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B C McWhinney

Publications and source records attributed to B C McWhinney.

11 recordsLinked to original sources
PubMed1989

Effect of citrate on the urinary excretion of calcium and oxalate: relevance to calcium oxalate nephrolithiasis.

Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.

Absorption↗
PubMed1987

Two-carbon oxalogenesis compared in recurrent calcium oxalate stone formers and normal subjects.

We used a xylitol load to test the two-carbon pathway to oxalate production in humans. Use of this pentose sugar caused a fourfold increase in glycolate excretion, indicating its suitability as a dynamic function test of two-carbon metabolism. However, despite this increase in glycolate excretion in 10 recurrent stone formers and six normal subjects, there was no concomitant increase in oxalate excretion in either group. By comparison, a sucrose load produced no increase in excretion of either glycolate or oxalate. In addition, when we studied four recurrent calcium stone formers on successive diets with various fat content, we found no correlation between high fat intake and increased glycolate or oxalate excretion. In summary, there was no evidence of abnormal fluxes through the two-carbon pathway to oxalate in recurrent stone formers, nor of hyperoxaluria as related to increased intake of sucrose or fat.

Adult↗
PubMed1987

Chemical factors important to calcium nephrolithiasis: evidence for impaired hydroxycarboxylic acid absorption causing hyperoxaluria.

An investigation of variables important to calcium stone formation in urine indicated significantly increased daily excretion of calcium and oxalate and decreased excretion of ascorbate and citrate by recurrent calcium stone formers. In addition, urine volume, sodium, mucopolysaccharide, and protein were also significantly increased. We compared the uptake of citrate and ascorbate from the gut into the blood in normal controls and stone formers. These studies indicated significantly depressed absorption of both these hydroxycarboxylic acids in recurrent calcium stone formers. We also found that concurrent administration of citrate inhibited ascorbate absorption and increased urinary oxalate excretion after an ascorbate load in normal subjects and stone formers. These findings suggest a mechanism that explains hyperoxaluria in stone patients on the basis of a malabsorption of citrate, ascorbate, and possibly other hydroxycarboxylic acids.

Absorption↗
PubMed1985

Stability of ascorbate in urine: relevance to analyses for ascorbate and oxalate.

Ascorbate is unstable in urine at room temperature at pH values ranging from 1 to 12. At pH 7 and above, oxalate is generated in amounts directly proportional to the ascorbate concentration. In 12 different urines, adjusted to pH 12 and incubated for 20 h at room temperature, there was a significant correlation between the amount of oxalate formed and the initial ascorbate concentration (r = 0.97, p less than 0.01). The mean (+/- SD) concentration of oxalate (1.32 +/- 0.70 mmol/L) formed during this period approximated the initial ascorbate concentration (1.57 +/- 1.09 mmol/L). Disodium EDTA, 10 mmol/L final concentration, stabilizes ascorbate in urine and inhibits its conversion to oxalate at pH values of 4.4 to 7.0 during a 24-h period. We therefore propose that urine specimens for ascorbate and oxalate analyses be collected with disodium EDTA present such as to give about this final concentration.

Ascorbic Acid↗