Tubular, Fluid, Electrolyte, and Acid-Base Disorders
Core concepts
Understand renal tubular handling of bicarbonate, sodium, potassium, and water. Proximal (type 2) renal tubular acidosis causes bicarbonate wasting, hypokalemia, and Fanconi syndrome; distal (type 1) RTA causes inability to acidify urine (urine pH above 5.5), hypokalemia, hypercalciuria, and nephrocalcinosis; type 4 RTA causes hyperkalemia from hypoaldosteronism or aldosterone resistance. Bartter syndrome resembles loop diuretic use (hypokalemia, metabolic alkalosis, hypercalciuria, normal blood pressure); Gitelman syndrome resembles thiazide use (hypokalemia, alkalosis, hypomagnesemia, hypocalciuria); Liddle syndrome is ENaC gain-of-function with hypertension, alkalosis, and low renin and aldosterone.
Traps
Check the urine anion gap (UNa + UK - UCl) in non-anion-gap acidosis: a negative gap suggests adequate ammonium excretion, while a positive gap suggests impaired acidification. Do not correct hyponatremia faster than 8-10 mEq/L per day because of osmotic demyelination risk. In hyperkalemia, ECG changes are not always present; treat with calcium first if unstable, then insulin/glucose and albuterol, and remove potassium with binders or dialysis. Winter's formula helps verify respiratory compensation.
Worked example / rule of thumb
A child with metabolic acidosis, hypokalemia, urine pH 6.8, and nephrocalcinosis has distal RTA. Treat with alkali (bicarbonate or citrate) and potassium replacement. Rule: expected pCO2 = 1.5 x HCO3 + 8 +/- 2; if measured pCO2 is higher than expected, there is superimposed respiratory acidosis; if lower, respiratory alkalosis. Anion gap = Na - (Cl + HCO3), corrected upward by 2.5 for every 1 g/dL fall in albumin.