ABSTRACT
We tested the possibility that the buffering agents in dialysis bath fluid might contribute to increased endogenous oxalate production in dialyzed patients. Using stable isotope dilution mass spectrometry, we obtained oxalate production rates and pool sizes directly for 10 patients in chronic renal failure, 5 of whom were undergoing continuous ambulatory peritoneal dialysis (lactate-buffered fluid). All peritoneal dialysis patients had either increased oxalate production rates or expanded oxalate pools when compared with undialyzed patients in renal failure. From a further four patients receiving maintenance hemodialysis we took blood samples immediately before and after three consecutive dialysis sessions in which the bath-fluid buffering agent (bicarbonate or acetate) was alternated; we analyzed these samples for oxalate and key precursors by capillary gas chromatography. Plasma glycine and serine concentrations remained within the physiological range. Glycolate and oxalate concentrations decreased, but the oxalate remained above normal after dialysis. All changes were independent of the bath-fluid buffering agent. We suggest that dialysis might stimulate the formation of oxalate by removing product inhibition of a late catabolic step.
Subject(s)
Dialysis Solutions/adverse effects , Kidney Failure, Chronic/therapy , Oxalates/blood , Peritoneal Dialysis, Continuous Ambulatory , Acetates , Bicarbonates , Buffers , Female , Glycolates/blood , Humans , Indicator Dilution Techniques , Kidney Failure, Chronic/blood , Kinetics , Male , Mass Spectrometry , Oxalic AcidABSTRACT
A capillary gas chromatographic method for plasma oxalate and an isotope dilution mass spectrometric reference method, both using the same tert.-butyldimethylsilyl derivatives, are described. Similar reference ranges for both were found (4.93 +/- 1.48 and 4.70 +/- 1.44 mumol/l, respectively), together with a close correlation for results covering a wide range of oxalate concentrations.
Subject(s)
Organosilicon Compounds , Oxalates/blood , Carbon Radioisotopes , Chromatography, Gas , Humans , Indicator Dilution Techniques , Indicators and Reagents , Mass Spectrometry , SiliconABSTRACT
We describe the clinical features of members of a family with an atypical form of thyroid hormone resistance syndrome, affecting thyroxine predominantly. Relevant diagnostic clinical and biochemical investigations are outlined and discussed.
Subject(s)
Hyperthyroxinemia/genetics , Thyroxine/therapeutic use , Adolescent , Adult , Child, Preschool , Diagnosis, Differential , Drug Resistance , Female , Humans , Hyperthyroxinemia/blood , Hyperthyroxinemia/diagnosis , Hyperthyroxinemia/physiopathology , Male , Middle Aged , Sex Hormone-Binding Globulin/analysis , Syndrome , Thyrotoxicosis/blood , Thyrotoxicosis/diagnosis , Thyrotoxicosis/drug therapy , Thyrotropin/blood , Thyrotropin-Releasing Hormone , Thyroxine/bloodABSTRACT
We describe two siblings with artefactually increased results for free thyroxin in serum as measured with the Amerlex analog method, despite normal thyroxin transport. The cause of the artefact is identified as a variant albumin with enhanced affinity for the Amerlex thyroxin-analog.
