1. Potassium (only 2% of body K+ is in extracellular fluids and it has to be regulated tightly)
Re-absorption by intercalated cells constantly
Around 90% reabsorbed here, little regulation
ATPases
Excretion by principal cells - REGULATED
ASC
Aldosterone
High tissue K+ increases K+ flow into cells thence out:
Low K+ diets tyrP of apical K+ channels channels removed from membrane
High K+ diets cause loss of tyrP and channels accumulate in membrane
Data from Giebisch GH. (2002) A trail of research on potassium. Kidney Int. 62:

2. Potassium flux is sensitive to body pH:
Re-absorption by intercalated cells constantly
Alkalosis: H+ out-pumping by intercalated cells reduced, so less K+ re-uptake (AND apical K+ channel activity increased in Prinicipal cells and so is the Na+/K+ ATPase -> more K+ loss)
hypokalaemia
ATPases
Acute acidosis: H+ out-pumping by intercalated cells increases so K+ reuptake increases. Also, apical K+ channels on Principal cells less active (by an effect on their intracellular regulation) so K+ secretion falls.
hyperkalaemia
Excretion by principal cells - REGULATED
ASC
(Chronic acidosis; Na pump less efficient in PCT, so urine more copious and helps flush K+ away)
Aldosterone
High tissue K+ increases K+ flow into cells thence out:
Low K+ diets tyrP of apical K+ channels channels removed from membrane
High K+ diets cause loss of tyrP and channels accumulate in membrane
Data from Giebisch GH. (2002) A trail of research on potassium. Kidney Int. 62:

3. Diuresis: increasing the amount of water (+ salts) lost from the body
through / of urine
65% salt and water
PCT
0.08
0.29
H2O
Renal corpuscle
0.1
More NaCl (2-5%)
0.29
Salt recovery
Water reabsorption driven by hypertonic zone
1.4
Up to 1.4
(you have seen this before)

4. (Henle's) Loop Diuretics:
(this still happens)
65% salt and water
If we block SLC12A2, we stop the salt being moved into the interstitium
PCT
TAL:
Renal corpuscle
More NaCl (2-5%)
Salt recovery
SLC12A2
Water reabsorption driven by hypertonic zone
(you have seen this before)

5. Features of loop diuretics:
They are powerful (up to 20% of filtrate to bladder: usually around 0.4%) 
They result in loss of Na+, K+ and Cl- because of failure to recover in the TAL of LoH 
They can result in hypercalcuria – less pull for Ca2+ recovery – and kidney stones.
More Na+ getting to the Coll Duct means more uptake there and more K+ loss 

6. Alternative diuretics:
Distal tubule diuretics ('thiazides')
65% salt and water
PCT
0.08
0.29
H2O
SLC12A3
Renal corpuscle
0.1
More NaCl (2-5%)
0.29
Salt recovery
You still loose some K+ for the same reason
Water reabsorption driven by hypertonic zone
(you have seen this before)
1.4
Up to 1.4

7. Alternative diuretics:
Distal tubule diuretics ('thiazides')
65% salt and water
PCT
0.08
Potassium-sparing diuretics (amiloride etc)
0.29
H2O
Renal corpuscle
0.1
More NaCl (2-5%)
0.29
ASC
Salt recovery
"amiloride sensitive sodium channel"
Water reabsorption driven by hypertonic zone
1.4
Up to 1.4
(you have seen this before)

8. Alternative diuretics:
aldosterone
Distal tubule diuretics ('thiazides')
65% salt and water
PCT
0.08
Potassium-sparing diuretics (amiloride etc)
H2O
Renal corpuscle
0.1
More NaCl (2-5%)
0.29
Spironolactone (problem – also antiandrogenic)
Salt recovery
Water reabsorption driven by hypertonic zone
1.4
Up to 1.4

9. Alternative diuretics:
Distal tubule diuretics ('thiazides')
65% salt and water
PCT
0.08
Potassium-sparing diuretics (amiloride etc)
H2O
Renal corpuscle
0.1
More NaCl (2-5%)
0.29
Spironolactone
Salt recovery
Carbonic anhydrase inhibitors (more bicarb in lumen, resists egress of water osmotically)
Water reabsorption driven by hypertonic zone
1.4
Up to 1.4

