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[Physiology](https://durgical.com/en/physiology/) · [Renal, fluids and acid–base](https://durgical.com/en/physiology/#s-renal)

# Potassium balance

- Regulation
- Exam priority: high

Almost all potassium sits inside cells. Small changes in the blood upset the heart and muscles, so the body controls it closely.

Updated 2026-11-01

Also called: Serum potassium, Kalemia

**See it in 3D:** [Kidneys](https://durgical.com/en/anatomy/kidney/) · [Left adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland/)

## Key points

- Plasma 3.5–5.0 mEq/L; inside cells ≈ 140 mEq/L.
- Shift K⁺ into cells: insulin, β2 agonists, aldosterone and alkalosis.
- Shift K⁺ out: insulin lack, acidosis (especially mineral acid), hyperosmolality, cell lysis, strenuous exercise, β blockade.
- The kidney regulates by excretion: collecting duct secretion depends on aldosterone, distal flow and delivered Na⁺.
- Hyperkalemia: peaked T waves, wide QRS, risk of arrest; hypokalemia: flat T waves, U waves, weakness and ileus.
- In ketoacidosis, serum K⁺ can be normal or high while total body potassium is very low; insulin makes it plunge.

## What it is

More than 98% of body potassium is inside cells, held there by the Na⁺/K⁺-ATPase. The plasma level (≈ 3.5–5.0 mEq/L) sets the resting potential of nerve and muscle, so it is controlled in two time frames: within minutes, by moving K⁺ into or out of cells; over hours, by adjusting its secretion in the collecting duct.

## How it works, step by step

- After a meal, absorbed K⁺ moves quickly into cells through the insulin-stimulated Na⁺/K⁺-ATPase.
- This prevents a dangerous plasma spike while the kidney has not yet removed it.
- Filtered K⁺ is almost all reabsorbed in the proximal tubule (≈ 65%) and thick ascending limb (≈ 25–30%).
- The amount excreted is decided in collecting duct principal cells, which secrete K⁺ through ROMK and BK.
- High plasma K⁺ directly stimulates aldosterone, which increases ENaC, Na⁺/K⁺-ATPase and K⁺ secretion.
- When K⁺ is short, α-intercalated cells reabsorb it with H⁺/K⁺-ATPase and secretion drops to a minimum.

### The nephron: segments, transporters and diuretics

**Na⁺ reabsorbed** ≈ 2–5% **Water reabsorbed** variable (ADH)

#### Collecting tubule and duct

- **What it does:** Fine tuning: reabsorbs ≈ 2–5% of Na⁺, secretes K⁺ and H⁺ and reabsorbs water as ADH allows (urine from ≈ 50 to ≈ 1200 mOsm/kg). Principal cells handle Na⁺, K⁺ and water; intercalated cells handle acid–base.
- **Transporters:** Principal: ENaC, ROMK and BK (K⁺ secretion; BK is flow-driven), apical AQP2 (ADH) and basolateral AQP3/4. α-intercalated: H⁺-ATPase and H⁺/K⁺-ATPase (secrete acid). β-intercalated: pendrin (secrete HCO₃⁻). Inner medulla: urea transporters (ADH).
- **Hormones:** Aldosterone (more ENaC, ROMK, Na⁺/K⁺-ATPase and H⁺-ATPase); ADH via the V2 receptor → cAMP → AQP2 insertion; atrial natriuretic peptide curbs Na⁺ reabsorption.
- **Drugs:** ENaC blockers (6) and mineralocorticoid receptor antagonists (7): K⁺-sparing (risk of hyperkalemia). V2 receptor antagonists (8, vaptans): aquaretics.
- **Disorders:** Liddle syndrome (overactive ENaC: hypertension, hypokalemia, low renin and aldosterone); nephrogenic diabetes insipidus (V2 or AQP2, lithium); type 1 distal renal tubular acidosis (H⁺ secretion fails: urine pH > 5.5, hypokalemia, stones) and type 4 (hypoaldosteronism: hyperkalemia); SIADH (excess ADH).

- Glomerulus and arterioles
- Proximal tubule
- Thin descending limb
- Thin ascending limb
- Thick ascending limb
- Distal convoluted tubule
- Collecting tubule and duct
- Juxtaglomerular apparatus (macula densa)
- Cortex
- Medulla
- Interstitial osmolality (≈ 300 → 1200 mOsm/kg)

Illustrative schematic drawn by Durgical (a long-loop juxtamedullary nephron); proportions and percentages are approximate and not for clinical decisions.

## Reference values

| Parameter | Value | Note |
| --- | --- | --- |
| Plasma K⁺ | 3.5–5.0 mEq/L | |
| Intracellular K⁺ | ≈ 140 mEq/L | |
| Total body K⁺ | ≈ 3500 mEq | > 98% inside cells |
| Daily renal excretion | ≈ 90% of intake | the rest in stool |

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

## Regulation

- *+* **Insulin**: Activates Na⁺/K⁺-ATPase: moves K⁺ into muscle and liver.
- *+* **β2 agonists (adrenaline)**: Move K⁺ into cells.
- *+* **Aldosterone**: More K⁺ secretion in the collecting duct (and some cell uptake).
- *+* **Distal flow and Na⁺ reaching the collecting duct**: More K⁺ secretion (loop and thiazide diuretics).
- *−* **Acidosis**: Moves K⁺ out of cells and reduces its renal secretion.
- *−* **Hyperosmolality**: Water leaves the cell and drags K⁺ with it (hyperglycemia).

