Control renal magnesium excretion and extracellular magnesium ion concentration

2021-05-05 10:56 AM

Modification of magnesium excretion is performed primarily by altering tubular reabsorption. The proximal tubule usually reabsorbs only about 25% of the filtered magnesium.

 

More than half of the body's magnesium is stored in the bones. Much of the rest is in the cells, with less than 1 percent in the extracellular fluid.

Although the total concentration of magnesium in the blood plasma is approximately 1.8 mEq / L, more than half of this concentration is bound to plasma proteins. Therefore, the free magnesium ion concentration is only about 0.8 mEq / L.

The normal daily intake of magnesium is between 250 and 300 mg/day, but only about half of this magnesium is absorbed from the gastrointestinal tract. To maintain magnesium balance, the kidneys must excrete this absorbed magnesium, about half of the daily magnesium intake, or 125 to 150 mg/day. The normal kidneys excrete about 10 to 15 percent of magnesium from the glomerular filtrate.

Renal adjustment of magnesium excretion can be markedly increased with excess magnesium or decreased to almost zero in the presence of magnesium deficiency. Since magnesium is involved in many biochemical processes in the body, including the activation of many enzymes, its concentration must be tightly regulated.

Modification of magnesium excretion is performed primarily by altering tubular reabsorption. The proximal tubule usually reabsorbs only about 25% of the filtered magnesium. The primary site for reabsorption in the Henle loop, where about 65% of the filtered magnesium is reabsorbed. Only a small amount (typically <5%) of filtered magnesium is reabsorbed in the distal tubule and the manifold.

The regulatory mechanism of magnesium excretion is not well understood, but the following disorders lead to an increase in magnesium excretion: (1) an increase in magnesium concentration in extracellular fluid, (2) an increase in extracellular fluid volume, and (3) ) increase the concentration of calcium in the extracellular fluid.

 

MOST VIEW

Pathophysiology of cardiogenic shock

Urine formation: Reabsorbed glomerular filtration

Air in and out of the lungs: pressure causes the movement of air

Mechanism of urine concentration: osmotic pressure changes in different segments of the renal tubule

Absorption and excretion of potassium through the kidneys

Nephron: The functional unit of the kidney

Prothrombin activation: initiates blood clotting

Estimated renal plasma flow: PAH clearance

Graphical analysis of high-volume heart failure

Pulmonary capillary dynamics: capillary fluid exchange and pulmonary interstitial fluid dynamics

Calculate the glomerular filtration rate (GFR): the forces that cause the filtration process

Red blood cells: differentiation and synthesis

Ammonia buffering system: excretes excess H + and creates new HCO3

Concentrated urine formation: urea contributes to increased osmotic pressure in the renal medullary

Reduced sodium chloride, dilates arterioles, increases Renin release.

Extracellular fluid distribution between interstitial space and blood vessels

The proximal tubule reabsorption: active and passive reabsorption

Origin of lymphocytes: the body's resistance to infection

Pathophysiology of fever

Acidosis causes a decrease in HCO3- / H + in renal tubular fluid: compensation mechanism of the kidney

The endocrine regulates tubular reabsorption

Sodium channel blockers: decrease the reabsorption of sodium in the manifold

Self-regulation of glomerular filtration rate and renal blood flow

Physiological anatomy of the kidneys and urinary system

The kidneys excrete sodium and fluid: feedback regulates body fluids and arterial pressure