Renal response to acute ammonium chloride acidosis in subjects with single kidney

The renal response to acute ammonium chloride ingestion (75 mEq per m²) is quantitated in 3 normal adults and 5 normal kidney donors (mean of 400 days after unilateral nephrectomy). The adequate renal tubular response to metabolic acidoses in the normal subjects is evident with nearly complete correction of the systemic acidosis at 1,920 min after ammonium chloride ingestion. This is sharply contrasted in the persistence of acidosis in the single kidney subjects. The net acid excretion is consistently lower in the single kidney subjects as compared to the normal subjects. The etiology of this acidification defect is best explained by invoking the role of the reduced renal mass despite a 20% compensatory increase in GFR. It is anticipated that this study will provide control data for the studies of kidney allograft recipients with abnormal renal function.