Bowman capsule

**Structure** - Parietal layer: simple squamous epithelium that forms the outer wall of the capsule. It is continuous with the proximal tubule epithelium at the urinary pole. - Visceral layer: made of podocytes, which wrap around the glomerular capillaries. Their foot processes interdigitate and form filtration slits. - Bowman (urinary) space: the space between the parietal and visceral layers. It receives the ultrafiltrate. - Vascular pole: where the afferent arteriole enters and the efferent arteriole exits. - Urinary pole: where the capsule opens into the proximal convoluted tubule.

**Glomerular filtration barrier (blood to Bowman space), 3 layers** 1. Fenestrated capillary endothelium. It blocks cells and is size-selective. 2. Glomerular basement membrane (GBM). It contains type IV collagen and heparan sulfate, which give it a negative charge and make it charge-selective against anions such as albumin. 3. Podocyte foot processes with slit diaphragms (nephrin, podocin).

**Filtration physiology** - Starling forces: GFR = Kf [(P_GC − P_BS) − (π_GC − π_BS)]. - Net filtration pressure = P_GC − P_BS − π_GC. π_BS is normally about 0 because filtrate has almost no protein. - Increased Bowman space hydrostatic pressure (P_BS) lowers GFR. Causes include ureteral obstruction and stones. - Efferent arteriole constriction (angiotensin II) raises P_GC and GFR, and raises filtration fraction. - Afferent arteriole constriction (NSAIDs) lowers GFR.

**Clinical correlations** - Nephrotic syndrome: podocyte injury or loss of GBM charge barrier causes massive proteinuria (>3.5 g/day), hypoalbuminemia, edema, and hyperlipidemia. - Minimal change disease (most common in children): effacement of foot processes on EM, normal light microscopy, responds to steroids. - Membranous nephropathy: subepithelial immune deposits ("spike and dome"), anti-PLA2R antibodies. - FSGS: segmental sclerosis, associated with HIV, heroin use, and obesity. - Nephritic syndrome: inflammation of the glomerulus causes hematuria, RBC casts, hypertension, and oliguria. - Poststreptococcal GN: subepithelial "humps," "lumpy-bumpy" immunofluorescence. - Rapidly progressive (crescentic) GN: proliferation of parietal epithelial cells of Bowman capsule plus macrophages and fibrin forms "crescents" in Bowman space. - Anti-GBM disease (Goodpasture): type IV collagen (α3 chain) antibodies, linear IF, hemoptysis plus GN. - Pauci-immune (ANCA-associated): GPA, MPA, EGPA. - Immune complex-mediated: lupus nephritis, IgA nephropathy. - Alport syndrome: type IV collagen mutation, which causes hematuria, sensorineural deafness, and ocular defects. EM shows a "basket-weave" GBM. - Diabetic nephropathy: GBM thickening and mesangial expansion, with Kimmelstiel-Wilson nodules.

**High-yield pearls** - The renal corpuscle = glomerulus + Bowman capsule. The nephron = renal corpuscle + tubule. - The parietal layer of Bowman capsule is the source of cells in crescents. - Mesangial cells lie between capillary loops and provide structural support and phagocytic function. - Normal filtrate has no cells and essentially no protein. Size cutoff is about 70 kDa, and albumin (~69 kDa) is mostly held back by charge.