Glomerulonephritis

Glomerulonephritis is immune-mediated injury to the glomerular capillary wall. Inflammation disrupts the filtration barrier, so red blood cells and protein escape into the urine. Swelling and damage within the glomerulus also reduce the filtration rate. The kidney then retains sodium and water, which contributes to oliguria, oedema, and hypertension. That mechanism produces the nephritic syndrome: hematuria, red blood cell casts, reduced urine output, rising creatinine, hypertension, and mild-to-moderate proteinuria, generally below 3.5 g in 24 hours. Red blood cell casts are especially useful because they indicate that bleeding occurred within the nephron rather than in the bladder or urethra. The nephrotic syndrome is dominated by protein loss rather than visible inflammatory bleeding. It is defined by proteinuria above 3.5 g per 24 hours, or a urine protein-to-creatinine ratio above 350 mg/mmol, together with serum albumin below 30 g/L, peripheral oedema, and hyperlipidaemia. Large urinary protein losses lower plasma oncotic pressure, pulling fluid into the tissues. The liver responds by increasing lipoprotein production, while urinary loss of anticoagulant proteins and immunoglobulins increases thromboembolism and infection risk. These are clinical syndromes, not...