1. Potassium homeostasis

2. Potassium homeostasis
TOTAL BODY K+ = mEq/kg
- intracellular – 98%
- extracellular – 2%
PLASMA K+ = 3.5 – 5.0 mEq/l K+
2K+
ATP K+
3Na+

4. RENAL REGULATION OF POTASSIUM HOMEOSTASIS
RESPONSE TO K+ DEFICIT
adaptation of kidneys during 2-3 days
minimal renal K+ excretion = 5 – 15 mEq/day
FEK+changes from 17% to 3-5%
minimal K+ intake of mEq/day is necessary to maintain balance
RESPONSE TO K+ EXCESS
Renal K+ excretion increases up to tenfold
renal reaction starts within hours
increased K+ secretion into the colon can support renal action

5. RENAL POTASSIUM EXCRETION
FILTRATION : 700 – 1000 mEq/day
EXCRETION: 25 – 100 mEq/day
Proximal tubules : reabsorption 40-50%
Descending limb of Henle loop: passive diffusion from the
interstitium to lumen
Thick ascending limb of Henle loop: reabsorption 35-45%
Cortical collecting tubules:
- reabsortpion in α-intercalated cells, in exchange for H+ secretion
- secretion from principal cells
Medullary collecting tubules:
- reabsorption in α-intercalated cells

6. K POTASSIUM CHANNELS PRINCIPAL CELL TUBULE K 0 mV Na - 90 mV
Na-K-ATPase Na
- 90 mV K
POTASSIUM CHANNELS
CHEMICAL GRADIENT
ELECTRICAL GRADIENT

7. RENAL POTASSIUM SECRETION FROM PRINCIPAL CELLS
Luminal K+ conc. = inversely proportional
Luminal Na+ conc. = proportional
3. Na+ and K+ conductance in the luminal membrane = proportional
4. Aldosterone = proportional
5. Nonreabsorbable anions in urine = proportional
6. Luminal flow rate = proportional
7. Intracellular K+ conc. = proportional

8. HYPOKALEMIA Plasma K < 3.5 mEq/L
Inadequate potassium intake (less than mEq/day)
Excessive nonrenal potassium excretion
- sweat 1-2 mEq/day => 100 mEq/day
- GI tract 10 mEq/day => 100 – 200 mEq/day
3. Renal potassium losses
- increased Na+ delivery to cortical tubule
- nonrebsorbable anions
- primary hyperaldosteronism
4. Potassium translocation into cells (Total K+ unchanged)
- hyperinsulinism, hyperaldosteronism, β-adrenergics
- rapid proliferation of cells

9. Membrane potential in hypokalemia
Hypokalemia - Muscles
- Hyperpolarisation of cells interior => increased threshold for depolarisation
K< 2.5 mEq/L => decreased muscles strength
Effect stronger in acute hypokalemia; with time its intensity decreases
Chronic hyperpolarisation=>Na+ channels are opened=>spontaneous depolarisation
Threshold potential
-60mV
Membrane potential
-90mV
Membrane potential in hypokalemia

10. HYPOKALEMIA - SYMPTOMS
1. Heart
- heart block and arrhytmias
2. Blood vessels
- lack of vasodilation => rhabdomyolysis
3. Endocrine
- decreased insulin synthesis

11. HYPOKALEMIA - SYMPTOMS
Kidneys
- decreased blood flow => renin synthesis
- impaired renal water conservation:
- inhibition of ADH renal effect
- metabolic alkalosis
- intracellular acidosis and extracellular alkalosis
- increased ammoniagenesis
- increased distal secretion of hydrogen

12. POTASSIUM DEFICIT REFLECTED BY PLASMA [K+]

13. HYPERKALEMIA Plasma K > 5.0 mEq/L
Excessive potassium load
Decreased renal potassium excretion
- renal failure
- decreased distal delivery of Na+
- hypoaldosteronism
Potassium redistribution ICF=>ECF (Total K+ unchanged)
- deficient insulin, aldosterone, β-adrenergics)
- acidosis
- hyperosmolality
- cell necrosis

14. Hyperkalemia - Muscles
- Hypopolarisation of the cell membrane => decreased threshold for depolarisation
Chronic hypopolarisation => Na+ channels are closed=> reduced depolarisation
Threshold potential
-60mV
Membrane potential in hyperkalemia
Membrane potential
-90mV

15. HYPERKALEMIA - SYMPTOMS
Muscles
- hypopolarisation =>decreased thereshold for depolarisation
- chronic hypopolarisation => closing of Na+ channels
2. Heart
- accelerated repolarisation and delayd depolarisation
- heart block
- arrhytmias
3. Blood vessels
- vasodilatation
4. Kidney
- decreased ammoniagenesis => metabolic acidosis
- natriuresis (via inhibition of proximal Na+ reabsorption)