyle adjustments—including low-sodium diets and avoidance of nephrotoxic substances.
In autoimmune-related cases, managing the primary condition (e.g., lupus or vasculitis) is equally important. With proper care, many individuals experience remission or significantly slowed disease progression, highlighting the importance of understanding glomerulonephritis as an immune-driven disorder rather than an infectious one.