The kidneys - the body's most important regulator of electrolytes, salts and minerals

Regulation of electrolytes, minerals, salts and metals in the kidneys

The kidneys play a crucial role in the regulation of the body's electrolytes, minerals, salts and metals. They filter the blood, reabsorbs necessary nutrients and secrete waste to maintain homeostasis. This process is controlled by hormonal mechanisms such as renin-angiotensin-aldosterone system (RAAS), antidiuretic hormone (ADH), parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23). These regulatory mechanisms ensure that the electrolytes maintain their critical functions in nerve cord, muscle contraction, acid-base balance and fluid balance in the body.

Benefits and effects

• Sodium (na⁺): Essential for fluid balance and blood pressure regulation. Maintained by aldosterone, which increases the sodium reabsence in the kidneys.

• Potassium (K⁺): Critical for heart and muscle activity. The RAAS system and aldosterone contribute to potassium separation to prevent hyperkalaemia.

• Magnesium (mg²⁺): Participates in enzymatic reactions, affects calcium and phosphate metabolism and is important for neuromuscular function.

• Calcium (Ca²⁺): Regulated by PTH, vitamin D and FGF23, and is important for muscle function, nerve transfer and skeletal health.

• Phosphorus (p): Calcium interacts and regulated by PTH and FGF23 to maintain skeletal structure and energy metabolism.

• Iron (Fe): Important for hemoglobin production. Copper is necessary for optimal iron metabolism.

• Zinc (zn) and copper (cu): Important for enzyme activity and immune function. Excess zinc can reduce copper absorption.

• Lithium (Li⁺) and sodium (na⁺): Competing for reabsorption in the kidneys, affecting the lithium concentration in the blood.

• Heavy metals (PB, HG, CD, AS): Can be accumulated in the kidneys and disrupt the electrolyte balance through interaction with essential minerals.

Technical specifications and mechanisms

The kidneys regulate electrolytes through the following mechanisms:

1. Glomerular filtration: Blood is filtered in the kidneys, where small molecules such as sodium, potassium, calcium and phosphorus pass through glomerulus.

2. Tubular reabsorption: The kidneys reabsorbs necessary electrolytes in proximal tubules to prevent losses.

3. Secretion and excretion: Surplus of electrolytes and waste materials are excreted via urine.

4. Hormonal regulation:

   • Raas increases sodium and water retention to regulate blood pressure.

   • PTH increases calcium reabsorption and phosphate excretion.

   • ADH promotes waterreaous absorption in collector pipes.

   • FGF23 regulates phosphate metabolism and interacts with PTH and vitamin D.

Interactions between electrolytes and minerals

• Sodium and potassium: Reverse regulated via aldosterone.

• Calcium and magnesium: High levels of calcium can inhibit magnesium absorption.

• Phosphorus and calcium: High phosphorus levels reduce the calcium concentration in the blood.

• Iron and copper: Excess copper can inhibit iron absorption.

• Zinc and copper: High zinc intake can cause copper shortages.

• Lithium and sodium: Increased sodium intake can reduce lithium retention, while low sodium intake increases lithium concentration.

• Heavy metals and minerals: Lead can replace calcium in bones, and mercury can bind to the harness and interfere with enzyme function.

Reverse regulated

By "reverse regulated" is meant that an increase in the concentration of one substance leads to a reduction of another, and vice versa. This is due to hormonal mechanisms or competition for transport mechanisms in the kidneys. Here are some examples of such inverted regulations:

1. Sodium (na⁺) and potassium (K⁺)

   • When sodium reabsorb in the kidneys, potassium is excreted in the urine through the influence of aldosterone.
   • High sodium intake often leads to increased potassium excretion, while low sodium absorption can lead to potassium retention.
     
     

2. Calcium (ca²⁺) and phosphorus (p)

   • Increased calcium levels stimulate the excretion of phosphorus through the kidneys, mainly regulated by parathyroid hormone (PTH).
   • High phosphorus concentration can reduce free calcium in the blood, which can trigger increased PTH secretion to increase calcium absorption.
     
     

3. Magnesium (mg²⁺) and calcium (ca²⁺)

   • Magnesium is necessary for normal calcium transport in cells, but very high levels of calcium can inhibit the magnesium absorption.
   • Low magnesium content can interfere with the PTH function and thus affect the calcium balance.
     
     

4. Iron (Fe) and copper (Cu)

   • Excess copper can inhibit the iron absorption, as these metals compete for the transport protein Ceruloplasmine.
   • Lack of copper can cause iron retention and secondary iron deficiency anemia.
     
     

5. Zinc (zn) and copper (cu)

   • High intake of zinc can reduce copper absorption, as both use metallothionein as a transport mechanism in the gut.
   • This can lead to copper deficiency, which in turn can cause anemia and neurological problems.
     
     

6. Lithium (Li⁺) and sodium (na⁺)

   • Sodium and lithium compete for the same reabsorption mechanisms in the kidneys.
   • High sodium intake increases lithium excretion, while low sodium levels can lead to increased lithium retention and possible toxicity.
     
     

7. Heavy metals and essential minerals

   • Lead (Pb) can displace calcium in bones and reduce its availability for metabolic processes.
   • Mercury (Hg) can bind to harness, reducing antioxidant protection and interferes with enzyme function.
   • Kadmium (CD) can inhibit zinc metabolism and cause kidney damage over time.

These conditions show how the body's electrolyte and mineral balance is strongly regulated through complex mechanisms, and why imbalances can lead to serious health consequences.

Disclaimer and reservation

Use of the information should be done in consultation with qualified health professionals. Uno Vita AS does not claim that the products can cure disease. Keep out of reach of children.

References

1. National Kidney Foundation - Electrolyte Balance.

2. American Journal of Physiology - Renal Physiology.

3. Kidney International Reports.

4. Advances in Chronic Kidney Disease.

5. The Lancet Nephrology.

6. PubMed - Electrolyte Homeostasis.

7. Journal of Nephrology.

8. European Renal Association Reports.

9. Clinical Kidney Journal.

10. Nature reviews nephrology.

11. Journal of Clinical Endocrinology & Metabolism.

12. International Journal of Molecular Sciences.