In respiratory acidosis, what is the primary mechanism by which the kidneys compensate?

Explanation

## Renal Compensation in Respiratory Acidosis **Key Point:** In respiratory acidosis, elevated PaCO₂ leads to decreased blood pH. The kidneys compensate by increasing reabsorption of filtered HCO₃⁻ and increasing excretion of H⁺ ions through multiple mechanisms. ### Mechanism of Renal Compensation 1. **Increased H⁺ secretion** in the proximal tubule, thick ascending limb, and collecting duct 2. **Enhanced HCO₃⁻ reabsorption** — nearly all filtered HCO₃⁻ is reclaimed 3. **Increased ammonia (NH₃) production** — provides additional buffer capacity for H⁺ excretion 4. **Increased titratable acidity** — phosphate and other weak acids bind H⁺ ### Timeline of Compensation - **Acute respiratory acidosis**: Minimal renal compensation (occurs over hours) - **Chronic respiratory acidosis**: Robust renal compensation (occurs over 3–5 days), HCO₃⁻ rises by ~3–4 mEq/L per 10 mmHg increase in PaCO₂ **High-Yield:** The kidney's response is **metabolic alkalosis** (elevated HCO₃⁻) superimposed on the respiratory acidosis. This partially offsets the pH drop. $$pH = 6.1 + \log \frac{[HCO_3^-]}{0.03 \cdot PaCO_2}$$ As PaCO₂ rises, HCO₃⁻ must also rise to prevent severe pH drop. **Clinical Pearl:** In chronic COPD, patients tolerate PaCO₂ levels of 50–60 mmHg because renal compensation raises HCO₃⁻ to 30–35 mEq/L, maintaining pH near 7.35.