1 / 20

Renal Regulation of Potassium, Calcium, Phosphate and Magnesium

Renal Regulation of Potassium, Calcium, Phosphate and Magnesium. http://www.biologymad.com/resources/kidney.swf. Regulation of Potassium (K) Excretion. Extracellular K concentration is about 4.2 mEq/L Daily K intake is between 50 to 200 mEq/L Hyperkalemia Hypokalemia.

skylar
Download Presentation

Renal Regulation of Potassium, Calcium, Phosphate and Magnesium

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Renal Regulation of Potassium, Calcium, Phosphate and Magnesium http://www.biologymad.com/resources/kidney.swf

  2. Regulation of Potassium (K) Excretion • Extracellular K concentration is about 4.2 mEq/L • Daily K intake is between 50 to 200 mEq/L • Hyperkalemia • Hypokalemia

  3. Regulation of Internal K Distribution • Insulin stimulates K uptake into cells • Aldosterone increases K uptake into cells • Beta-adrenergic stimulation increases cellular uptake of potassium • Acid-base abnormalities can cause changes in K distribution • Metabolic acidosis increases and alkalosis decreases extracellular K levels • Cell lysis causes increased extracellular K concentration • Strenuous exercise can cause hyperkalemia by releasing K from skeletal muscle • Increased extracellular fluid osmolarity causes redistribution of K from the cells to extracellular fluid

  4. Renal Potassium Excretion • K excretion is determined by three processes: • Rate of K filtration • Rate of K reabsorption and • Rate of K secretion by the tubules

  5. Renal Potassium Excretion • The most important sites for regulating K excretion are the principal cells of the late distal tubules and cortical collecting tubules

  6. Renal Potassium Excretion • Increased extracellular K concentration • Increased aldosterone and • Increased tubular flow rate stimulate secretion of K by the principal cells

  7. Renal Regulation of Potassium Excretion

  8. Lack of Aldosterone Feedback Mechanism Impairs Control of K Concentration • In the absence of aldosterone secretion (as in Addison’s disease) extracellular K levels are impaired (increase) • Conversely, with excess aldosterone secretion (primary aldosteronism) K loss by the kidneys is greatly increased (hypokalemia)

  9. Control of Renal Calcium Excretion • Extracellular Ca concentration is regulated tightly (2.4 mEq/L) • Hypercalcemia • Hypocalcemia • Changes in plasma H concetration can influence the degree of Ca binding to plasma proteins • With acidosis, less Ca is bound to proteins, in alkalosis great amount of Ca is bound to plasma proteins • Patients with alkalosis are more suceptible to hypocalcemic tetany

  10. Control of Renal Calcium Excretion • 99 % of the total Ca is stored in the bone • Only 1 % is in the extracellular fluid • And 0.1% in the intracellular fluid • Daily dietary intake is about 1000 mg • About 900 mg Ca is lost in feces daily • One of the most important regulators of bone uptake and release of Ca is PTH • PTH stimulates bone resorption • Stimulates Vit D which increases GI absorption of Ca • Directly increases renal tubular reabsorption of Ca

  11. Control of Renal Calcium Excretion

  12. Control of Calcium Excretion by the Kidneys • Renal Ca excretion = Ca filtered – Ca reabsorbed • Normally, 99 % of the Ca filtered is reabsorbed • 65% of it is absorbed in the PCT • 25% in the ascending Henle • And 5-10% in the distal and collecting tubules • Its reabsorption pattern is similar to that of Na

  13. Control of Calcium Excretion by the Kidneys • Primary controller of renal tubular reabsorption is PTH • Another factor is the plasma concentration of phosphate • Increased phosphate stimulates (??) PTH which increases reabsorption of Ca (thus reduces excretion) • Ca reabsorption is also stimulated by metabolic acidosis and inhibited by metabolic alkalosis

  14. Factors That Alter Renal Calcium Excretion

  15. Regulation of Renal Phosphate Excretion • The renal tubules have a normal transport maximum for reabsorbing phosphate of about 0.1mM/min • When less than this amount is present in the glomerular filtrate, all phosphate is reabsorbed … • PTH plays a significant role in phosphate excretion: 1) PTH promotes bone resorption (Ca and phosphate) 2) It decreases transport maximum of phosphate • Thus whenever PTH is increased, phosphate reabsorption is decreased and excretion is increased

  16. Overview of Calcium-Phosphate Regulation

  17. Role of PTH • Stimulates renal reabsorption of calcium • Inhibits renal reabsorption of phosphate • Stimulates bone resorption • Inhibits bone formation and mineralization • Stimulates synthesis of calcitriol ↑ serum calcium ↓ serum phosphate Net effect of PTH 

  18. Control of Renal Magnesium Excretion • Most of the Mg is stored in the bones • Most of the other half is found in the cells • Only about 1 % is located in the extracellular fluid • Total plasma Mg level is about 1.8 mEq/L • Most of it is bound to plasma proteins • Free ionized Mg concentration is only about 0.8 mEq/L • Daily intake of Mg is about 250 mg • Only about half of it is absorbed in the GI tract • Thus the kidneys must excrete this absorbed amount

  19. Control of Renal Magnesium Excretion • Regulation of Mg is mainly achieved by tubular reabsorption • Only about 25 % of filtered Mg is reabsorbed in the PCT • Most of it (65%) is reabsorbed in the ascending Henle • The remaining 5-10% is reabsorbed in the distal and proxymal collecting tubules

  20. Tubular Reabsorption

More Related