Renal: Potassium Balance Flashcards
What is the importance of potassium balance?
Ratio of the intracellular [130-140 mmol/L] to extracellular [3.5-4.7 mmol/L] K+ conc determines resting membrane potential, maintained by Na/K ATPase (2K+ in, 3Na+ out)
Maintenance of intracellular K+ is critical in:
nerve conduction
muscle contraction
Heart function
Give some dietary K+ sources
Fruit: bananas, avocado, dried fruit, citrus etc
Veg: unboiled, green veg, tomato based all high in potassium
Stratchy foods- anything potato based
Reduced sodium salts
What is hyperkalaemia and its causes?
Hyperkalaemia (raised potassium, >5.5 mmol/L)
Causes:
Drugs e.g. potassium sparing diuretics, ACEi or ARBs,
Advanced CKD/ESKD
Addison’s
Food ingestion
What is hypokalaemia and its causes?
Hypokalaemia (low potassium, <3.5 mmol/L)
Causes:
Drugs e.g. diuretics
GI loss in vomiting + diarrhoea
Genetic disease
Mineralocorticoid excess
How does hypokalaemia affect the resting membrane potential?
In hypokalaemia hay hyperpolarization of the RMP due to the altered K+ gradient.
The cells thus become less excitable.
An increased a.potential threshold and lack of K+ for membrane repolarization decreases muscle contraction.
This leads to muscle weakness, impaired nerve signaling, constipation (smooth muscle effect) and change in heartbeat
What are the 4 mechanisms of K+ balance?
K+ intake through diet
GI losses and renal losses
Transcellular K+ shift
Overall K+ stores remain the same but redistribute between the ICF and ECF
Describe renal handling of potassium in the PCT
Potassium is freely filtered in the glomerulus
Absorption in the PCT is via passive para cellular transport (movement of electrolyte between cells).
This is K+ reabsorption via diffusion and solvent drag. Solvent drag involves electrochemical gradient and diffusion.
Describe renal handling of K+ in the TAL of Henle
The TAL has an active trans cellular mechanism.
Na/KATPase channel in the baso lateral membrane pumps 3 Na+ out into the bloodstream in exchange for 2 K+ into the ascending limb.
Na conc decreases, which triggers the NKCC2 transporter which brings Na, K+ and Cl- into the cell. Buildup of K+ causes it to leave into the bloodstream
Describe renal handling of K+ in the DCT and CD
Occurs via a transcellular pathway, mediated by alpha and beta intercalated cells which reabsorb K+.
Step 1: the apical H+/K/ATPase mediates H+ movement into the lumen, driving K+ into the intercalated cell
Step 2: the basolateral K+ channel allows the K+ inside the intercalated cell to leak out into the bloodstream
How do principal cells excrete potassium?
Hay a conc gradient across luminal membrane
Electrical gradient generated by reabsorption of Na+ via ENaC
Number of open K+ channels in luminal membrane
All of these cause potassium excretion
How does aldosterone affect K+ secretion?
Aldosterone opens more Na+ and K+ channels in luminal membrane which increases K+ secretion
Enhances activity of Na+K+ ATPase
This causes K+ secretion in principal cells which will efflux into the tubular fluid (see diagram).
How does raised plasma potassium affect its secretion?
Raised plasma K:
- Increases number of open Na+ and K+ channels in luminal membrane
- Enhances activity of Na+K+ATPase pump
- This increases K+ secretion into the tubular fluid
What factors affect K+ secretion into the tubular fluid?
•Distal flow rate: increased distal flow rate washes secreted K+ away and replaces it w K+ free fluid. This allows a good gradient for K+ secretion into tubular fluid
•Distal sodium delivery:
Entry of Na+ via ENaC makes lumen more electronegative
Transport of Na+ into peritubular capillary by ATPase pumps more K+ into cell
More K+ secreted into electronegative lumen
How loop and thiazide diuretics work
How is K+ reabsorbed in cases of severe K+ deficiency
•Active re-absorption by H+ K+ ATPase by intercalated cells in the collecting duct enables urinary K+ excretion to decrease to <15mmol/d in severe K+ deficiency
What happens to the RAAS system in Conns syndrome?
In Conns syndrome the adrenal gland produces too much aldosterone. This will lead to mucho Na retention, potassium diuresis from the distal tubule.
It also increases the hydrogen iron secretion from the collecting ducts.
How would you treat hyperkalaemia based on severity?
Mild (K+ is 5.5-5.9mmol/l): repeat test within 14 days, if result is unexpected repeat within 3 days. If the patient is clinically unwell/has AKI consider hospital referral
Moderate (K+ is 6-6.4mmol/l): repeat test within 1 day, if result is unexpected repeat within 24hrs. If the patient is clinically unwell/has AKI refer to hospital
(K+> 6.5 mmol/l): hospital referral asap
For each case assess the cause (drugs diet etc)
How do you treat hyperkalaemia?
- Protect the heart: use Calcium gluconate or CaCl to stabilise the membrane potential
- Shift potassium into cells using drugs like Insulin + Dextrose, Salbutamol, NaHCO3
- Remove potassium from body using Dialysis
- Drugs to increase K+ secretion in the gut like Sodium Zirconium Cyclosilicate, Patiromer
- Drugs which increase renal potassium loss like Frusemide, Bumetinide
How do you prevent reoccurrence of hyperkalaemia?
Stop drugs which cause high potassium
Low potassium diet
