Thick ascending limb of Henle (NKCC2)

Loop of Henle · 25% Na+ NKCC2 Loop diuretics

The engine of the concentrating mechanism: it reabsorbs ~25% of filtered sodium via the luminal Na+/K+/2Cl- cotransporter without water, diluting the tubular fluid and salting the medullary interstitium. It is the site of loop diuretic action.

Traced from the start

  1. Glomerular filtration barrier
  2. Proximal tubule: Na+/H+ exchange and bicarbonate reclamation
  3. Thick ascending limb of Henle (NKCC2)

Detail

Reabsorbs
~25% of filtered Na+, K+ and Cl-; ~25% of Ca2+ and 60-70% of Mg2+ paracellularly (claudin-16/19) driven by a lumen-positive potential; ~10-15% of HCO3- via NHE3
Transporter
Apical NKCC2 (SLC12A1) and ROMK (K+ recycles back into the lumen, creating the ~+8 mV lumen-positive voltage); basolateral Na+/K+-ATPase and ClC-Kb chloride channel with its barttin subunit
Water
Impermeable: the 'diluting segment'; fluid leaves at ~100-150 mOsm/kg regardless of ADH
Hormone
ADH (V2, cAMP) and angiotensin II increase NKCC2 activity; the TAL also secretes uromodulin (Tamm-Horsfall protein), the matrix of urinary casts
Diuretic
Loop diuretics (frusemide, bumetanide, ethacrynic acid) bind the Cl- site of NKCC2 from the lumen; the strongest natriuretics, excreting up to 20-25% of filtered Na+; also venodilate acutely and abolish the medullary gradient

When it goes wrong

Loop diuretic

Hypovolaemia; hypokalaemic hypochloraemic metabolic alkalosis (more distal Na+ delivery plus secondary hyperaldosteronism); hypocalcaemia and hypomagnesaemia (lumen-positive drive lost); hyperuricaemia; ototoxicity (NKCC1 in the stria vascularis) with high IV doses, aminoglycosides or ethacrynic acid

Loop diuretic after IV saline repletion in severe hypercalcaemia

Calciuresis: an adjunct once the patient is volume-replete, never before

Bartter syndrome (loss of NKCC2 type I, ROMK type II, ClC-Kb type III, barttin type IV with sensorineural deafness)

The picture of chronic loop-diuretic use: hypokalaemic metabolic alkalosis, hypercalciuria with nephrocalcinosis, polyuria, normal or low blood pressure, high renin and aldosterone; antenatal polyhydramnios

Medullary ischaemia from hypotension, NSAIDs, contrast or rhabdomyolysis

TAL and S3 cells are the most oxygen-hungry in the worst-perfused zone, so they die first in acute tubular necrosis: muddy brown casts, FE Na over 2%, isosthenuria

Practise this structure

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