of a comprehensive metabolic panel. Patients with CKD Stages G3-G5 should be routinely screened for metabolic acidosis. Diagnostic approach and causes Metabolic acidosis is defined as a reduced serum pH, and an abnormal serum bicarbonate concentration of <22 mEq/L, below the normal range of 22 to 29 mEq/L. However, if a patient has other coexisting acid-base disorders, the pH level may be low, normal or high in the setting of metabolic acidosis. In the absence of chronic respiratory alkalosis, metabolic acidosis can be clinically diagnosed by measuring serum bicarbonate levels in the blood, which is generally a standard component of blood panels. Imperatively, when weighing a metabolic acidosis diagnosis, the change in serum bicarbonate levels over time should be considered; if baseline bicarbonate results are unknown, a single set of values may be misinterpreted. Causes Generally, metabolic acidosis occurs when the body produces too much acid (e.g., lactic acidosis, see below section), there is a loss of bicarbonate from the blood, or when the kidneys are not removing enough acid from the body. Chronic metabolic acidosis is most often caused by a decreased capacity of the kidneys to excrete excess acids through renal ammoniagenesis. The typical Western diet generates 75-100 mEq of acid daily, and individuals with normal kidney function increase the production of ammonia to get rid of this dietary acid. As kidney function declines, the tubules lose the ability to excrete excess acid, and this results in buffering of acid using serum bicarbonate, as well as bone and muscle stores. There are many causes of acute metabolic acidosis, and thus it is helpful to group them by the presence or absence of a normal anion gap. Increased anion gap Causes of increased anion gap include: Lactic acidosis Ketoacidosis (e.g., Diabetic, alcoholic, or starvation) Chronic kidney failure Transient 5-oxoprolinemia due to long-term ingestion of high-doses of acetaminophen (often seen with sepsis, liver failure, kidney failure, or malnutrition) Intoxication: Salicylates, methanol, ethylene glycol Organic acids, paraldehyde, ethanol, formaldehyde Carbon monoxide, cyanide, ibuprofen, metformin Propylene glycol (metabolized to L and D-lactate and is often found in infusions for certain intravenous medications used in the intensive care unit) Massive rhabdomyolysis Isoniazid, iron, phenelzine, tranylcypromine, valproic acid, verapamil Topiramate Sulfates Normal anion gap Causes of normal anion gap include Inorganic acid addition Infusion/ingestion of HCl, Gastrointestinal base loss Diarrhea Small bowel fistula/drainage Surgical diversion of urine into gut loops Renal base loss/acid retention: