Tubular Reabsorption and Secretion Along the Nephron
Segment-by-segment transporters of the nephron and the drugs that block them.
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Questions Covered in This Set
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What is the 'battery' driving nearly all tubular reabsorption?
The basolateral Na⁺/K⁺-ATPase (3 Na⁺ out, 2 K⁺ in), which keeps intracellular Na⁺ low (~10–30 mM) and creates the Na⁺ electrochemical gradient spent by apical transporters.
How much of the filtered load does the PCT reabsorb?
~65% of Na⁺ and water, ~100% of glucose and amino acids, ~85% of bicarbonate, ~80% of phosphate — and it does so isosmotically (fluid leaves at ~300 mOsm).
Which transporters reabsorb glucose in the PCT, and what is the Tm/threshold?
SGLT2 (early, high-capacity/low-affinity) then SGLT1 (late mop-up); exit via GLUT2/GLUT1. Tm ≈ 375 mg/min; glucosuria appears above plasma glucose ~180–200 mg/dL, with 'splay' from nephron heterogeneity.
Describe proximal bicarbonate reabsorption and the effect of acetazolamide.
Apical NHE3 secretes H⁺; brush-border carbonic anhydrase IV converts H⁺+HCO₃⁻ to CO₂+H₂O; CO₂ enters, CA II rehydrates it, HCO₃⁻ exits via basolateral NBCe1. Acetazolamide blocks CA → bicarbonate wasting, mild diuresis, hyperchloremic metabolic acidosis.
What do OAT and OCT transporters do, and why does it matter clinically?
PCT secretion of organic anions/cations: penicillin, furosemide, PAH, uric acid, creatinine, metformin. Probenecid blocks OAT and prolongs penicillin; furosemide must be secreted into the lumen, so renal failure requires larger doses.
What is Fanconi syndrome physiologically?
Generalized PCT damage (heavy metals, myeloma) causing loss of everything the PCT handles: glucosuria with normal blood glucose, aminoaciduria, phosphaturia, and proximal (type 2) RTA.
Contrast the thin descending limb and the thick ascending limb.
Thin descending limb: water-permeable (AQP1), solute-impermeable → fluid concentrates. TAL: water-impermeable, actively pumps salt via NKCC2 → fluid dilutes to ~100 mOsm ('diluting segment').
What does NKCC2 transport and how much Na⁺ does the TAL reclaim?
1 Na⁺, 1 K⁺, 2 Cl⁻ across the apical membrane; the TAL reabsorbs ~25% of filtered Na⁺.
How are Ca²⁺ and Mg²⁺ reabsorbed in the TAL?
K⁺ recycles into the lumen via ROMK, creating a lumen-positive transepithelial potential that drives paracellular Ca²⁺ and Mg²⁺ reabsorption.
Why do loop diuretics cause calcium and magnesium wasting?
Furosemide/bumetanide block NKCC2, abolishing K⁺ recycling and the lumen-positive potential, so paracellular Ca²⁺ and Mg²⁺ reabsorption stops — useful in hypercalcemia.
