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*From the Medizinische Universitaetsklinik Kantonsspital Bruderholz, Bruderholz, Switzerland; and
Institute of Physiology, Departement of Veterinary Medicine, University of Zurich, Switzerland; and
Genentech Inc., South San Francisco, California.
Correspondence to Dr. Reto Krapf, Medizinische Universitaetsklinik, Kantonsspital Bruderholz, CH 4101 Bruderholz/Basel, Switzerland. Phone: 0041-61-436-21-81; E-mail: reto.krapf{at}ksbh.ch
ABSTRACT. Despite the high incidence of acute metabolic acidosis, there are no reliable human data to enable physicians to accurately diagnose this disorder. In addition, there is uncertainty about the direction and magnitude of plasma potassium changes in acute metabolic acidosis. The systemic and renal acid-base, electrolyte, and endocrine response to acute acid loads (imposed by three timed NH4Cl infusions into the duodenum, 0.9 mmol of NH4Cl per kg of body weight over 30 min each) was characterized in six healthy male subjects in whom a metabolic steady-state had been established. Arterialized blood CO2 tension decreased by 0.85 mmHg per mmol/L decrease in plasma bicarbonate concentration and blood hydrogen ion concentration increased by 0.45 nmol/L per mmol/L decrease in plasma bicarbonate concentration. Plasma potassium did not change significantly (+0.02 ± 0.02 mmol/L per mmol decrease in plasma bicarbonate concentration). Plasma insulin increased and plasma glucagon levels decreased in acute metabolic acidosis, while catecholamines and aldosterone were not affected significantly. These data provide the first diagnostic criteria for the diagnosis of acute metabolic acidosis in humans. The finding of a hyperinsulinemic response in acute metabolic acidosis suggests that an insulin response counterregulates any acidemia-induced cellular potassium efflux, resulting in stable plasma potassium concentrations.
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