Renal Physiology - Electrolyte Homeostasis

Question 1

What is the role of sodium within the body, and what are the daily requirements?

Answer 1

It is the dominant cation in the extracellular fluid, with an important role in membrane potential & AP transmission.

Responsible for 90% of the osmotic effect of solutes within the ECF, and therefore determines the volume of ECF.

Usual concentration is 135-145mmol/L
Daily requirement 1-1.4mmol/kg/day

It is lost via the following routes:
Sweat (10mmol/day)
Urine (150-450mmol/day)
Faeces (10mmol/day)

Question 2

What is the role of potassium in the body, and what are normal plasma levels? What are the causes of hypo/hyperkalaemia?

Answer 2

Main intracellular cation in the body - particularly important for electrochemical gradients and AP conduction. Involved in protein synthesis and osmolality regulation.

Normal plasma levels 3.5-5mmol/L, with a requirement of approximately 1mmol/kg/day depending on losses.

Hypokalaemia (3 categories as per all ‘hypo’ questions)
Reduced intake
Overhydration with water/dextrose
Poor dietary intake
Malabsorption/short gut syndrome
Increased losses
D&V
Renal disease & excessive diuresis (RTA (other than type 4) or diuretic induced)
Cushing’s syndrome/Hyperaldosteronism (Can be mimicked by high licorice consumption)
Intracellular shifts
Where total body potassium may even be high, but it has been sequestered intracellularly
Insulin, Salbutamol, Adrenaline, Alkalosis

Hyperkalaemia
Increased intake (or release from tissues)
Overadministration of IV/PO potassium
Haemolysis, Rhabdomyolysis
Trauma
Malignant hyperthermia
Reduced losses
AKI
Acidosis & DKA (Technically whole body potassium is low, but it has shifted extracellularly)
Drugs
Potassium sparing diuretics
ACE-i and ARBs
Suxamethonium (in those at risk)

Question 3

How does sodium concentration change in the tubular fluid throughout the nephron?

IMAGE - graph

https://derangedphysiology.com/main/cicm-primary-exam/renal-system/Chapter-013/renal-handling-sodium

Answer 3

Starts around 190mmol/litre in the proximal tubule
As the filtrate descends into the loop of Henle, the extreme osmotic gradient draws water out of the tubule, increasing the sodium concentration dramatically to around 500mmol/litre
By the end of the ascending loop, relatively dilute urine is formed as a reesult of the countercurrent multiplier system & the active removal of sodium from the tubular fluid, hence the urinary sodium concentration drops at this point.

ADH acts on the distal convoluted tubule and collecting duct, where it can concentrate the urine if necessary, therefore increasing the sodium concentration again.

Question 4

How does potassium concentration change in the tubular fluid throughout the nephron?

EXPAND HERE

Answer 4

Potassium reabsorption is largery determined by flow rate through the tubular system

Question 5

Where in the body is magnesium found and what is its normal concentration?

Answer 5

It is the fourth most abundant cation in the body
Predominantly intracellular
50% stored in bone, 48% in soft tissues and muscles
Some in RBCs
1% in extracellular fluid
0.7-1mmol/L plasma concentration

It is responsible for maintenence of electrochemical gradients, a physiological calcium antagonist, and plays a role in DNA, RNA and protein synthesis,

Question 6

What are the systemic effects of magnesium?

Answer 6

Cardiovascular
Negative inotrope and chronotrope (Slows SA node conduction & increases refractory period) - Reduced cardiac output
Vasodilation, reduced systemic/pulmonary vascular resistance
Hypotension
Respiratory
Muscle weakness (may affect ventilation)
Bronchodilation
Neurological
Anticonvulsant
Reduces ACh production at the NMJ
Genitourinary
Inhibits spontaneous labour (tocolytic)
Neuroprotective to the baby in preterm labour
Used in pre-eclampsia

Question 7

What are the causes and features of hypo/hypermagnesaemia?

Answer 7

Hypomagnesaemia
Causes:
Reduced intake
Deficiency, overhydration with magnesium-deplete fluid
Increased losses
Diuretics, alcoholism, diarrhoea, GI fistula
Intracellular shifts
Insulin, hyperparathyroidism, citrate

Features:
Early
Nausea & anorexia, muscle cramps and weakness, weight loss, lethargy
Late
Convulsions & tetany
Stridor & muscle spasm
HTN, Pulmonary oedema
PR & QT prolongation
ST depression/flattened T waves
Trousseau’s and Chvostek’s signs
Hypocalacaemia due to reduced PTH production & increased renal excretion

Hypermagnesaemia
Causes:
Increased intake
IV fluids, excessive antacid/laxative intake
Reduced loss
CKD, hypothyroidism, cortico-adrenal insufficiency, lithium
Extracellular redistribution
DKA, Tumour lysis syndrome

Features:
Early
Vomiting & headache, diarrhoea, muscle weakness (above 4mmol/L), Reduced muscle tone
Late
Respiratory depression
Hypotension & bradycaqrdia
Wide QRS
Cardiac arrest (Above 10mmol/L)