Hyponatremia and hyperkalemia in relation to hyperglycemia in insulin-treated diabetic out-patients.

Interrelations between glucose and electrolyte homeostasis were evaluated in 193 insulin-treated diabetic out-patients. All had normal serum creatinine and were studied during their everyday metabolic control. Although the patients were selected to be without proteinuria and ketonuria, they exhibited wide ranges of blood glucose values (2.5-29.5 mmol/l) and urine glucose excretions (0-301 mmol/mmol creatinine). Patients with blood glucose values within 2.5-10 mmol/l (n = 80) had entirely normal levels of serum sodium (140.6 +/- 2.7 (SD) versus 141.0 +/- 2.6 mmol/l) and potassium (4.35 +/- 0.38 versus 4.40 +/- 0.38 mmol/l) as compared with normals (n = 371). In contrast, diabetics with higher blood glucose concentrations (n = 113) showed hyponatremia (137.7 +/- 2.6 mmol/l, p less than 0.001) and a moderate increase of serum potassium (4.60 +/- 0.39 mmol/l, p less than 0.001). On stratification into classes of blood glucose, serum sodium declined from 142 to 135 mmol/l (r = -0.61, p less than 0.001), whereas serum potassium rose from 4.33 to 4.87 mmol/l (r = 0.37, p less than 0.001). Despite these reciprocal changes the urinary excretion rates relative to creatinine of sodium potassium and water rose with rising degrees of glycosuria (r = 0.24, p less than 0.001; r = 0.28, p less than 0.001; and r = 0.63, p less than 0.001, respectively). The decline in serum sodium represents a well-known osmoregulatory response to hyperglycemia. However, the rising level of serum potassium in virtual absence of renal failure and ketonuria suggests an abnormality in potassium homeostasis. Diabetic dysregulation, or rather insulin deficiency may be its cause.