NephrologyTier 2Topic

Laboratory tests - electrolytes

Focus in nephrology

Electrolyte interpretation in nephrology centres on sodium, potassium, calcium, phosphate, and magnesium - the kidney is the principal regulator of all five
Electrolyte derangement is near-universal in advanced CKD and a leading cause of dialysis-related emergencies (hyperkalaemia especially)

Hyperkalaemia - reduced GFR reduces distal potassium secretion; worsened by RAAS inhibitors (ACEi/ARB/MRA), acidosis (shifts K+ extracellularly), and reduced dietary restriction adherence
CKD-mineral bone disorder (CKD-MBD): reduced phosphate excretion -> hyperphosphataemia -> reduced activation of vitamin D -> hypocalcaemia -> secondary hyperparathyroidism
Hyponatraemia - usually dilutional in advanced CKD/fluid overload rather than true sodium deficiency

Regular monitoring is standard of care in CKD stages 3b-5 and on dialysis, given the rate of change and risk of asymptomatic severe hyperkalaemia
ECG changes with hyperkalaemia - peaked T waves -> flattened P waves -> widened QRS -> sine wave -> arrest; ECG severity does not always correlate tightly with the potassium level

Hyperkalaemia - calcium gluconate (cardiac membrane stabilisation, no effect on K+ level), insulin/dextrose and salbutamol (shift K+ intracellularly), and definitive removal via potassium binders (patiromer, sodium zirconium cyclosilicate) or dialysis
CKD-MBD - dietary phosphate restriction, phosphate binders (calcium-based or non-calcium-based), active vitamin D analogues, calcimimetics (cinacalcet) for secondary hyperparathyroidism refractory to other measures

RAAS inhibitor use, secondary hyperparathyroidism, renal osteodystrophy, vascular calcification

CKD-MBD progresses insidiously over years and drives cardiovascular calcification - a major contributor to excess cardiovascular mortality in CKD/dialysis populations

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