renal cortex

**Anatomy** - Outermost parenchyma of the kidney, deep to the fibrous capsule. It extends inward between the pyramids as the renal columns of Bertin. - Contains: all renal corpuscles (glomerulus + Bowman capsule), proximal convoluted tubules (PCT), distal convoluted tubules (DCT), cortical thick ascending limb, the macula densa and juxtaglomerular apparatus, cortical collecting ducts, and the medullary rays (straight tubules and collecting ducts that extend into the cortex). - Vasculature: interlobar → arcuate → interlobular (cortical radiate) arteries → afferent arterioles → glomerular capillaries → efferent arterioles → peritubular capillaries. The cortex gets about 90% of renal blood flow. The medulla gets about 10% and has the vasa recta. - Cortical (superficial) nephrons have short loops of Henle. Juxtamedullary nephrons have glomeruli at the corticomedullary junction and long loops that are important for urine concentration.

**Physiology** - Glomerular filtration: the filtration barrier consists of fenestrated endothelium, glomerular basement membrane (type IV collagen, heparan sulfate, negative charge), and podocyte foot processes with slit diaphragms (nephrin, podocin). - PCT reabsorbs about 65% of filtered Na⁺ and water. It reabsorbs nearly all glucose (SGLT2), amino acids, and bicarbonate, and it handles phosphate (PTH-sensitive) and organic acid/base secretion. - DCT: Na⁺/Cl⁻ cotransporter (NCC), which thiazides block. Ca²⁺ reabsorption is PTH-stimulated. - Cortical collecting duct: principal cells (ENaC, ROMK; aldosterone-sensitive; ADH-responsive via aquaporin-2) and α-intercalated cells (H⁺ secretion). - JG apparatus: JG cells secrete renin, and the macula densa senses NaCl delivery (tubuloglomerular feedback). - Endocrine: peritubular interstitial fibroblasts in the cortex make erythropoietin. 1α-hydroxylase in the PCT activates vitamin D (25-OH → 1,25-(OH)₂ vitamin D).

**Clinical significance/associations** - Diseases that affect the cortex: glomerulonephritides (nephritic and nephrotic syndromes), acute tubular necrosis (PCT and the thick ascending limb are especially vulnerable), and acute cortical necrosis (for example in septic shock or abruptio placentae, with DIC and diffuse ischemia). - Renal cell carcinoma arises from PCT epithelium (clear cell type, VHL/3p deletion). Angiomyolipoma (tuberous sclerosis) is also cortical. - Medulla versus cortex: the papilla is vulnerable to ischemia and to NSAID injury (papillary necrosis, seen in sickle cell disease, diabetes, analgesic nephropathy, and pyelonephritis), whereas the cortex is more vulnerable to glomerular disease and to ATN. - Chronic kidney disease: loss of cortical mass leads to small, echogenic kidneys with cortical thinning on ultrasound. Loss of EPO production causes normocytic anemia, and loss of 1α-hydroxylase causes secondary hyperparathyroidism and renal osteodystrophy. - Imaging: normal cortex is slightly hypoechoic relative to the liver or spleen. Increased cortical echogenicity suggests intrinsic medical renal disease. - Polycystic kidney disease (ADPKD, PKD1/PKD2) produces cysts in both the cortex and the medulla. - Pyelonephritis scarring: cortical scars (often over a blunted calyx) are classic for chronic pyelonephritis and vesicoureteral reflux. - Cortical thinning with a "thyroidization" pattern (eosinophilic casts in dilated tubules) is typical of chronic pyelonephritis.

**High-yield pearls** - Cortex: filtration, bulk reabsorption, and EPO and renin production. Medulla: concentration and dilution of urine. - The cortex is highly vascular, so it appears dark red-brown on gross specimens. The medulla is paler. - Renal oxygen tension is higher in the cortex than the medulla, so the medulla is more hypoxic and vulnerable to ischemia (especially the thick ascending limb in the outer medulla).