Which is a common etiology of acute glomerulonephritis?

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Multiple Choice

Which is a common etiology of acute glomerulonephritis?

Explanation:
Acute glomerulonephritis is classically immune complex–mediated and often follows a streptococcal infection of the throat or skin. After such an infection, antibodies form against streptococcal antigens and circulate as immune complexes. These complexes can deposit in the glomeruli, triggering inflammation and activating complement. The resulting damage to the glomerular basement membrane leads to the hallmark nephritic picture: abrupt onset of hematuria (often dark or tea-colored urine), mild to moderate proteinuria, edema, and sometimes hypertension. The complement level, especially C3, can be reduced during the acute phase, supporting this mechanism. This sequence commonly occurs about 1–3 weeks after throat infection or 3–6 weeks after skin infection, making post-streptococcal illness a quintessential cause of acute GN. The other options describe conditions that are not typical causes of acute glomerulonephritis. Diabetic nephropathy and polycystic kidney disease are chronic, long-standing diseases that cause progressive kidney dysfunction rather than an abrupt nephritic presentation. Hydronephrosis results from obstruction and can affect kidney function, but it isn’t a primary immune-mediated glomerular inflammation leading to acute GN.

Acute glomerulonephritis is classically immune complex–mediated and often follows a streptococcal infection of the throat or skin. After such an infection, antibodies form against streptococcal antigens and circulate as immune complexes. These complexes can deposit in the glomeruli, triggering inflammation and activating complement. The resulting damage to the glomerular basement membrane leads to the hallmark nephritic picture: abrupt onset of hematuria (often dark or tea-colored urine), mild to moderate proteinuria, edema, and sometimes hypertension. The complement level, especially C3, can be reduced during the acute phase, supporting this mechanism. This sequence commonly occurs about 1–3 weeks after throat infection or 3–6 weeks after skin infection, making post-streptococcal illness a quintessential cause of acute GN.

The other options describe conditions that are not typical causes of acute glomerulonephritis. Diabetic nephropathy and polycystic kidney disease are chronic, long-standing diseases that cause progressive kidney dysfunction rather than an abrupt nephritic presentation. Hydronephrosis results from obstruction and can affect kidney function, but it isn’t a primary immune-mediated glomerular inflammation leading to acute GN.

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