Acid–Base Regulation
by the Kidney
Discover how the kidneys maintain blood \(\text{pH}\) within a narrow range by reabsorbing bicarbonate, secreting hydrogen ions, and producing new buffers.
Why Blood pH Matters
Normal arterial blood pH is maintained between \(7.35\) and \(7.45\). Even small deviations disrupt enzyme function, oxygen delivery, and cardiac rhythm. The kidneys are the slow but powerful arm of pH homeostasis: they cannot correct in seconds like the lungs, but they can generate new bicarbonate and permanently eliminate acid.
Core Vocabulary
The Henderson–Hasselbalch Equation
$$ \text{pH} = 6.1 + \log \frac{[\text{HCO}_3^-]}{0.03 \times P_{\text{CO}_2}} $$
Three Renal Mechanisms
Bicarbonate Reabsorption in the PCT
\(\text{H}^+\) Secretion and New \(\text{HCO}_3^-\)
When all filtered bicarbonate has already been reclaimed, any additional \(\text{H}^+\) secreted into the tubule must be buffered by other molecules. This is how the kidney generates brand-new bicarbonate:
Titratable acid: excreted in urine. Each \(\text{H}^+\) trapped = 1 new \(\text{HCO}_3^-\) to blood.
Ammonia produced from glutamine in PCT cells. \(\text{NH}_4^+\) trapped in urine = 1 new \(\text{HCO}_3^-\) to blood.
Acidosis vs Alkalosis: Key Distinction
| Acidosis (pH < 7.35) | Alkalosis (pH > 7.45) | |
|---|---|---|
| Kidney response | Increases \(\text{H}^+\) secretion | Decreases \(\text{H}^+\) secretion |
| \(\text{HCO}_3^-\) handling | Reabsorbs 100% + makes new | Excretes excess in urine |
| \(\text{NH}_4^+\) production | Greatly increased | Decreased |
| Urine pH | As low as 4.5 | As high as 8.0 |
| Time to full effect | 2–3 days | 2–3 days |
Metabolic vs Respiratory Imbalances
| Metabolic | Respiratory | |
|---|---|---|
| Primary change | \([\text{HCO}_3^-]\) | \(P_{\text{CO}_2}\) |
| Compensated by | Lungs (change \(P_{\text{CO}_2}\)) | Kidneys (change \([\text{HCO}_3^-]\)) |
| Speed of compensation | Minutes (respiratory) | Hours to days (renal) |
| Example acidosis | Diabetic ketoacidosis | COPD (CO₂ retention) |
| Example alkalosis | Severe vomiting (HCl loss) | Hyperventilation |
How the Kidney Corrects Acidosis
Example 1: Diabetic Ketoacidosis
A patient with uncontrolled diabetes produces excess ketoacids. Lab values: pH = 7.28, \([\text{HCO}_3^-]\) = \(14 \text{ mEq/L}\) (normal: 24), \(P_{\text{CO}_2}\) = \(30 \text{ mmHg}\) (normal: 40).
Example 2: Chronic COPD
A patient with chronic obstructive pulmonary disease retains \(\text{CO}_2\). Lab values: pH = 7.33, \(P_{\text{CO}_2}\) = \(58 \text{ mmHg}\), \([\text{HCO}_3^-]\) = \(32 \text{ mEq/L}\).
Example 3: Prolonged Vomiting
A patient vomits repeatedly, losing gastric HCl. Lab values: pH = 7.52, \([\text{HCO}_3^-]\) = \(38 \text{ mEq/L}\), \(P_{\text{CO}_2}\) = \(48 \text{ mmHg}\).
The Ammonium Pathway
Common Mistakes
Summary of Renal Acid–Base Tools
| Mechanism | Location | Effect on Blood | New HCO₃⁻? |
|---|---|---|---|
| \(\text{HCO}_3^-\) reabsorption | PCT (80–90%) | Prevents loss | No |
| \(\text{H}^+\) secretion via \(\text{Na}^+/\text{H}^+\) antiporter | PCT, DCT | Acidifies urine | No (reclaims) |
| Phosphate buffering | Collecting duct | Adds \(\text{HCO}_3^-\) | Yes |
| Ammonium excretion | PCT + collecting duct | Adds \(\text{HCO}_3^-\) | Yes |
| \(\text{HCO}_3^-\) excretion | Collecting duct (type B) | Removes excess base | N/A (alkalosis) |
Question 1 of 5
In the proximal convoluted tubule, filtered \(\text{HCO}_3^-\) is reclaimed by first combining with which ion in the lumen?
Question 2 of 5
Which process allows the kidney to generate brand-new bicarbonate (not merely reclaim filtered bicarbonate)?
Question 3 of 5
A patient has: pH = 7.30, \(P_{\text{CO}_2}\) = 60 mmHg, \([\text{HCO}_3^-]\) = 29 mEq/L. What is the primary disorder?
Question 4 of 5
During metabolic alkalosis, the kidney compensates primarily by:
Question 5 of 5
In the Henderson–Hasselbalch equation \(\text{pH} = 6.1 + \log \frac{[\text{HCO}_3^-]}{0.03 \times P_{\text{CO}_2}}\), the kidneys regulate which variable?