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  • Image not available. The kidney plays a central role in the regulation of acid–base homeostasis through the excretion or reabsorption of filtered bicarbonate (HCO3), the excretion of metabolic fixed acids, and generation of new HCO3.
  • Image not available. Arterial blood gases (ABGs), along with serum electrolytes, physical findings, medical and medication history, and the clinical condition of the patient, are the primary tools to determine the cause of an acid–base disorder and to design and monitor a course of therapy.
  • Image not available.Metabolic acidosis and metabolic alkalosis are generated by a primary change in the serum bicarbonate concentration. In metabolic acidosis, bicarbonate is lost or a nonvolatile acid is gained, whereas metabolic alkalosis is characterized by a gain in bicarbonate or a loss of nonvolatile acid.
  • Image not available. Renal tubular acidosis (RTA) refers to a group of disorders characterized by impaired tubular renal acid handling despite normal or near-normal glomerular filtration rates. These patients often present with hyperchloremic metabolic acidosis.
  • Image not available. Respiratory compensation for a primary metabolic acidosis begins rapidly (within 15 to 30 minutes) but does not reach a steady state for 12 to 24 hours after the onset of metabolic acidosis.
  • Image not available. Primary therapy of most acid–base disorders must include treatment or elimination of the underlying cause, not just correction of the pH and electrolyte disturbances.
  • Image not available. Potassium supplementation is always necessary for patients with chronic metabolic acidosis, as the bicarbonaturia resulting from alkali therapy increases the renal potassium wasting.
  • Image not available. Effective treatment of the underlying cause of some organic acidoses (e.g., ketoacidosis) can result in the regeneration of bicarbonate within hours, thus mitigating the need for alkali therapy.
  • Image not available. Loss of gastric acid from vomiting or nasogastric suctioning is often responsible for the development of a metabolic alkalosis, characterized by hypochloremia and hyperbicarbonatemia.
  • Image not available. Aggressive diuretic therapy can produce a metabolic alkalosis, and the accompanying hypokalemia can be serious.
  • Image not available. The patient’s response to volume replacement can be predicted by the urine chloride concentration and permits the differential diagnosis of metabolic alkalosis.
  • Image not available. Management of these disorders usually consists of treatment of the underlying cause of mineralocorticoid excess. In patients in whom the mineralocorticoid excess cannot be corrected, chronic pharmacologic therapy can be required.
  • Image not available. In most cases of acute metabolic acidosis, such as following cardiopulmonary arrest, sodium bicarbonate therapy is not indicated and can be detrimental. Blood gas analysis should guide therapy.

On completion of this chapter, the reader will be able to:

  1. State the mechanisms by which the kidney participates in the maintenance of acid–base homeostasis.

  2. Determine the likely cause of an acid–base disorder given the patient history, arterial blood gases, and medication history.

  3. Differentiate the likely type of metabolic acidosis that is present on the basis of the serum anion gap.

  4. Propose an initial treatment plan for the management of patients with acute severe metabolic acidosis.

  5. Select the optimal oral alkali therapeutic agent and regimen for a patient with chronic metabolic acidosis secondary to proximal renal tubular acidosis.

  6. Contrast the common causes of sodium chloride-responsive with those associated ...

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