Chloride

Serum Chloride (96–106 milliequivalents per litre (mEq/L):

Urine Cl⁻ has diagnostic power, and serum Cl⁻ does not. Serum chloride tells you the direction of acid–base disturbance, but cannot identify the cause. Cl⁻ and HCO₃⁻ behave like a seesaw. When one rises, the other falls. 

• If Cl⁻ goes down → HCO₃⁻ goes up  → alkalosis

• If Cl⁻ goes up → HCO₃⁻ goes down → acidosis

Urine Chloride:

1. It determines whether metabolic alkalosis is saline-responsive (urine chloride low) or saline-resistant (urine chloride high)

2. Renal hydrogen and potassium handling

Causes:

• Chloride responsive: Vomiting, volume depletion, or diuretics

• Chloride resistant (mineralocorticoid): Conn's, Liddle, Cushing

Kidney's role in chloride-responsive metabolic alkalosis: 

"The kidney cannot clear bicarbonate without chloride"

"Pendrin" is the anion transporter (a protein) in the body (kidney, inner ear, thyroid, lung)

1. In the DCT, the pendrin (Cl⁻/HCO₃⁻ exchanger) removes HCO₃⁻ only if chloride is available

So   ↓ Cl⁻ = ↓ bicarbonate secretion = alkalosis stays “locked in”

2. With low volume (vomiting) → RAAS activation → aldosterone ↑ -> Na⁺ retention & K⁺ & H⁺ loss

Without chloride, the kidney cannot dump bicarbonate, so alkalosis cannot be corrected, no matter how much K⁺ or fluid you give. Only chloride reverses it.