Aldosterone In Dka

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Hyperaldosteronism In Ketoacidosis And In Poorly Controlled Non-ketotic Diabetes

Summary PLASMA aldosterone concentrations were measured in 14 patients in diabetic ketoacidosis and in 20 patients with poorly controlled non-ketotic diabetes, both before treatment and again when metabolic control was achieved. Plasma aldosterone was above normal in 12 of 14 patients in ketoacidosis and there was a highly significant fall in mean plasma aldosterone concentration when metabolic control improved. Plasma aldosterone concentration in ketoacidosis was significantly related to plasma angiotensin //, arterial pH and indirect indices of dehydration. Plasma aldosterone was also above normal before treatment in 7 of 20 patients with poorly controlled non-ketotic diabetes. When metabolic control improved there was a small but significant reduction in mean plasma aldosterone concentration. However, plasma aldosterone and angiotensin were not significantly related in these patients. It is concluded that ketoacidosis is usually associated with marked hyper-aldosteronism. Poorly controlled nonketotic diabetes is sometimes associated with mild aldosterone excess, which may contribute to the potassium wasting associated with poorly controlled diabetes. Continue reading >>

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Popular Questions

  1. metalmd06

    Does acute DKA cause hyperkalemia, or is the potassium normal or low due to osmotic diuresis? I get the acute affect of metabolic acidosis on potassium (K+ shifts from intracellular to extracellular compartments). According to MedEssentials, the initial response (<24 hours) is increased serum potassium. The chronic effect occuring within 24 hours is a compensatory increase in Aldosterone that normalizes or ultimatley decreases the serum K+. Then it says on another page that because of osmotic diuresis, there is K+ wasting with DKA. On top of that, I had a question about a diabetic patient in DKA with signs of hyperkalemia. Needless to say, I'm a bit confused. Any help is appreciated.

  2. FutureDoc4

    I remember this being a tricky point:
    1) DKA leads to a decreased TOTAL body K+ (due to diuresis) (increase urine flow, increase K+ loss)
    2) Like you said, during DKA, acidosis causes an exchange of H+/K+ leading to hyperkalemia.
    So, TOTAL body K+ is low, but the patient presents with hyperkalemia. Why is this important? Give, insulin, pushes the K+ back into the cells and can quickly precipitate hypokalemia and (which we all know is bad). Hope that is helpful.

  3. Cooolguy

    DKA-->Anion gap M. Acidosis-->K+ shift to extracellular component--> hyperkalemia-->symptoms and signs
    DKA--> increased osmoles-->Osmotic diuresis-->loss of K+ in urine-->decreased total body K+ (because more has been seeped from the cells)
    --dont confuse total body K+ with EC K+
    Note: osmotic diuresis also causes polyuria, ketonuria, glycosuria, and loss of Na+ in urine--> Hyponatremia
    DKA tx: Insulin (helps put K+ back into cells), and K+ (to replenish the low total potassium
    Hope it helps

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