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

# Renal handling of calcium, phosphate and magnesium

- Mechanism
- Exam priority: medium

The kidney decides how much calcium, phosphate and magnesium the body keeps; each one is reclaimed mainly in a different part of the tubule.

Updated 2026-11-01

Also called: Calciuria, Phosphaturia, Paracellular reabsorption

**See it in 3D:** [Kidneys](https://durgical.com/en/anatomy/kidney/) · [Parathyroid glands](https://durgical.com/en/anatomy/parathyroid-glands/)

## Key points

- Calcium: ≈65 % proximal, ≈20–25 % thick ascending limb (paracellular, driven by the lumen-positive voltage), ≈5–10 % distal (transcellular, PTH-regulated); ≈1–2 % excreted.
- Loop diuretics: more calcium in urine. Thiazides: less calcium in urine (useful in calcium stones).
- Phosphate: ≈80–85 % proximal (NaPi-IIa/IIc); PTH and FGF-23 remove the transporters (phosphaturia).
- Magnesium: only ≈15–25 % proximal; ≈60–70 % in the thick ascending limb; ≈5–10 % distal (TRPM6).
- The calcium-sensing receptor in the loop curbs reabsorption when calcium rises: hypercalcaemia causes calciuria and polyuria.
- Hypomagnesaemia causes hypokalaemia that won’t correct (K⁺ leak via ROMK) and hypocalcaemia (less PTH secretion and action).

## What it is

Only the non-protein-bound fraction of calcium and magnesium is filtered. Calcium is reclaimed mostly in the proximal tubule and the loop (passively, between cells), with the fine-tuning done by the distal tubule under PTH control. Phosphate is reclaimed almost only in the proximal tubule, and PTH and FGF-23 make the kidney excrete it. Magnesium is different: its main site is the thick ascending limb.

### The nephron: segments, transporters and diuretics

**Na⁺ reabsorbed** ≈ 25% **Water reabsorbed** 0%

#### Thick ascending limb of the loop of Henle

- **What it does:** Reabsorbs ≈ 25% of filtered Na⁺ but is impermeable to water: the diluting segment (fluid leaves at ≈ 100 mOsm/kg) and the engine of the medullary gradient. The lumen-positive potential drives paracellular Ca²⁺ and Mg²⁺ reabsorption.
- **Transporters:** Apical NKCC2 (Na⁺-K⁺-2Cl⁻); ROMK recycles K⁺ to the lumen; basolateral ClC-Kb with barttin; claudins 16 and 19 (paracellular path); Ca²⁺-sensing receptor.
- **Hormones:** ADH (V2) increases NaCl reabsorption; PTH increases Ca²⁺ reabsorption.
- **Drugs:** Loop diuretics (4): block NKCC2; Na⁺, K⁺, Ca²⁺ and Mg²⁺ are lost (hypokalemia, metabolic alkalosis, hypercalciuria).
- **Disorders:** Bartter syndrome (like a loop diuretic: hypokalemic alkalosis, hypercalciuria, high renin and aldosterone).

- 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.

### The nephron: segments, transporters and diuretics

**Na⁺ reabsorbed** ≈ 5% **Water reabsorbed** 0%

#### Distal convoluted tubule

- **What it does:** Reabsorbs ≈ 5% of Na⁺; impermeable to water (keeps diluting). Actively reabsorbs Ca²⁺, under PTH control, and Mg²⁺.
- **Transporters:** NCC (Na⁺-Cl⁻ cotransporter); TRPV5 (Ca²⁺) with the basolateral Na⁺/Ca²⁺ exchanger; TRPM6 (Mg²⁺).
- **Hormones:** PTH (more Ca²⁺ reabsorption); aldosterone and Ang II in the late part.
- **Drugs:** Thiazides (5): block NCC; lower Ca²⁺ excretion (hypocalciuria) and cause hypokalemia and hyponatremia.
- **Disorders:** Gitelman syndrome (like a thiazide: hypokalemic alkalosis, hypomagnesemia, hypocalciuria). Gordon syndrome (pseudohypoaldosteronism type 2): the opposite, hypertension with hyperkalemia.

- 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.

## Plasma values (adult, approx.)

| Parameter | Value | Note |
| --- | --- | --- |
| Total calcium | ≈8.5–10.5 mg/dL | ≈40 % bound to albumin |
| Ionised calcium | ≈1.1–1.3 mmol/L | the active fraction |
| Phosphate | ≈2.5–4.5 mg/dL | higher in children |
| Magnesium | ≈1.7–2.2 mg/dL | |

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

## Regulation

- *+* **PTH on the distal tubule**: More TRPV5 channels and basolateral transport: more calcium reabsorbed.
- *−* **PTH on the proximal tubule**: Removes NaPi transporters: more phosphate excreted.
- *−* **FGF-23 (with Klotho)**: Phosphaturia and less renal calcitriol.
- *+* **Calcitriol**: Increases distal calcium transport proteins.
- *−* **Calcium-sensing receptor (hypercalcaemia, hypermagnesaemia)**: Curbs paracellular reabsorption in the loop: calciuria and magnesiuria.
- *−* **Volume expansion and loop diuretics**: Less proximal and loop reabsorption: more calcium in the urine.

