Effect of acute acid loading on acid–base and calcium metabolism

Abstract

Objective. To investigate the acid–base and calcium metabolic responses to acute non-carbonic acid loading in idiopathic calcium stone-formers and healthy males using a quantitative organ physiological approach. Material and methods. Five-h ammonium chloride loading studies were performed in 12 male recurrent idiopathic calcium stone-formers and 12 matched healthy men using a randomized, placebo-controlled, cross-over design. Arterialized capillary blood, serum and urine were collected hourly for measurement of electrolytes, ionized calcium, magnesium, phosphate, parathyroid hormone and acid–base status. Concentrations of non-metabolizable base (NB) and acid (NA) were calculated from measured concentrations of non-metabolizable ions. Results. The extracellular acid–base status in the stone-formers during basal conditions and acid loading was comparable to the levels in the healthy controls. The stone-formers tended to have lower renal excretion rates of NA during acid loading; however, for a given degree of non-carbonic acidosis, controls and stone-formers excreted approximately the same amount of NA in the urine, suggesting that the capacity of tubular regeneration of NB was comparable in the two groups. Acid loading resulted in significantly increased concentrations of ionized calcium in serum in both controls and stone-formers. The increase in serum ionized calcium in response to acid loading was, however, significantly higher in the calcium stone-formers than in the healthy individuals. Acid loading resulted in massive calciuria in both groups, with significantly higher urinary calcium excretion rates in the stone-formers compared to the healthy subjects. Renal excretion rates of NA correlated significantly with renal calcium excretion rates in both groups. However, the stone-formers excreted significantly more calcium in the urine at a given rate of renal NA excretion. Conclusions. The hypercalciuric and hypercalcaemic responses to loading with non-carbonic acid are more pronounced in recurrent idiopathic calcium stone-formers than in healthy individuals. Acid loading (i.e. protein ingestion) may contribute to disturbed bone metabolism in idiopathic calcium nephrolithiasis as well as calcium stone formation.

• Acid–base
• bone
• calcium
• kidney calculi
• magnesium
• parathyroid hormone
• phosphorous
• protein catabolism