Anatomy – Urinary/Excretory (2026)

Overview

Aiden Xie. Renal physiology regulates volume, osmolality, electrolytes, and acid–base via filtration, reabsorption, secretion, and excretion across specialized nephron segments.

Nephron organization and transport (survey)

• Glomerulus: filtration barrier (fenestrated endothelium, basement membrane, podocytes). GFR depends on hydrostatic/oncotic pressures; autoregulation (myogenic, tubuloglomerular feedback via macula densa).
• Proximal tubule: bulk reabsorption (Na⁺, glucose/AA via cotransport, HCO₃⁻ reclamation via Na⁺/H⁺ exchanger + carbonic anhydrase); water follows iso‑osmotically; secretion (organic acids/bases).
• Loop of Henle: thin descending (water permeable, solute‑impermeable), thick ascending (Na⁺–K⁺–2Cl⁻, impermeable to water). Countercurrent multiplier creates corticomedullary gradient.
• Distal convoluted tubule: Na⁺–Cl⁻ cotransport; Ca²⁺ reabsorption (PTH‑regulated).
• Collecting duct: principal cells (ENaC, aldosterone ↑Na⁺ reabsorption/K⁺ secretion; ADH inserts aquaporin‑2 for water reabsorption); intercalated cells (Type A secrete H⁺, reabsorb HCO₃⁻; Type B reverse in alkalosis).

Concentrating mechanism

• Countercurrent multiplier (loop) + countercurrent exchanger (vasa recta) preserve gradient; urea recycling contributes to inner medullary osmolality (ADH facilitates urea permeability in IMCD).

Hormonal control

• RAAS: ↓renal perfusion → renin → Ang II (efferent constriction, ↑proximal Na⁺ reabsorption) → aldosterone (↑ENaC/Na⁺/K⁺‑ATPase in principal cells) → ↑Na⁺ and water retention.
• ADH: acts on V₂ receptors → aquaporin‑2 insertion; ↑water reabsorption; V₁ vasoconstriction (survey).
• ANP: opposes RAAS; ↑natriuresis; dilates afferent, constricts efferent; inhibits Na⁺ reabsorption.

Acid–base handling (survey)

• Proximal: HCO₃⁻ reclamation via CA; NH₄⁺ generation from glutamine enables net acid excretion.
• Distal: Type A intercalated cells secrete H⁺ (H⁺‑ATPase/H⁺‑K⁺‑ATPase) and reabsorb HCO₃⁻; Type B secrete HCO₃⁻.

Worked micro‑examples

1. Diuretic sites

• Loop diuretic blocks NKCC2 → ↓medullary gradient → ↑diuresis; thiazide blocks NCC in DCT; K⁺‑sparing blocks ENaC or aldosterone effects.

2. Water deprivation

• ↑ADH → ↑aquaporins in collecting duct → concentrated urine; high urea recycling augments inner medullary gradient.

3. Metabolic acidosis

• Kidney increases NH₄⁺ production and H⁺ secretion; urine anion gap becomes negative in GI loss vs positive in distal RTA (conceptual distinction).

Pitfalls

• Confusing water permeability along nephron (descending limb vs ascending limb).
• Overlooking urea’s role in concentration at high ADH.
• Mixing intercalated cell types.

Practice prompts

• Trace a filtered glucose molecule from glomerulus to peritubular capillary; identify transporters.
• Predict effects of ACE inhibitor on GFR in bilateral renal artery stenosis (concept level).
• Explain why thiazides increase Ca²⁺ reabsorption while loops increase Ca²⁺ excretion.

References

• SciOly Wiki – Anatomy & Physiology (Renal)
• OpenStax Anatomy & Physiology (Urinary system)