Glomerular diseases are classified by their clinical presentation into nephritic and nephrotic syndromes. Nephritic syndrome results from inflammation of the glomerular capillaries (glomerulonephritis), causing disruption of the glomerular basement membrane (GBM). Inflammatory cells infiltrate the glomerulus, allowing red blood cells and some protein to pass into the urine. The hallmark is hematuria (often with RBC casts indicating glomerular origin). The inflammatory process reduces GFR, causing oliguria, azotemia, hypertension, and mild-moderate proteinuria (<3.5 g/day). Classic causes include post-streptococcal GN (immune complex deposition 1-3 weeks after group A strep pharyngitis), IgA nephropathy (most common worldwide), and rapidly progressive GN (RPGN - crescentic GN with rapid loss of kidney function). Nephrotic syndrome results from increased glomerular permeability to proteins without significant inflammation. Massive proteinuria (>3.5 g/day) causes hypoalbuminemia, which reduces plasma oncotic pressure and leads to generalized edema (anasarca). Loss of antithrombin III and immunoglobulins increases risk of thromboembolism and infection. Hyperlipidemia develops as the liver increases lipoprotein synthesis in response to low albumin. Key causes include minimal change disease (most common in children), membranous nephropathy, focal segmental glomerulosclerosis (FSGS), and diabetic nephropathy.