Clinical Investigation

Kidney International (1995) 47, 269–273; doi:10.1038/ki.1995.34

Acid-base balance in chronic peritoneal dialysis patients

Jaime Uribarri, Joey Buquing and Man S Oh

The Departments of Medicine, Mount Sinai Medical Center, New York, and State University of New York Health Science Center at Brooklyn, New York, USA

Correspondence: Jaime Uribarri MD, Mount Sinai Medical Center, One Gustave Levy Place, New York, New York 10029, USA.

Received 22 April 1994; Revised 29 June 1994; Accepted 25 July 1994.

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Abstract

Acid-base balance in chronic peritoneal dialysis patients. Endogenous acid production has never been measured directly in dialysis patients and an empiric formula is used to estimate acid production from their protein catabolic rate. We have studied acid-base balance in 19 stable CAPD patients attending the peritoneal dialysis clinic of Mount Sinai Hospital. They obtained a 24 hour collection of peritoneal dialysis fluid and urine while consuming their usual diet and performing their usual activities. Total alkali gain was calculated from net GI alkali absorption plus urinary net acid excretion plus alkali gain from dialysate, while total acid production was measured directly from the urinary and dialysate excretions of sulfate and organic anions. Net GI alkali absorption was estimated from the difference between cations (Na + K + Ca + Mg) and anions (Cl + 1.8P) in the 24 hour dialysate and urine collections minus the daily total amount of lactate infused. All of our patients had a normal or high serum bicarbonate concentration, which was stable with time. Total alkali gain was virtually identical to total acid production (54.2 vs. 52.4 mEq/day) which suggests that these patients were in neutral acid-base balance. Net GI alkali absorption (22.7 mEq/day) was one of the same range as that of chronic renal failure patients not on dialysis and represented almost one half of the total daily alkali gain. The daily acid production of 52.4 mEq/day was numerically equal to 84% of the protein catabolic rate expressed as g/day, which is similar to the predicted value of 77% of PCR reported in the literature. However, the main source of alkali loss, that is, acid production, was the loss of organic anions in dialysate and urine. Daily sulfate excretion (16 mEq/day) was lower than expected for the level of protein intake (protein catabolic rate of 62 g/day). The stable serum bicarbonate concentrations on long-term dialysis suggests a steady state and neutral acid-base balance in these patients. The almost perfect agreement between acid production and total alkali gain supports the validity of our methods for measuring the various parameters of acid-base balance, including net GI absorption of alkali.

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