Renal Physiology: Potassium and Magnesium

Question 1

Where is magnesium stored in the body?

Answer 1

99% in bone, muscle and soft tissue
Most of it in the ICF (99%), but in the ECF, found in red cells.
Is bound or free (active). Needs to be pushed into cells

About 20mmol/kg in a human, so on average 24g

Question 2

Roles of magnesium physiologically

where does it come from

Answer 2

• Cofactor in >300 enzymatic reactions, such as ATP metabolism, muscle contraction/relaxation, NT release.
• Regulates vascular tone and cardiac rhythm
• Platelet activated thrombosis

Diet, leafy greens or water, cereals, nut. Processed not so good. 300mg a day roughly. SI absorption

Question 3

Magnesium reabsorption in PCT, TAL of LoH, DCT

Answer 3

10-20% PCT: paracellularly
TAL 60-70%: NKCC2 influence, by Claudin16-19 paracellular channel. Rare mutation in childhood, hypomagnesaemia
DCT 10%: Transient receptor (TRPM6), same thing, paediatric

Question 4

Mg assessment

Answer 4

Serum Mg: most common and frequently used. Sometimes not good due to majority in bones etc
Red cell Mg
24 hour excretion: (low in serum, high urine, kidney prob, low in both, absorption)
Mg retention
isotope analysis

Question 5

Causes of hypomagnesaemia

Drugs that cause

Answer 5

• Low dietary intake
• GI malabsoprtion (Crohns, UC)
• Endocrine: hyperaldosteronism (K+ excretion); DM (increase flow, increase filtered load, lessinsulin enhances uptake); SIADH
• Renal loss: Congenital (Gittlemans/Barrters) (mutation); acquired by DRUGS, most common

Drugs: Aminoglycosides, amphotericin, omeprazole*

Question 6

Hypomagnesaemia symptoms

Answer 6

• Muscle weakness/fatigue
• Fasciculations/cramps
• tetany/carpopedalspasm (often with hypocalcaemia)
• numbness and parathesia

-Severe: seizures and arrythmias

Question 7

Hypomagnesaemia treatments

Answer 7

-Primary cause with replacement

Question 8

Potassium intake

Answer 8

Mostly fruit and vege.

90-95% excreted in urine, small amount in faeces

Question 9

Internal potassium balance

-Potassium concentration is primarily regulated by the ____.
Initial changes in ___ conc are buffered by influx/efflux into ____ ____, regulated by ____ and catecholamines. Later excreted in kidney.
-Hyperglycaemia will cause potassium ___, as fluid moves out of cell in this instance
-pH: Acidosis: K ____, buffered by H+ ____, alkalosis drives potassium ___, with H+ being ____
-____ will increase Na+/K+ ATPase activity, driving potassium ___ cell

Answer 9

-Potassium concentration is primarily regulated by the kidneys.
Initial changes in ECF conc are buffered by influx/efflux into skeletal muscle, regulated by insulin and catecholamines. Later excreted in kidney.
-Hyperglycaemia will cause potassium efflux, as fluid moves out of cell in this instance
-pH: Acidosis: K efflux, buffered by H+ influx, alkalosis drives potassium influx, with H+ being effluxed
-Insulin/B agonist will increase Na+/K+ ATPase activity, driving potassium into cells

Question 10

K+ reabsorption in tubules, PCT, TAL, CD, DCT

Answer 10

PCT: 60%, paracellular, due to Na+/K+ ATPase
TAL: 30%, NKCC2 (In) and ROMK (into tubule) along with Na+/K+ ATPASE
DCT: variable
CD: variable
Hormones: aldosterone will increase renal excretion

Question 11

Hypokalaemia symptoms

HPP

Answer 11

not present till lower than 3mmo/L, but defined as <3.5
Muscle weakness+ paralysis
cardiac conduction abnormalities
Cramps
Constipation

Hypokalaemic periodic paralysis: Autosomal dominant condition, or thyrotoxic. Abnormal K+ channels, triggered after a high carb meal, causing excessive K+ influx, HYPOKALAEMIA

Question 12

How do we get potassium losses. two kinds

Answer 12

Renal: hyperaldosteronism (e.g Conn’s syndrome HT), licorice (glycyrrhizin,mimics aldosterone), diuretics(may increase or lower, e.g loop diuretics ‘waste’ potassium)
Gut: vomiting, diarrrhoea, laxatives, ileostomy, bowel fistulae, NG tube loss

Diuretics: Potassium sparing can cause hyperkalaemia, rest cause hypo, as less reabsorbed (spirinolactone, amiloride)

Question 13

Hypokalaemia treatement

Answer 13

Underlying problem, if mild oral replacement, severe IV replacement. Monitor for development of arrythmia

Question 14

Hyperkalaemia symptoms

Emergency

Pseudohyperkalaemia

Answer 14

Defined above 5mmol/L
fatigue, weak, parasthesiae, nausea/vomiting, dyspnoea, palpitations

Emergency: >6, can chnage cardiac rhythm, prolongs te action potential, widening QRS

Pseudo: when samples its around, cells break down. Samples need to be processed quickly

Question 15

Causes of hyperkalaemia

Answer 15

Increased intake
Disruption of cell intake (Beta blockers, acidosis, rhabdomyolysis
Less excretion: Renal failure, hypoaldosteronism, ACEi/ARB, drugs, Addisons (less aldosterone/cortisol)

Question 16

Addisons disease
symptoms
treatment

Answer 16

Deficiency of adrenocortical hormones (aldosterone, cortisol)
Symptoms: hyperpigmeted skin (excess ACTH stumlates melanocytes); lethargy/weakness, weight loss, low BP hyperkalaemia, hyponatraemia

treat with dexamethasone, fludrocortisone

Question 17

Ways to treat Hyperkalaemia
Stabilise AP, push K+ into cells, reduce absorption, increase excretion, fix underlying problem

In order

Answer 17

Stabilise AP: IV Calcium/glutamine. Normalises membrane excitability by pushing calcium into cell. short lasting

Push K+ into cells:

• Beta agonists, that cause K+ uptake into cells, e.g nebulised salbutamol. Hour long last.
• Insulin, short acting with dextrose to not lower blood sugar. 4-6 hour duration of action. Peak effect at 30m-1hr
• Treat acidosis, oral bicarbonate or IV, will drive potassium uptake (note this occurs due to bicarbonate contransport with sodium, up regulating Na+/K+ ATPase)

Reduce K+ absorption: Cation exchange products, that bind K+ in gut, and increase faceal elimination. calcium resonium, can cause constipation

Increase elimination: K+ wasting diuretic, e.g furosemide, thiazide. Dialysis