Nephrology and Fluid-Electrolyte Disorders
Questions target acute kidney injury staging, the prerenal-renal distinction, chronic kidney disease classification, hyperkalaemia and the sodium disorders.
Acute kidney injury
KDIGO defines AKI as a creatinine rise of 0.3 mg/dL or more within 48 hours, a rise to 1.5 times baseline within 7 days, or urine output below 0.5 mL/kg/h for 6 hours. Prerenal states show fractional excretion of sodium below 1% and urine sodium below 20 mmol/L; established acute tubular necrosis shows values above 2% with muddy brown casts. When diuretics are in play, fractional excretion of urea below 35% supports a prerenal cause.
Chronic kidney disease
Classify by both eGFR category (G1–G5) and albuminuria category (A1–A3). Use the CKD-EPI equation, and remember that eGFR loses accuracy at extremes of muscle mass.
Sodium disorders
Confirm hypotonicity with serum osmolality before treating. Then use urine osmolality and urine sodium: a urine osmolality above 100 mOsm/kg with urine sodium above 40 mmol/L in a euvolemic patient suggests SIADH. Correct by no more than 8–10 mmol/L in 24 hours to avoid osmotic demyelination.
Hyperkalaemia
Calcium gluconate stabilises the myocardium without lowering potassium; insulin with glucose and nebulised salbutamol shift potassium intracellularly; dialysis is definitive.
Worked example
A 74-year-old with sodium 118 mmol/L, urine osmolality 520 mOsm/kg, urine sodium 60 mmol/L and no oedema has SIADH. Treat with fluid restriction and address the cause rather than giving isotonic saline, which may worsen the sodium.
Traps that cost marks
- Relying on fractional excretion of sodium in CKD or on diuretics.
- Correcting hyponatraemia faster than 8 mmol/L per day.
- Missing that calcium gluconate does not change the serum potassium.