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Renal

Nephron explorer

Renal physiology is taught as a list and tested as a location. Click a segment to see what it reabsorbs, which transporter does it, which drug blocks that transporter and which syndrome breaks it, all in one place because that is how the question will come.

Click a segment

The nephron

CORTEX · 300 mOsmINNER MEDULLA · 1200 mOsmGlomerulusProximal tubuleDescending limbThick ascending limbDistal tubuleCollecting duct

The segment

Thick ascending limb of Henle

25% of filtered sodium

Two things happen here and both matter. Salt is pulled out of water-impermeable tubule, which dilutes the fluid inside and, by the same act, salts the medulla outside. That medullary saltiness is the gradient the descending limb and the collecting duct both depend on, which is why a loop diuretic does not merely lose sodium: it dismantles the machinery that lets the kidney concentrate urine at all. Separately, the potassium leaking back through ROMK leaves the lumen positive, and that charge pushes calcium and magnesium out between the cells.

The diluting segment, and the maker of the medullary gradient. Block it and you lose the ability to concentrate urine, plus calcium and magnesium.

Water

What happens to the fluid here

Impermeable to water. Salt leaves and water cannot follow, so the fluid is diluted.

Fluid leaving this segment100 mOsm/kg
Share of the filtered sodium load reclaimed here25%

Takes back

What is reabsorbed

  • About a quarter of filtered sodium
  • Potassium and chloride, on the same carrier
  • Calcium and magnesium, between the cells rather than through them

How

Transporters

  • NKCC2

    Brings in one sodium, one potassium and two chlorides together. The single most drugged transporter in the kidney.

  • ROMK

    Leaks the reabsorbed potassium back into the lumen. That leak is what makes the lumen electrically positive.

Where drugs act

Blocked here

  • Loop diuretics

    Block NKCC2. Sodium loss is large, and because the lumen-positive potential collapses with it, calcium and magnesium are lost too. That is why loops lower serum calcium and thiazides raise it.

When it breaks

What goes wrong here

Thick ascending limb
  • Bartter syndrome

    Loss of function in this segment's transport. It looks exactly like a patient permanently on a loop diuretic: hypokalaemia, metabolic alkalosis, hypercalciuria, normal or low blood pressure.

The whole journey

What the fluid concentration does

3006009001200ProximalLoopDistalUrinemOsm/kg

Everything before the collecting duct is identical in both cases. The proximal tubule takes two thirds of the volume without changing the concentration at all, the loop drives it to 1200 and then back down below plasma, and the fluid arriving at the collecting duct is dilute either way. Only the last stretch differs, and it differs completely: with antidiuretic hormone the duct is open to water and urine leaves at 1200, without it the duct is shut and urine leaves at 50.

The kidney concentrates urine by making a salty medulla in the loop and then deciding, separately and later, whether to let water out into it.

A schematic drawn for teaching, not an anatomical illustration, and the numbers are the conventional teaching values. Nothing here is medical advice. How this content is written.