Nephrology and Fluid/Electrolyte Disorders
Core concepts
Know AKI staging, prerenal versus intrinsic versus postrenal physiology, urine indices, CKD staging by GFR and albuminuria, glomerular disease patterns, and acid-base interpretation. Prerenal AKI shows bland urine sediment, fractional excretion of sodium below 1% in the absence of diuretics, and rapid response to volume. Acute tubular necrosis shows muddy brown casts. Hyperkalemia with ECG changes is treated first with intravenous calcium, then insulin and glucose, a beta-agonist, and definitive removal. Hyponatremia requires assessment of volume status, urine osmolality, and urine sodium; correct slowly to avoid osmotic demyelination.
Traps
- Relying on FENa in patients on diuretics.
- Correcting hyponatremia faster than 8-10 mEq/L in 24 hours.
- Treating hyperkalemia without checking for ECG changes.
- Missing the anion gap in a normal-pH acidosis.
- Assuming all elevations in creatinine are prerenal without a urinalysis.
- Overlooking obstructive uropathy in an older man with rising creatinine.
Worked example
A 60-year-old with vomiting has Na 128, K 3.4, Cl 90, HCO3 12, pH 7.28, PCO2 28. The anion gap is 26, and the expected PCO2 by Winter formula is 1.5 times 12 plus 8, plus or minus 2, so 24-28; respiratory compensation is appropriate. The picture is a high-anion-gap metabolic acidosis with vomiting. Evaluate for ketoacidosis, lactate, toxins, or renal failure. Rule of thumb: always calculate the gap and apply Winter formula before naming the disorder.