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

2021-05-06 01:47 PM

Both respiratory and metabolic acidosis causes a decrease in the ratio of HCO3- / H + in the renal tubular fluid. As a result, excess of H + in the renal tubules reduces HCO3 А reabsorption and leaves more H + available to combine with urinary buffers NH4 + and HPO4--.

The mechanism by which the kidneys excrete H + and re-absorb HCO3 А, which may explain how the kidney regulates extracellular fluid pH as it changes.

In the Henderson - Hasselbalch equation, acidosis occurs when the ratio of HCO3- / CO2 in the extracellular fluid decreases, causing a decrease in pH. If this leakage is reduced due to a decrease in HCO3 А, metabolic acidosis occurs. If the pH is decreased by increasing PCO2, acidosis is acidosis.

Both respiratory and metabolic acidosis causes a decrease in the ratio of HCO3- / H + in the renal tubular fluid. As a result, excess of H + in the renal tubules reduces HCO3 А reabsorption and leaves more H + available to combine with urinary buffers NH4 + and HPO4--. Thus, in acidosis, the kidneys reabsorb both filtered HCO3 А and from new HCO3 А through the reaction of NH4 + and titratable acid.

In metabolic acidosis, the excess of H + compared to HCO3 А occurs in the tubular fluid mainly due to decreased HCO3 А filtration. This is due to a decrease in the concentration of HCO3 А in the extracellular fluid.

In respiratory acidosis, the excess of H + in a renal tubular fluid is mainly due to the increase in the concentration of extracellular fluid PCO2, which stimulates H + secretion.

In chronic acidosis, whether respiratory or metabolic, there is an increase in NH4 + production, contributing to an increase in H + secretion and an increase in new HCO3 А in the extracellular fluid. With severe chronic acidosis, H + can be excreted up to 500 mEq/day in the urine, mainly from NH4 +; This excretion contributes up to 500 mEq/day of new HCO3 А into the bloodstream.

Board. Main features of acid-base disorders

Major transformations are described with a ↑↑ or ↓↓ sign. Note, respiratory acid-base disorders begin with an increase or decrease in PCO2, while metabolic disorders begin with an increase or decrease in HCO3 А.

Thus, in chronic acidosis, the renal tubular secretion of H + helps to remove excess H + and increase the amount of HCO3 А in the extracellular fluid. This process increases the HCO3 А in the bicarbonate buffer, according to the Henderson-Hasselbalch equation, to increase the extracellular pH and repair acidosis. If the acidosis is metabolic, the increase in ventilation reduces the PCO2 also helps correct the acidosis.

A summary of properties related to respiratory and metabolic acidosis, as well as respiratory and metabolic alkalosis, is included below. Note that in respiratory acidosis, a decrease in pH, an increase in the concentration of extracellular fluid H +, and an increase in PCO2 cause acidosis. The compensatory response is an increase in renal plasma HCO3 А. This increase helps compensate for an increase in PCO2, which in turn brings blood pH back to normal.

In metabolic acidosis, there is also a decrease in pH and an increase in extracellular H + concentration. In this case, however, the first abnormality is a decrease in HCO3 А. The first compensation mechanism includes hyperventilation, a decrease in PCO2, and renal compensation by adding new HCO3 А to the extracellular fluid, helping to minimize extracellular HCO3 А loss.

Adjustment of the kidneys in alkalosis - reduces renal tubular secretion and increases HCO3 А absorption.

Compensation for alkalosis was essentially the opposite of acidosis. In alkaline individuals, the extracellular HCO3- / CO2 ratio increases, leading to increased pH, as shown in the Henderson-Hasselbalch equation.

The alkaline infection causes an increase in the ratio of HCO3- / H + in the renal tubules.

Alkaline infection, whether the cause is due to respiratory or metabolic disorders, has an increased ratio of HCO3- / H + in the renal tubules. The real cause of the increased HCO3- concentration is the renal tubular non-reabsorption of HCO3- but excretion in the urine. In alkalosis, HCO3 А is eliminated from the extracellular fluid through the kidney, having the same effect as increasing the retention of H + in the extracellular fluid. This mechanism helps to keep Ph back to normal value. The table shows all properties of respiratory alkalosis and metabolic alkalosis. In the case of respiratory alkalosis, there is an increase in extracellular pH and a decrease in the H + concentration. The cause of alkalosis is a decrease in PCO2 and a decrease in the renal tubular secretion of H +. As a result, there is not enough H + in renal tubular urine to react with HCO3 А. Therefore, HCO3- will increase the excretion and reduce reabsorption, leading to a decrease in compensation and alkalosis. Therefore, the primary compensatory response in respiratory alkalosis is a decrease in the HCO3 А concentration. In metabolic alkalosis, there is also a decrease in the concentration of H + and an increase in pH. The cause of alkalization is the increase in the concentration of HCO3 А in the extracellular fluid. The body has a compensatory mechanism by reducing breathing to increase PCO2 and return the pH to normal values. In addition, an increase in extracellular fluid HCO3 А concentration decreases HCO3 А transport, leading to an increase in the proportion of HCO3- / H + in the tubular urine. Although the concentration of HCO3- in tubular urine is high, it is not reabsorbed due to the absence of combined H +. Therefore, HCO3- will be excreted in the urine. In metabolic alkalosis, the main compensatory mechanism is to increase PCO2 through increased excretion of HCO3 А. An increase in extracellular fluid HCO3 А concentration decreases HCO3 А transport, leading to an increase in the proportion of HCO3- / H + in the tubular urine. Although the concentration of HCO3- in tubular urine is high, it is not reabsorbed due to the absence of combined H +. Therefore, HCO3- will be excreted in the urine. In metabolic alkalosis, the main compensatory mechanism is to increase PCO2 through increased excretion of HCO3 А. An increase in extracellular fluid HCO3 А concentration decreases HCO3 А transport, leading to an increase in the proportion of HCO3- / H + in the tubular urine. Although the concentration of HCO3- in tubular urine is high, it is not reabsorbed due to the absence of combined H +. Therefore, HCO3- will be excreted in the urine. In metabolic alkalosis, the main compensatory mechanism is to increase PCO2 through increased excretion of HCO3 А.

 

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