Nephrology
Core framework
Think in three axes: acute versus chronic, prerenal versus renal versus postrenal, and the urine sediment plus biochemistry. Acute kidney injury is staged by creatinine and urine output criteria; the key early step is excluding obstruction (bladder scan, ultrasound) and assessing volume status. Chronic kidney disease is staged by eGFR and albuminuria, with attention to anaemia, mineral bone disease and cardiovascular risk.
Concepts examiners test
Fractional excretion of sodium and urea in distinguishing prerenal from intrinsic disease (with caveats in diuretic use and contrast); the nephritic versus nephrotic syndrome distinction and which serology to order (ANA, anti-dsDNA, complement, ANCA, anti-GBM, hepatitis, HIV); glomerulonephritis urgency and when to biopsy; hyperkalaemia management by cardiac membrane stabilisation, intracellular shift, and removal; acid-base interpretation using the anion gap and delta ratio; dialysis indications (AEIOU); and hyponatraemia assessment by volume status and urine osmolality.
Traps
- Fractional excretion of sodium is unreliable with diuretics; consider fractional excretion of urea.
- Normal anion gap acidosis points to bicarbonate loss or renal tubular acidosis, not ketosis or lactate.
- Do not give intravenous contrast or nephrotoxins to a deteriorating kidney without indication.
- Hyperkalaemia with ECG changes needs calcium first, not insulin-glucose alone.
- Hyponatraemia correction must be slow to avoid osmotic demyelination; rapid correction risk is highest in chronic, malnourished patients.
Worked rule of thumb
A patient with creatinine rise, oliguria and muddy-brown casts after sepsis: this is acute tubular necrosis, not prerenal. Treat the cause, stop nephrotoxins, and reserve dialysis for refractory hyperkalaemia, acidosis, fluid overload, uraemic complications or toxin removal.