K+ balance

Question 1

K+ in the body

Answer 1

normal: 3.5-5.0 mEq/L
most abundant intracellular cation (98% in ICF)
balance important for RMP
Na/K ATpase
insulin/beta stimuliation of Na/K ATPase

Question 2

K+ in kidney

Answer 2

1-2% of K+ in plasma, freely filtered

cannot perform min-min homeostasis (done by Na/K ATpase)

Question 3

K+ handling

Answer 3

daily: 50-150 mEq/day intake - must excrete all
determined by secretion, not reabsorption
- all filtered K+ is reabsorbed
- secretion from principal cells in CD controls balance

Question 4

K+ reabsorption

Answer 4

55% in PT: diffusion due to increased intratubular [K+] due to water resorption (follows NaCl)
30% in LOH: NKCC, linked to Na+
Medullary CD

no control over resorption
can be impaired by glucosuria - osmotic diuresis, prevents creation of high concentration gradients of K+ in the urine
resorption inhibited by Lasix, which blocks NKCC

Question 5

K+ secretion

Answer 5

Mostly in CCD by principal cells, determined by

1) aldosterone: release stimulated by high K+ and AII
- increase Na/K ATpase and ENaC
- more negative lumen –> K+ secretion
- also favours H+ secretion
- steroid hormone - long-term only
- short term: changes Na/K ATpase on basolateral side of principal cell

2) tubular flow rate
- higher flow rate = decreased intratubular [K+], increased secretion

3) Distal Na Delivery
- more Na+ delivery to CCD = more Na+ resorption in CCD
- Na+ resorption paired with K+ secretion

4) H+ ions
- low basolateral [H+] - movement of H+ out of cell and K+ into cell (from blood), secretion
- alkalosis - secrete more K+
- acidosis - secrete less K+

Question 6

Hyperkalemia threshold

Answer 6

> 5
6 is potentially dangerous
6.5 must be treated urgently

Question 7

Causes of hyperkalemia

Answer 7

Increased GI load - rare
Impaired renal excretion: drop in GFR, impaired secretion (aldosterone insufficiency, K+ sparing diuretics)
Shift from ICF –> ECF (acidosis, digoxin - impairs Na/K ATPase, insulin deficiency, beta blockers, hyperglycemia (water to ECF to compensate for hyperosmolality), familial causes, rhabdomyolysis, tumor lysis, hemolysis)

Question 8

Tx of hyperkalemia

Answer 8

Correct first, then treat underlying cause

• insulin
• maintain cell membrane stability and avoid cardiac effects: hyperkalemia: iv calcium
• shift K+ into cells (insulin + glucose, beta-adrenergic agonists)
• promote K+ secretion (improve volume status/flow, sodium polystyrene to promote GI excretion, hemodialysis)
• stop offending agents (ACEi/ARBs, K+ sparing diuretics, NSAIDs)