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Metabolic acidosis is a **serious electrolyte disorder** characterized by a primary reduction in serum bicarbonate concentration and decreased blood pH due to either increased acid production, loss of base, or reduced renal excretion of acids.[1][7] It is not itself a molecular target but rather a clinical syndrome resulting from various underlying diseases including kidney failure, diabetes mellitus (ketoacidosis), severe diarrhea, toxin ingestion, or sepsis-induced lactic acid accumulation.[1][10] The condition can be acute or chronic; acute forms often result from rapid organic acid buildup while chronic forms are usually related to impaired renal function or ongoing base loss.[1] Diagnosis relies on laboratory findings such as low serum bicarbonate and arterial blood gas analysis showing low pH; further classification uses the anion gap calculation.[7][8] Treatment focuses on correcting the underlying cause and may include administration of alkalinizing agents like sodium bicarbonate when appropriate,[5] but this approach carries risks if not carefully monitored. Note: **Metabolic acidosis is not a molecule/receptor/therapeutic target**, but rather a pathophysiological state/syndrome caused by dysfunction at various molecular targets within metabolism—such as enzymes involved in acid-base homeostasis—or organ systems like kidneys. Therefore "is_target" should be marked false and "is_incorrect" true for use as a drug discovery/target entry.[5]
Sodium bicarbonate and sodium citrate act as alkalinizing agents, neutralizing excess acid in the blood. Insulin corrects diabetic ketoacidosis by reducing ketone production. IV fluids restore fluid balance and help correct underlying causes such as dehydration or shock. Oxygen improves tissue oxygenation in lactic acidosis. Antibiotics treat underlying infections that may be causing lactic acid buildup.[2][4]
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