NaHCO3 and KHCO3 ingestion rapidly increases renal electrolyte excretion in humans
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This paper describes and quantifies acute responses of the kidneys in correcting plasma volume, acid-base, and ion disturbances resulting from NaHCO3 and KHCO3 ingestion. Renal excretion of ions and water was studied in five men after ingestion of 3.57 mmol/kg body mass of sodium bicarbonate (NaHCO3) and, in a separate trial, potassium bicarbonate (KHCO3). Subjects had a Foley catheter inserted into the bladder and indwelling catheters placed into an antecubital vein and a brachial artery. Blood and urine were sampled in the 30-min period before, the 60-min period during, and the 210-min period after ingestion of the solutions. NaHCO3 ingestion resulted in a rapid, transient diuresis and natriuresis. Cumulative urine output was 44 ± 11% of ingested volume, resulting in a 555 ± 119 ml increase in total body water at the end of the experiment. The cumulative increase (above basal levels) in renal Na+ excretion accounted for 24 ± 2% of ingested Na+. In the KHCO3 trial, arterial plasma K+ concentration rapidly increased from 4.25 ± 0.10 to a peak of 7.17 ± 0.13 meq/l 140 min after the beginning of ingestion. This increase resulted in a pronounced, transient diuresis, with cumulative urine output at 270 min similar to the volume ingested, natriuresis, and a pronounced kaliuresis that was maintained until the end of the experiment. Cumulative (above basal) renal K+ excretion at 270 min accounted for 26 ± 5% of ingested K+. The kidneys were important in mediating rapid corrections of substantial portions of the fluid and electrolyte disturbances resulting from ingestion of KHCO3 and NaHCO3 solutions.
