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The effects of altered acid-base balance on the production of urea and the metabolism of glutamine were investigated in the isolated perfused liver and hindquarter of the rat. In the isolated perfused rat liver, lowering of perfusate pH without altering bicarbonate concentration significantly reduced urea production and increased net glutamine synthesis, although the converse did not obtain. In the isolated perfused rat hindquarter when perfusate pH and bicarbonate were simultaneously reduced glutamine synthesis was significantly increased. The combined hepatic and muscle increase in glutamine synthesis accounted for 89% of the decrease in hepatic urea synthesis under these experimental conditions. These changes in nitrogen metabolism are interpreted in terms of adaptations which offset the initial alterations in hydrogen ion homeostasis.

The cause of secondary hyperoxalemia and oxalosis in patients on maintenance dialysis is unknown. The oxalate removal rate was determined in 26 patients on maintenance hemodialysis and 6 on continuous ambulatory peritoneal dialysis by measuring oxalate removed by dialysis and urinary excretion. The role of vitamin B6 deficiency and ascorbate in the raised plasma oxalate concentrations of these patients was evaluated. Plasma oxalate in hemodialysis patients, 442 +/- 41 micrograms/100 mL (mean +/- SE), and peritoneal patients, 394 +/- 115 micrograms/100 mL, were significantly higher than that in normal subjects, 11 +/- 1 microgram/100 mL (P less than 0.001). Average daily oxalate removal in subjects on hemodialysis, based on dialysis losses and urinary excretion, 35 +/- 3 mg/24 h, was significantly greater than urinary excretion of normal subjects, 26 +/- 1 (P less than 0.01). Oxalate removal from peritoneal dialysis patients, 28 +/- 2 mg/24 h, was not significantly different from that of hemodialysis patients or urinary excretion of normal subjects. Plasma ascorbate and B6 status were not correlated with plasma oxalate. A positive correlation between B6 deficiency and oxalate removal rate was not found. Plasma oxalate was correlated with time on dialysis (all patients) (P = 0.02). In a separate study of 15 hemodialysis patients followed over 2.3 +/- 0.2 yr, both plasma oxalate and oxalate removal rate significantly increased, P less than 0.001 and 0.05, respectively. It was concluded that oxalate removal rate is increased in hemodialysis patients and that the increased total body oxalate burden in these patients is not due to decreased removal. Although the increase may result from increased oxalate synthesis or gastrointestinal absorption, B6 deficiency and increased plasma ascorbate do not play a role.

The methods used for determination of oxalate in blood are reviewed, and the advantages and disadvantages of the two basic approaches--direct methods and in vivo isotope-dilution techniques--are compared. Possible reasons for the previous discrepancies between direct and isotopic methods are discussed, as are the effects of protein binding, sample handling, and storage conditions on oxalate values in plasma. Necessary precautions for obtaining reproducible results are presented. We recommend and critically review several direct methods, and describe the application of a direct method for oxalate determination in some other biological fluids.

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