1. Stable urea isotopes can be used to study urea kinetics in humans. The use of stable urea isotopes for studying urea kinetic parameters in humans on a large scale is hampered by the high costs of the labelled material. We devised a urea dilution for measurement of the distribution volume, production rate and clearance of urea in healthy subjects and renal failure patients using the inexpensive single labelled [ 13 C]urea isotope with subsequent analysis by headspace chromatography—isotope ratio MS (GC—IRMS) of the [ 13 C]urea enrichment. 2. The method involves measurement of the molar percentage excess of [ 13 C]urea in plasma samples taken over a 4 h period after an intravenous bolus injection of [ 13 C]urea. During the sample processing procedure, the plasma samples together with calibration samples containing a known molar percentage excess of [ 13 C]urea are acidified with phosphoric acid to remove endogenous CO 2 , and are subsequently incubated with urease to convert the urea present in the plasma samples into CO 2 . The 13 C enrichment of the generated CO 2 is analysed by means of GC—IRMS. This method allows measurement of the molar percentage excess of [ 13 C]urea to an accuracy of 0.02%. 3. Reproducibility studies showed that the sample processing procedure [within-run coefficient of variation (CV) <2.8% and between-run CV <8.8%] and the GC—IRMS analysis (within-day CV <1.3% and between-day CV <1.3%) could be repeated with good reproducibility. 4. In clinical urea kinetic studies in a healthy subject and in a renal failure patient without residual renal function, reproducible values of the distribution volume, production rate and clearance of urea were determined using minimal amounts of [ 13 C]urea (25–50 mg). 5. Because only low [ 13 C]urea enrichments are needed in this urea dilution method using GC—IRMS analysis, the costs of urea kinetic studies are reduced considerably, especially in patients with renal failure.

1. In order to find out whether hyperoxaluria can be demonstrated in patients on chronic (twice a week) haemodialysis, a group of 13 patients was investigated. These included one patient with proven primary hyperoxaluria, one suspected of having this disease and 11 patients in whom no information was available as to their oxalate metabolism. 2. Oxalate concentrations in haemodialysate fractions and blood samples, taken before and after dialysis, were determined. 3. The patient with primary hyperoxaluria had a plasma oxalate concentration before dialysis above 100 μmol/l and after dialysis above 25 μmol/l, while the oxalate concentration in haemodialysate at the start of dialysis was above 25 μmol/l and at the end above 10 μmol/l. The patient suspected of hyperoxaluria had similar values. Of the remaining 11 patients, one was shown to exhibit a transient hyperoxaluria, but the others showed a normal oxalate metabolism. 4. A plasma oxalate/creatinine concentration ratio exceeding 0.1, and the calculated total quantity of oxalate removed by dialysis exceeding 2 mmol, also enabled a diagnosis of hyperoxaluria to be made. 5. Hyperoxaluria can still be demonstrated in patients, who because of renal failure are subjected to haemodialysis. Measurements of oxalate in haemodialysate and plasma are valuable in cases where kidney transplantations are considered, especially when the particular patient exhibits hyperoxaluria.