Bit · Renal

Bartter vs Gitelman vs Liddle

Three inherited tubular disorders that all cause hypokalemic metabolic alkalosis with normal-to-low blood pressure (except Liddle). The pivot is which tubule segment is broken and what happens to calcium.

Mechanism

Each mimics a diuretic:

Differentiator Table

BartterGitelmanLiddle
SegmentThick ascending limbDistal convoluted tubuleCollecting duct
MimicsLoop diureticThiazideHyperaldosteronism
Blood pressureNormal or lowNormal or low↑↑ (HTN, often young)
K⁺
pHAlkalosisAlkalosisAlkalosis
Ca²⁺ (urine)↑ (hypercalciuria)↓ (hypocalciuria)Normal
Mg²⁺Normal / low↓↓ (hypomagnesemia is classic)Normal
Renin / Aldo↑ / ↑↑ / ↑↓ / ↓ (suppressed)
OnsetChildhood, severeAdolescent / adult, milderYoung HTN, family hx

The Pivot

Three quick questions:

  1. Hypertension? Yes → Liddle. (Renin and aldo both low.)
  2. No HTN, what is urinary calcium? High → Bartter. Low → Gitelman.
  3. Hypomagnesemia? Strongly suggests Gitelman.

NBME-Style Stem

A 17-year-old girl presents with muscle cramps and fatigue. Blood pressure is 110/70 mm Hg. Labs: K⁺ 2.8 mEq/L, Mg²⁺ 1.2 mg/dL, bicarbonate 32 mEq/L. Urine calcium is low. Renin and aldosterone are elevated. Which of the following is the most likely diagnosis?
Concept Anchor
If a tubular disorder gives you hypokalemic alkalosis, ask first about blood pressure: high → Liddle (ENaC stuck open). If normal, calcium splits the loop (Bartter, high urine Ca) from the thiazide (Gitelman, low urine Ca) phenotype.

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