10. Alternative diuretics:
Distal tubule diuretics ('thiazides')
65% salt and water
PCT
0.08
Potassium-sparing diuretics (amiloride etc)
H2O
Renal corpuscle
0.1
More NaCl (2-5%)
0.29
Spironolactone
Salt recovery
Carbonic anhydrase inhibitors
Water reabsorption driven by hypertonic zone
Osmotic agents (eg mannitol): stay in the lumen and resist water egress osmotically)
Clinical use controversial
1.4
Up to 1.4

11. Alternative diuretics:
Distal tubule diuretics ('thiazides')
65% salt and water
PCT
0.08
Potassium-sparing diuretics (amiloride etc)
H2O
Renal corpuscle
0.1
More NaCl (2-5%)
0.29
Spironolactone
Salt recovery
Carbonic anhydrase inhibitors
Water reabsorption driven by hypertonic zone
Osmotic agents (eg mannitol): stay in the lumen and resist water egress osmotically)
1.4
Up to 1.4
Very high plasma glucose can exceed recovery capacity and act in this way: diabetic thirst because water lost by Na+ not lost as much -> hypernatraemia.

12. Diuretics summary slide:
Carbonic anhydrase inhibitors
Thiazides
Amiloride, spironolactone
Loop diuretics
NB – this info is given from the point of view of basic understanding – the pharmacology vertical theme will give you the clinical details.

13. What can go wrong? – Hereditary disorders of tubule function.
Bartter's syndrome (Type 1) – impaired SLC12A2
CLICKER QUIZ
Effects (choose one)
a) Loss of Na+, K+, hypocalcuria
b) Loss of Na+ K+, H2O; hypercalcuria
c) Na+ loss, K+ retention, high aldosterone
d) Diabetes insipidus (polyuria, polydipsia)
e) Volume expansion (body), hypertension
TAL cells:

14. What can go wrong? – Hereditary disorders of tubule function.
Gitelman's syndrome – impaired SLC12A3
CLICKER QUIZ
SLC12A3
Effects (choose one)
a) Loss of Na+, K+
b) Loss of Na+ K+, H2O; hypercalcuria
c) Na+ loss, K+ retention, high aldosterone
d) Diabetes insipidus (polyuria, polydipsia)
e) Volume expansion (body), hypertension

15. What can go wrong? – Hereditary disorders of tubule function.
Liddle's syndrome – hyperactive ASC (=ENaC)
CLICKER QUIZ
Effects (choose one)
a) Loss of Na+, High K+, hypocalcuria
b) Loss of Na+ K+, H2O; hypercalcuria
c) Na+ loss, K+ retention, high aldosterone
d) Diabetes insipidus (polyuria, polydipsia)
e) Volume expansion (body), hypertension
ASC

16. What can go wrong? – Hereditary disorders of tubule function.
Pseudohypoaldosteronism – inactive ASC (=ENaC)
CLICKER QUIZ
Effects (choose one)
a) Loss of Na+, K+, hypocalcuria
b) Loss of Na+ K+, H2O; hypercalcuria
c) Na+ loss, K+ retention, high aldosterone
d) Diabetes insipidus (polyuria, polydipsia)
e) Volume expansion (body), hypertension
ASC

17. What can go wrong? – Hereditary disorders of tubule function.
Inactivating Mutations of Aquaporins
CLICKER QUIZ
AVP +
Effects (choose one)
a) Loss of Na+, K+, hypocalcuria
b) Loss of Na+ K+, H2O; hypercalcuria
c) Na+ loss, K+ retention, high aldosterone
d) Diabetes insipidus (polyuria, polydipsia)
e) Volume expansion (body), hypertension

18. What can go wrong? – Problems outside the kidney
CLICKER QUIZ
Addison's disease (destruction of adrenal glands)
Effects (choose one)
Loss of Na+, High K+, hypovolaemia
Loss of Na+ K+, H2O; hypercalcuria
c) Whole body hypo- osmolarity
d) Diabetes insipidus (polyuria, polydipsia)
e) Volume expansion (body), hypertension

19. What can go wrong? – Problems outside the kidney
Psychogenic polydipsia
CLICKER QUIZ
Effects (choose one)
Loss of Na+, K+, hypovolaemia
Loss of Na+ K+, H2O; hypercalcuria
c) Whole body hypo- osmolarity