Step by Step
PCT
Proximal convoluted tubule — bulk reabsorption
Reabsorbs 65% of sodium, 65% of water, 100% of glucose and amino acids, 90% of bicarbonate, and 50% of urea. Sodium/potassium ATPase on the basolateral membrane powers essentially all of this. Glucose specifically is reabsorbed via SGLT2 (on the apical membrane) and GLUT2 (on the basolateral membrane) — but there's a transport maximum of about 180 mg/dL; exceeding this threshold (as in diabetes) causes glucosuria, since the transporters become saturated.
Loop
Loop of Henle — building the concentration gradient
The descending limb allows water to leave (concentrating the fluid); the ascending limb actively pumps NaCl out (without losing water) — together, this builds up the hypertonic gradient in the medulla.
DCT
Distal convoluted tubule — hormone-sensitive fine-tuning
Sodium reabsorption here is aldosterone-sensitive, and calcium reabsorption is PTH (parathyroid hormone)-sensitive.
CD
Collecting duct — ADH-controlled water reabsorption
Water reabsorption here is ADH-sensitive, working via the insertion of aquaporin-2 channels. ADH itself comes from the posterior pituitary. Without ADH, the collecting duct can't reabsorb water effectively, resulting in diabetes insipidus — a condition marked by massive, dilute urine output.
Applied Walkthrough
1
As filtrate passes through the PCT, 65% of the filtered sodium and water, along with essentially all of the glucose and amino acids, are reabsorbed back into the blood.
2
In a patient with uncontrolled diabetes, blood glucose exceeds 180 mg/dL, surpassing the PCT's glucose transport maximum — meaning some glucose can no longer be reabsorbed and instead appears in the urine (glucosuria).
3
As remaining filtrate passes through the loop of Henle, the descending limb allows water to leave while the ascending limb pumps out NaCl, together establishing the hypertonic medullary gradient needed to concentrate urine.
4
In the DCT and collecting duct, aldosterone fine-tunes sodium reabsorption while ADH controls final water reabsorption via aquaporin-2 — a patient lacking sufficient ADH (diabetes insipidus) would be unable to concentrate their urine properly, producing large volumes of dilute urine despite potential dehydration.
Exam Application
Exams test whether you can match each nephron segment to what it reabsorbs and which hormones control it, and specifically whether you understand the concept of transport maximum (Tm) and what happens when it's exceeded, as in diabetic glucosuria.
⚠ Common Trap
The most common trap is assuming glucose reabsorption in the PCT has no limit — in reality, the SGLT2/GLUT2 transport system has a maximum capacity (Tm) of about 180 mg/dL; blood glucose above this threshold overwhelms the transporters and spills into the urine.
✓ Quick Self-Check
1. What percentage of filtered glucose does the PCT normally reabsorb?
100% (all of it), under normal blood glucose conditions.
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2. What is the transport maximum for glucose reabsorption, and what happens when it's exceeded?
About 180 mg/dL; exceeding it causes glucosuria (glucose in the urine).
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3. What hormone controls sodium reabsorption in the DCT?
Aldosterone.
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4. What hormone controls water reabsorption in the collecting duct, and via what mechanism?
ADH, via insertion of aquaporin-2 channels.
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5. What condition results from insufficient ADH, and what does it cause?
Diabetes insipidus, causing massive, dilute urine output.
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