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Biomedical subjects

D Corish

Publications and source records attributed to D Corish.

2 recordsLinked to original sources

The electrolytes in hyponatremia.

It is commonly taught that retention of free water is the dominant factor reducing the serum sodium concentration in hyponatremia. To determine whether the concentrations of other electrolytes are similarly diluted, we identified 51 patients with hyponatremia (Na = 121 +/- 1 mmol/L [mEq/L]) and compared electrolyte and laboratory values at the time of hyponatremia with values at a time when serum sodium was in the normal range (138 +/- 1 mmol/L). The medium interval between these measurements was 12 days. At the time of hyponatremia, serum sodium and chloride were substantially and significantly reduced by 12% to 15%. Although many hyponatremic patients had overtly increased or decreased concentrations of the other measured electrolytes, there were no significant changes in the mean concentration for any of these at the time of hyponatremia. Unchanged mean values were found for the plasma concentration of bicarbonate (26.1 +/- 0.6 normal v 25.2 +/- 0.8 mmol/L at the time of hyponatremia), potassium (4.31 +/- 0.10 v 4.33 +/- 0.15 mmol/L), albumin, phosphate, and creatinine. The stability of these laboratory values was observed both in patients with clinically normal extracellular fluid (ECF) volume and in those with true or effective ECF depletion. The urinary sodium (UNa) concentration was found to be a reliable predictor of the ECF volume status, whereas the fractional sodium excretion (FENa) was not. Electrolyte derangements are common in patients with hyponatremia, but are usually confined to patients on diuretics or who have an abnormal ECF volume. In the absence of these complicating situations, the plasma electrolytes are typically normal and are not reduced by dilution to the same extent as Na and CI. Based on a review of both the classic and recent knowledge concerning electrolyte regulation in hyponatremia, we propose that two factors explain these observations. First, the degree of dilution is overestimated because of Na losses in urine and perhaps Na shift into cells. Second, both renal and extrarenal adaptive mechanisms are activated by hyponatremia that stabilizes the concentration of other ions. One of these mechanisms is cell swelling, which triggers a volume-regulatory response leading to the release of ions and water into the ECF. Other adaptive mechanisms are mediated by antidiuretic hormone (ADH) per se, and by atrial natriuretic peptide (ANP).

Adaptation, Physiological↗

Thrombocytosis elevates serum potassium.

Spurious elevation of the serum potassium can be seen if the platelet count exceeds 1,000 x 10(9)/L in patients with myeloproliferative disease. To see if serum potassium is increased at more modest elevations of the platelet count we studied these parameters in 283 controls and 161 patients with reactive thrombocytosis. The incidence of hyperkalemia was 34% in patients with over 500 x 10(9) platelets/L compared with 9% if the platelet count was below 250 x 10(9)/L. Over this range there was a significant correlation of potassium increasing with the platelet count. The higher potassium values could not be explained on the basis of leukocytosis, renal insufficiency, or acidosis, suggesting that the elevated serum levels were often spurious. In support of this conclusion, the serum potassium exceeded plasma potassium by a larger amount in patients with thrombocytosis. We conclude that serum potassium rises in direct proportion to the platelet count in normal patients and in those with thrombocytosis, and that this increment is an artifact.

Humans↗