In respiratory acidosis, the kidneys compensate by increasing the reabsorption of which ion in the proximal convoluted tubule?

Explanation

## Renal Compensation in Respiratory Acidosis **Key Point:** In respiratory acidosis, the kidneys increase HCO₃⁻ reabsorption and H⁺ secretion to restore the 20:1 HCO₃⁻:H₂CO₃ ratio and normalize pH. ### Mechanism of Renal Compensation 1. **Increased CO₂ → ↑ H⁺ in blood** 2. **Proximal tubule cells increase H⁺ secretion** via Na⁺-H⁺ exchanger and H⁺-ATPase 3. **Filtered HCO₃⁻ is reabsorbed** (normally ~99% reabsorbed, increases further) 4. **New HCO₃⁻ is generated** in proximal tubule cells 5. **Result**: Plasma HCO₃⁻ rises, pH normalizes ### Metabolic Compensation Timeline ```mermaid flowchart TD A[Respiratory Acidosis<br/>↑ PaCO₂, ↓ pH]:::outcome --> B[Kidneys sense ↓ pH]:::action B --> C[↑ H⁺ secretion in PCT]:::action C --> D[↑ HCO₃⁻ reabsorption]:::action D --> E[↑ Plasma HCO₃⁻]:::outcome E --> F[pH normalizes toward 7.35-7.45]:::outcome G[Timeline: 3-5 days] -.-> F ``` **High-Yield:** For every 10 mmHg increase in PaCO₂ above 40, plasma HCO₃⁻ increases by ~3-4 mEq/L (chronic respiratory acidosis). ### Why HCO₃⁻ and Not Other Ions? | Ion | Role in Compensation | Reason | | --- | --- | --- | | **HCO₃⁻** | **Primary** | Directly restores buffer ratio; generated by H⁺ secretion | | Cl⁻ | Secondary | Reabsorption ↓ to maintain electroneutrality | | PO₄³⁻ | Minimal | Acts as urinary buffer, not primary compensation | | SO₄²⁻ | Minimal | Minor urinary buffer, not involved in compensation | **Mnemonic:** **CHOP** — Compensation Happens Over Proximal tubule (HCO₃⁻ reabsorption is the key mechanism). **Clinical Pearl:** In chronic respiratory acidosis (e.g., COPD), renal compensation can raise HCO₃⁻ to 50+ mEq/L, partially normalizing pH. This is why patients with chronic hypercapnia tolerate higher CO₂ levels than acute cases.