A renal mechanism limiting the degree of potassium loss in severely hyperglycemic patients.

Potassium (K) secretion in the cortical 'distal nephron' was assessed in vivo in 29 consecutive patients presenting with diabetic ketoacidosis (DKA) or the hyperglycemic hyperosmolar syndrome (HHS). The only selection criteria applied were that the electrolytes and osmolality be measured in the urine on admission. Five patients with DKA and 3 patients with HHS were reported in detail as plasma aldosterone levels were also measured in these patients on admission. K secretion in the 'cortical distal nephron' was assessed by a semiquantitative index, the transtubular K concentration gradient (TTKG). TTKG values less than 6.0, consistent with less than maximal renal K secretion, were found in 28 of 29 patients despite the presence of hyperkalemia and/or stimuli for renin and aldosterone release. Plasma aldosterone levels on admission were very elevated in 4 patients, at the upper end of the usual normal range in 3 and in the low part of the normal range in 1 patient. Treatment with intravenous saline, KCl and insulin corrected the fluid and electrolyte abnormalities in the plasma over 24-48 h. Concurrently, plasma aldosterone levels fell, but the TTKG rose; this suggest that there was an increased renal tubular response to aldosterone after initial therapy. The mechanism responsible for this reversible impairment of renal K secretion is unknown. It may limit total body K depletion in patients presenting with DKA and HHS by diminishing renal K excretion.