Nature of hypochloremic alkalosis induced by adrenal steroids

Hypokalaemia, Metabolic Alkalosis, and Hypernatraemia due to "Massive" Sodium Penicillin Therapy

“…This means that even in maximally acidic urine over 90% will be ionized, (Clapp et al, 1962). Hypokalaemia should secondarily augment hydrogen ion excretion by stimulating ammonia production (Seldin et al, 1954) as well as sustain metabolic alkalosis by increasing bicarbonate reabsorption in the proximal tubule (Rector et al, 1964). The importance of chloride depletion causing increased hydrogen ion excretion (Gulyassy et al, 1962) (Schwartz et al, 1955) with mild secondary aldosteronism due to clinically apparent or inapparent heart failure or inadequate food intake, form the necessary background for penicillin to cause potassium depletion.…”

“…The increased transtubular potential difference in the distal tubule generated by non-reabsorbable anions should enhance not only potassium secretion but hydrogen ion secretion as well (Clapp et al, 1962). Hypokalaemia should secondarily augment hydrogen ion excretion by stimulating ammonia production (Seldin et al, 1954) as well as sustain metabolic alkalosis by increasing bicarbonate reabsorption in the proximal tubule (Rector et al, 1964). The importance of chloride depletion causing increased hydrogen ion excretion (Gulyassy et al, 1962) Though five patients suffering from subacute bacterial endocarditis were rendered hypokalaemic by 100 mega units of sodium penicillin G daily, there was one patient with coxitis who did not develop any electrolyte disturbance.…”