The incidence of tubular proteinuria measured as urinary excretion of β2-microglobulin was evaluated in 68 consecutive renal calcium stone formers, 14 of whom had impaired urinary acidification capacity. During normal conditions 13% of these stone formers had tubular proteinuria. There was no statistical difference in the incidence of tubular proteinuria between subgroups with proximal or distal acidification defects. During transient metabolic acidosis induced by an ammonium chloride load a pronounced increase in β2-minicrglobulin excretion was noticed in all patient groups but especially in those with urinary acidification defects. In stone formers with normal acidification capacity the degree of acidosis-induced β2-microglobulinuria was moderate but a small group of patients exhibited a large urine excretion of β2-microglobulin. This finding may reflect a latent tubular defect of importance for stone genesis.
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