Glomerulonefriitin

Glomerulonefriitin, commonly referred to as glomerulonephritis, is an inflammation of the glomeruli, the tiny filtering units of the kidneys. It can be acute or chronic and arises from immune-mediated injury, infections, vasculitis, or systemic diseases. The inflammatory process often involves immune complex deposition or autoantibodies, leading to damage of the glomerular capillary walls and impaired filtration.

Clinical features vary but commonly include hematuria (blood in the urine), which may be visible or microscopic, proteinuria, hypertension, edema, and reduced kidney function. In some cases, patients present with nephritic syndrome (hematuria, hypertension, and modest proteinuria) or nephrotic syndrome (heavy proteinuria, hypoalbuminemia, edema).

Diagnosis relies on history, examination, urinalysis (showing red blood cell casts and proteinuria), and blood tests. Complement levels may be low in certain post-infectious or immune-mediated forms; serologic tests for specific causes (such as anti-streptolysin O, ANA, anti-dsDNA, ANCA, or anti-GBM antibodies) may be helpful. A kidney biopsy is often performed to determine the precise type and guide treatment.

Causes are diverse and include post-infectious glomerulonephritis (often after streptococcal infection), IgA nephropathy, membranoproliferative GN, lupus nephritis, ANCA-associated vasculitis, and anti-GBM disease.

Treatment targets the underlying cause and supportive management. This includes control of blood pressure and proteinuria (commonly with ACE inhibitors or ARBs), management of edema, and, in many inflammatory or vasculitic forms, immunosuppressive therapy (corticosteroids and/or other agents). Plasma exchange may be needed in anti-GBM disease or severe vasculitis. Infections should be treated, and kidney function monitored.

Prognosis varies; many patients recover after acute GN, while others progress to chronic kidney disease or renal failure, influenced by etiology, severity, and treatment response.