Pathogenesis and Cellular-Renal Mechanisms
The underlying pathology is driven by excessive processes occurring within the renal tubules and tissue cells:
- Renal Mechanisms:
- Renal tubular epithelium increases the secretion of hydrogen ($H^+$) and potassium ($K^+$) ions into the tubular fluid.
- Sodium ($Na^+$) reabsorption from the tubular lumen back into the blood increases.
- Cellular Mechanisms:
- The intracellular accumulation of $H^+$ ions leads to intracellular acidosis.
- Intracellular retention of $Na^+$ occurs.
- Increased osmotic pressure resulting from sodium accumulation causes cellular hyperhydration.
This acid-base disorder is termed metabolic because it develops through a sequential cascade of metabolic reactions.
Excretory Acid-Base Disorders
The etiology of excretory acid-base disturbances involves impaired elimination of acids or bases from the body—either through their excessive loss or retention.
There are two main groups of such disorders:
- Excretory acidosis;
- Excretory alkalosis.
Defensive responses in excretory alkalosis are fundamentally similar to the compensatory mechanisms seen in metabolic acidosis. They include an immediate phase (involving non-bicarbonate extracellular and cellular buffers) followed by long-term adaptive responses.
Immediate Compensatory Mechanisms
The primary goal of compensatory processes is to reduce the concentration of bicarbonate ($HCO_3^-$) in extracellular fluids and blood plasma. Because the body lacks highly efficient direct pathways to eliminate excess base, a complex set of immediate indirect reactions is utilized:
- Respiratory compensation: A drop in alveolar ventilation (hypoventilation) leads to $CO_2$ retention. The resulting respiratory acidosis compensates for the metabolic alkalosis.
- Activation of cellular systems: Protein buffers are engaged, and glycolysis along with the tricarboxylic acid (TCA) cycle are stimulated to generate acidic metabolic products.
- Ion exchange: Intracellular chloride ($Cl^-$) is shifted into the extracellular space in exchange for bicarbonate ($HCO_3^-$) entering the cells.
- Extracellular buffering: Extracellular buffers are activated, although their buffering capacity against alkali is limited.
Long-Term Compensation
Following the immediate protective shifts, long-term processes are activated to completely correct or minimize the degree of alkalosis.
Renal compensation plays the key role here. The kidneys increase the excretion of excess bicarbonate ($HCO_3^-$) from the body, ensuring durable normalization of acid-base balance parameters.