Hypomagnesemia, D-Lactic Acidosis, & Short Bowel Syndrome!

Pearls from today’s case:
1) The two major mechanisms of hypomagnesemia are gastrointestinal & renal loss.

2) D-lactic acidosis is an unusual form of lactic acidosis that can be seen in patients with short bowel syndrome.

3) The standard enzymatic lab assay for lactate does NOT detect D-lactate because it uses L-lactate dehydrogenase.

For a great review of Renal Tubular Acidoses and the urinary anion gap, check out Jess Beaman’s recent blog post!

Causes of Hypomagnesemia

    1) Gastrointestinal Losses
    a. diarrhea
    b. malabsorption
    c. small bowel bypass surgery
    d. acute pancreatitis
    e. PPIs (presumed mechanism is impaired absorption of intestinal epithelial cells)
    f. Genetic disorders

    2) Renal Losses
    a. alcoholism (alcohol-induced tubular dysfunction!)
    b. uncontrolled diabetes mellitus
    c. acquired tubular dysfunction
    – post-ATN, post-transplant, post-obstructive diuresis
    d. medications
    – diuretics (loop and thiazide)
    – abx (aminoglycosides, amphotericin, pentamidine)
    – calcineurin inhibitors
    – cisplatin
    – monoclonal Abs targeting EGF receptor
    e. hypercalcemia
    f. volume expansion
    g. genetic disorders
    – Bartter/Gitelman syndromes

    D-lactic acidosis
    Accumulation of D-lactic acid occurs in three settings:
    1) in a patient with short bowel syndrome after consumption of a carbohydrate load
    2) in a patient after large amount of propylene glycol
    3) in a patient with diabetic ketoacidosis

    Clinical manifestations of D-lactic acidosis are largely neurologic and include an altered sensorium. They include confusion, cerebellar ataxia, slurred speech, memory loss.

    The standard enzymatic lab assay for lactate with NOT detect D-lactic acid because it uses L-lactate dehydrogenase.

    Patient with D-lactic acidosis, the anion gap may not be as large as expected due to a stereospecific effect in the proximal tubule (D-lactate is more readily excreted than L-lactate; this leads to a decreased serum anion gap but does not increase the serum bicarb).

    D-lactic acidosis may result in both an elevated anion gap and a hyperchloremic metabolic acidosis and can occasionally be confused with renal tubular acidosis! (both can have a positive urine anion gap too — you would need to check the urine osm gap to differentiate!)


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