Clinical Manifestations In glomerulonephritic diseases, damage to the glomerular capillary wall results in the leakage of red blood cells and proteins, which are normally too large to cross the glomerular capillary, into the renal tubular lumen, giving rise to hematuria and proteinuria. The GFR falls either because glomerular capillaries are infiltrated with inflammatory cells or because contractile cells (eg, mesangial cells) respond to vasoactive substances by restricting blood flow to many glomerular capillaries. Decreased GFR leads to fluid and salt retention that clinically manifests as edema and hypertension. A fall in serum complement is observed as a result of immune complex and complement deposition in the glomerulus, as can be seen with lupus nephritis, membranoproliferative GN and post-infectious GN. An elevated titer of antibody to streptococcal antigens is observed in cases associated with group A β-hemolytic streptococcal infections. Another characteristic of the clinical course in poststreptococcal acute GN is a lag between clinical
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