## Causes by mechanism

| Mechanism | Hyperkalemia | Hypokalemia |
| --- | --- | --- |
| Shift between compartments | Insulin lack, acidosis, cell lysis, β blockade | Insulin, β2 agonists, alkalosis |
| [Kidney](https://durgical.com/en/conditions/chronic-kidney-disease/) | Kidney disease, ACE inhibitors/ARBs, K⁺-sparing diuretics, low aldosterone | Loop and thiazide diuretics, aldosterone excess, vomiting |
| [Losses outside the kidney](https://durgical.com/en/conditions/acute-gastroenteritis/) | — | Diarrhea |
| Spurious | Sample hemolysis | — |

## Clinical notes

- Hyperkalemia partly depolarizes cells, inactivates Na⁺ channels and slows conduction; calcium stabilizes the membrane and insulin with glucose shifts K⁺ in.
- In diabetic ketoacidosis, starting insulin drives K⁺ into cells and it can fall dangerously, so it is checked before and during.
- Hypokalemia from vomiting is mainly renal loss (aldosterone and alkalosis), not the K⁺ in the vomit.
- Hypokalemia increases toxicity of digoxin, which competes for the Na⁺/K⁺-ATPase.

## Memory aid

'Potassium lives at home': insulin and β2 let it in, acidosis throws it out on the street, and aldosterone sends it away in urine.

## Test yourself

Think of the answer, then tap the question to see it.

## Why can a patient with diabetic ketoacidosis have high serum K⁺ with low total body potassium?

Insulin lack and hyperosmolality move K⁺ out of cells while osmotic diuresis loses it in urine. Plasma is high, but the cell store is empty.

## Why do loop and thiazide diuretics cause hypokalemia?

They raise the flow and Na⁺ reaching the collecting duct, and hypovolemia activates aldosterone; both increase K⁺ secretion by principal cells.

## Why does insulin with glucose lower serum potassium within minutes without changing total potassium?

Insulin activates Na⁺/K⁺-ATPase and moves K⁺ into muscle and liver: it is a shift between compartments, not removal.

## What does hyperkalemia do to the resting potential and cardiac conduction?

It makes it less negative; many Na⁺ channels become inactivated, conduction slows (wide QRS) and repolarization speeds up (peaked T waves).

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/potassium-balance/)

## See it in 3D

The structures of Durgical's 3D anatomy where it happens.

- [Kidneys](https://durgical.com/en/anatomy/kidney/)
- [Left adrenal gland](https://durgical.com/en/anatomy/suprarenal-gland/)

## Related topics

- [Distal tubule and collecting duct](https://durgical.com/en/physiology/distal-tubule-and-collecting-duct/)
- [Where and how diuretics act](https://durgical.com/en/physiology/where-and-how-diuretics-act/)
- [The ECG in potassium and calcium disorders](https://durgical.com/en/physiology/the-ecg-in-potassium-and-calcium-disorders/)
- [The resting membrane potential](https://durgical.com/en/physiology/the-resting-membrane-potential/)
- [Reasoning through fluid and electrolyte imbalances](https://durgical.com/en/physiology/reasoning-through-fluid-and-electrolyte-imbalances/)
- [Aldosterone: actions and control](https://durgical.com/en/physiology/aldosterone-actions-and-control/)

## Related conditions

- [Hyperkalaemia](https://durgical.com/en/conditions/hyperkalaemia/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)
- [Diabetic ketoacidosis](https://durgical.com/en/conditions/diabetic-ketoacidosis/)
- [Chronic kidney disease](https://durgical.com/en/conditions/chronic-kidney-disease/)
- [Adrenal insufficiency](https://durgical.com/en/conditions/adrenal-insufficiency/)

## In Biochemistry

- [Na⁺/K⁺-ATPase (sodium pump)](https://durgical.com/en/biochemistry/enzymes/na-k-atpase/)
- [Aldosterone](https://durgical.com/en/biochemistry/molecules/aldosterone/)
- [Insulin signalling](https://durgical.com/en/biochemistry/topics/insulin-signalling/)

## In Pharmacology

- [Regular human insulin](https://durgical.com/en/pharmacology/regular-human-insulin/)
- [Insulins](https://durgical.com/en/pharmacology/classes/insulins/)
- [Beta blockers](https://durgical.com/en/pharmacology/classes/beta-blockers/)
- [ACE inhibitors](https://durgical.com/en/pharmacology/classes/ace-inhibitors/)
- [Digoxin](https://durgical.com/en/pharmacology/digoxin/)

[← All of physiology](https://durgical.com/en/physiology/)

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: [26.3 Electrolyte Balance](https://openstax.org/books/anatomy-and-physiology-2e/pages/26-3-electrolyte-balance) (OpenStax (Rice University), 2022); [High potassium level: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/001179.htm) (MedlinePlus, US National Library of Medicine, 2026); [Low blood potassium: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000479.htm) (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 30). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/physiology/potassium-balance/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/potassium-balance/