Why does the kidney produce only 1.5 L of urine from 180 L of filtrate?
Because the PCT reabsorbs 65–70% of the filtrate (obligatory osmosis following active solute reabsorption), the loop of Henle exchanges additional water and creates the medullary gradient, the DCT reabsorbs additional water and ions under hormonal control, and the collecting duct reabsorbs water under ADH influence as it passes through the hyperosmotic medulla. The combined 99% reabsorption leaves only 1.5 L (0.83%) as urine.
Why does dehydration produce concentrated urine?
Dehydration → blood osmolarity rises → hypothalamic osmoreceptors detect this → ADH released from posterior pituitary → aquaporin-2 channels inserted into DCT and collecting duct membranes → water exits collecting duct by osmosis into hyperosmotic medullary interstitium → concentrated urine produced. Simultaneously, reduced blood volume activates RAAS → aldosterone → more Na+ reabsorbed → more water follows (additional concentration effect).
Why must the ascending limb of the loop of Henle be water-impermeable?
If the ascending limb were permeable to water, the NaCl pumped out would draw water back in by osmosis, preventing net solute accumulation in the medullary interstitium. The water impermeability ensures that NaCl accumulates in the medullary interstitium without water following it — this is the only way to build a hyperosmotic medullary gradient. The impermeable ascending limb is structurally essential for the counter-current multiplier to function.
Why does glomerulonephritis cause oedema even though the kidney is not directly involved in fluid storage?
Glomerulonephritis damages the glomerular filtration barrier → proteins (primarily albumin) pass into filtrate → proteinuria → hypoalbuminaemia in blood. Albumin is the primary contributor to plasma oncotic (colloid osmotic) pressure, which normally opposes the outward filtration pressure at capillaries and keeps fluid in the bloodstream. When albumin falls, plasma oncotic pressure drops → net Starling force shifts to push fluid out of capillaries into interstitial spaces → oedema. Additionally, reduced GFR → Na+ and water retention further aggravates fluid accumulation.
How does the RAAS raise blood pressure?
Low BP → JG cells detect reduced stretch → renin released → cleaves angiotensinogen (from liver) to angiotensin I → ACE (pulmonary capillary endothelium) converts to angiotensin II → (1) angiotensin II directly causes vasoconstriction (raises peripheral resistance → raises BP immediately); (2) angiotensin II stimulates aldosterone from adrenal cortex → Na+ reabsorption in DCT → water follows → increased blood volume → raised BP (slower, volume effect); (3) angiotensin II stimulates ADH release → more water retained → further volume increase.