Renal response to acute acid loading--an organ physiological approach

OBJECTIVE: In previous studies of the renal response to acute NH4Cl acidosis no correlation was found between systemic acid-base status and the traditionally used quantity, renal net acid excretion (NAE). If NAE is to be considered a physiologically meaningful quantity then this is surprising, as th...

Full description

Bibliographic Details
Published in:Scandinavian Journal of Urology and Nephrology
Main Authors: Osther, P J, Engel, K, Kildeberg, P
Format: Article in Journal/Newspaper
Language:English
Published: 2004
Subjects:
Online Access:https://portal.findresearcher.sdu.dk/da/publications/ba0ce690-0667-11df-aefb-000ea68e967b
https://doi.org/10.1080/00365590310018838
Description
Summary:OBJECTIVE: In previous studies of the renal response to acute NH4Cl acidosis no correlation was found between systemic acid-base status and the traditionally used quantity, renal net acid excretion (NAE). If NAE is to be considered a physiologically meaningful quantity then this is surprising, as the extracellular acid-base status would be expected to be the key physiological trigger for renal NAE. The object of this study was to investigate the renal response to acute non-carbonic acid loading using a quantitative organ physiological approach. MATERIAL AND METHODS: Five-h NH4Cl loading studies were performed in 10 healthy men using a randomized, placebo-controlled, crossover design. Arterialized capillary blood, serum and urine were collected hourly during the loading studies for the measurement of electrolytes and acid-base status. Concentrations of non-metabolizable base (NB) and acid (NA) were calculated from measured concentrations of non-metabolizable ions according to Kildeberg. RESULTS: In the steady state (placebo) the rate of renal excretion of NA (=-NB) was close to zero, indicating that the net extrarenal input of NA (endogeneous production, gastrointestinal absorption. skeletal release, etc.) was likewise about zero. An inverse correlation was found between blood pH and the rate of renal excretion of NA. Only a small amount of the acid load (approximately 8%) was excreted during the 5-h study period and this was accompanied by massive calciuria, indicating that mobilization of NB from bone contributed substantially to the current net extrarenal NA input. CONCLUSION: From a physiological point of view, NB can be regarded as the actual substrate for renal acid-base control, and measurement of renal turnover of NB may give a more precise description of renal acid-base metabolism during acid loading than previously described methods.