## Where each ion is reclaimed (approx. % of filtered load)

| Segment | Calcium | Phosphate | Magnesium |
| --- | --- | --- | --- |
| Proximal tubule | ≈65 % | ≈80–85 % | ≈15–25 % |
| Thick ascending limb | ≈20–25 % | minimal | ≈60–70 % |
| Distal tubule and collecting duct | ≈5–10 % (PTH, calcitriol) | small | ≈5–10 % |
| Excreted | ≈1–2 % | ≈10–15 % | ≈3–5 % |

## Clinical notes

- Primary hyperparathyroidism: hypercalcaemia with low phosphate; although PTH reabsorbs calcium, the filtered load is so high that there is hypercalciuria and stones.
- Chronic kidney disease: phosphate is retained, and FGF-23 and PTH rise (secondary hyperparathyroidism).
- Bartter syndrome (loop) causes hypercalciuria; Gitelman syndrome (distal) causes hypocalciuria and hypomagnesaemia.

## Memory aid

“The loop belongs to magnesium, the distal tubule to PTH, and the proximal tubule takes the phosphate”: each ion has its star segment.

## Test yourself

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

## Why do loop diuretics increase calciuria while thiazides reduce it?

Loop diuretics abolish the lumen-positive voltage that drives paracellular Ca²⁺ reabsorption. Thiazides lower distal cell Na⁺ (more basolateral Na⁺/Ca²⁺ exchange) and mildly contract volume (more proximal reabsorption).

## In a patient whose hypokalaemia does not improve with potassium replacement, which ion should be checked, and why?

Magnesium. With low intracellular Mg²⁺, collecting-duct ROMK channels let more K⁺ out: renal potassium loss persists until magnesium is corrected.

## What does PTH do to urinary calcium and phosphate, and in which segments?

It lowers calcium excretion (more reabsorption in the distal tubule) and raises phosphate excretion (inhibits NaPi in the proximal tubule).

[Add to my cards (3)](https://durgical.app/estudiar/?add=/en/physiology/renal-handling-of-calcium-phosphate-and-magnesium/)

## See it in 3D

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

- [Kidneys](https://durgical.com/en/anatomy/kidney/)
- [Parathyroid glands](https://durgical.com/en/anatomy/parathyroid-glands/)

## Related topics

- [Calcium regulation: PTH, vitamin D and calcitonin](https://durgical.com/en/physiology/calcium-regulation-pth-vitamin-d-and-calcitonin/)
- [Phosphate and FGF-23](https://durgical.com/en/physiology/phosphate-and-fgf-23/)
- [Transport in the loop of Henle](https://durgical.com/en/physiology/transport-in-the-loop-of-henle/)
- [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/)
- [Bone remodeling](https://durgical.com/en/physiology/bone-remodeling/)

## Related conditions

- [Hypocalcaemia](https://durgical.com/en/conditions/hypocalcaemia/)
- [Hypercalcaemia](https://durgical.com/en/conditions/hypercalcaemia/)
- [Kidney stones (urolithiasis)](https://durgical.com/en/conditions/kidney-stones/)
- [Primary hyperparathyroidism](https://durgical.com/en/conditions/primary-hyperparathyroidism/)
- [Hypokalaemia](https://durgical.com/en/conditions/hypokalaemia/)

## In Biochemistry

- [Calcium and phosphate](https://durgical.com/en/biochemistry/topics/calcium-and-phosphate/)
- [Magnesium](https://durgical.com/en/biochemistry/topics/magnesium/)
- [Vitamin D (calcitriol)](https://durgical.com/en/biochemistry/molecules/vitamin-d/)

[← 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); [Calcium Blood Test: MedlinePlus Medical Test](https://medlineplus.gov/lab-tests/calcium-blood-test/) (MedlinePlus, US National Library of Medicine, 2024); [Magnesium Blood Test: MedlinePlus Medical Test](https://medlineplus.gov/lab-tests/magnesium-blood-test/) (MedlinePlus, US National Library of Medicine, 2024); [Phosphate in Blood: MedlinePlus Medical Test](https://medlineplus.gov/lab-tests/phosphate-in-blood/) (MedlinePlus, US National Library of Medicine, 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (chs. 30, 80). 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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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/renal-handling-of-calcium-phosphate-and-magnesium/