Renal system potassium and urea handling

1. RENAL HANDLING OF POTASSIUM
AND UREA
Datu Agasi Bin Mohd Kamal

2. LEARNING OBJECTIVES :
 To describe potassium distribution within the
body.
 To know the role of hormones in the movement
of potassium between intracellular and
extracellular pools.
 To explain the factors that regulate K+ secretion
in collecting duct.
 To know the harmful effect of hyperkalemia
 To understand renal handling of urea

3. CASE
Blood urea and electrolyte test of a 59-year-old
man with chronic kidney disease showed high
level of creatinine and urea.
Patient was treated with angiotensin-converting
enzyme inhibitor drug and developed
hyperkalemia.

4. HYPERKALEMIA
 Rise in ECF K+ reduces resting potential
which decreases excitability of neuron &
muscle
 By keep voltage-gated Na+ in inactive
state + cell membrane unable to
repolarize completely
 Hyperkalemia is defined as a serum potassium
concentration greater than approximately 5.0-5.5 mmol/L
in adults.
 Reduce cardiac cell excitability may cause
cardiac arrhythmia or cardiac arrest

5. POTASSIUM DISTRIBUTION
 98% of K+ is in ICF due to Na+-K+ pump.
 ECF regulated at 4.2mEq/L ±0.3mEq/L
 Control of K+ distribution in ECF and ICF – first line of
defence against K+ ECF changes
Factor that
shift K+ into
cells
Factor that shift K+ out
of cells
Insulin Insulin deficiency
(diabetes melitus)
Aldosterone Aldosterone deficiency
(Addison’s disease)
β-adrenergic
stimulation
β-adrenergic blockade
Alkalosis Acidosis
Cell lysis
Strenous exercises
Increased ECF osmalarity

6. RENAL POTASSIUM HANDLING
• K+ actively reabsorbed
at proximal tubule &
thick ascending loop of
Henle.
• Early tubule-K+
constantly reabsorbed
without regulation.
• K+ secreted at late
distal tubules and
collecting ducts by
principal cell.
• K+ secretion at later
tubule subjected to
regulation.

7. MECHANISM OF K+ REABSORPTION

8. MECHANISM OF K+ SECRETION

9. REGULATION OF K+ SECRETION
Principal tubular cell
1.Aldosterone

10. REGULATION OF K+ SECRETION
2. Acid-base balance
Type A intercalated
cell
• H+ secreting
• HCO3
-
reabsorbing
• K+ reabsorbing
• More active at
normal condition
• Increases during
acidosis
Type B intercalated
cell
• Opposite action
of type A
• More active
during alkalosis

11. UREA
• Urea is a waste product from
breakdown of protein
• Reabsorption of water in
proximal tubule make urea
more concentrated and
creating concentration
gradient to passively diffuse
to peritubular capillary.
• Only 50% filtered urea being
reabsorbed because urea is
not fully permeable to the wall
of proximal tubule
• Inner medullary collecting
duct – urea transporter
• Remainder of urea is excreted
as urine

12. THANK YOU

13.  ROMK – renal outer medullary potassium
 BK-High conductance big potassium
 Distal tubular flow

14.  A cell model for K+ transport in the proximal
tubule. K+ reabsorption in the proximal tubule primarily
occurs through the paracellular pathway. Active
Na+ reabsorption drives net fluid reabsorption across the
proximal tubule, which in turn, drives K+ reabsorption
through a solvent drag mechanism. As fluid flows down
the proximal tubule, the luminal voltage shifts from
slightly negative to slightly positive. The shift in
transepithelial voltage provides an additional driving
force favoring K+ diffusion through the low-resistance
paracellular pathway. Experimental studies suggest that
there may be a small component of transcellular
K+ transport; however, the significance of this pathway is
not known. K+uptake through the Na+-K+-ATPase pump
can exit the basolateral membrane through a conductive
pathway or coupled to Cl−. An apically located K+ channel
functions to stabilize the cell negative potential,
particularly in the setting of Na+-coupled cotransport of
glucose and amino acids, which has a depolarizing effect
on cell voltage.