renal corpuscle

STRUCTURE - Glomerulus: tuft of fenestrated capillaries between afferent (larger, wider) and efferent arterioles. Located in renal cortex. - Bowman capsule: parietal layer (simple squamous epithelium) and visceral layer (podocytes). Space between = Bowman (urinary) space, which drains into the proximal convoluted tubule at the urinary pole. The vascular pole is where the afferent/efferent arterioles enter/exit. - Mesangial cells: lie between capillary loops; provide structural support, phagocytose debris/immune complexes, secrete matrix, and are contractile (regulate GFR). Related to the juxtaglomerular apparatus (extraglomerular mesangium/lacis cells).

GLOMERULAR FILTRATION BARRIER (3 layers) 1. Fenestrated capillary endothelium (70–100 nm pores): blocks blood cells; has negatively charged glycocalyx. 2. Fused basement membrane (GBM): type IV collagen, laminin, and heparan sulfate (negative charge) - main charge barrier. 3. Podocyte foot processes (pedicels) with filtration slits bridged by slit diaphragms (nephrin, podocin, CD2AP). Size and charge selectivity: small, cationic molecules pass more readily; albumin (~69 kDa, anionic) is mostly repelled.

PHYSIOLOGY - GFR = Kf × [(PGC − PBS) − (πGC − πBS)]; normal ~100–125 mL/min. Filtration fraction = GFR/RPF (~20%). - Afferent arteriole constriction: ↓RPF, ↓GFR, ↓FF. Efferent constriction (e.g., angiotensin II): ↓RPF, ↑GFR, ↑FF. NSAIDs dilate-block afferent dilation (↓PGE2) → ↓GFR; ACE inhibitors/ARBs dilate efferent → ↓GFR. - Juxtaglomerular apparatus at vascular pole: JG cells (renin), macula densa (NaCl sensing in the DCT), mesangial cells.

CLINICAL CORRELATIONS - Nephrotic syndrome (proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia, hypercoagulability): loss of charge/size barrier. Minimal change disease (effacement of foot processes on EM, normal light microscopy, responds to steroids; kids; post-infection/Hodgkin), FSGS (HIV, heroin, sickle cell; Black patients), membranous nephropathy (anti-PLA2R; "spike and dome" subepithelial deposits), diabetic nephropathy (Kimmelstiel-Wilson nodules, GBM thickening, mesangial expansion), amyloidosis (Congo red, apple-green birefringence). - Nephritic syndrome (hematuria, RBC casts, HTN, oliguria, azotemia): inflammation of the corpuscle. Post-streptococcal GN (subepithelial humps, "lumpy-bumpy" IF, ↓C3), IgA nephropathy (Berger; mesangial IgA, 1–3 days post-URI), RPGN (crescents of parietal epithelial cells/fibrin; anti-GBM/Goodpasture with linear IF; pauci-immune ANCA), lupus nephritis (wire-loop lesions, "full-house" IF), MPGN. - Alport syndrome: X-linked, COL4A5 mutation (type IV collagen) → hematuria, sensorineural hearing loss, ocular defects, "basket-weave" GBM. - Congenital nephrotic syndrome (Finnish type): nephrin (NPHS1) mutation. - Histology: PAS stains basement membrane/mesangium; EM best for localizing deposits (subendothelial vs subepithelial) and foot process effacement.

HIGH-YIELD MNEMONIC: Filtration barrier layers from blood to urine = Endothelium → GBM → Podocytes ("EGP").