OBJECTIVES: To investigate the correlations and agreements between the solute/creatinine ratios from the 24-hour and early morning spot urine samples for metabolic evaluation in stone-formers given the various pitfalls with the 24-hour urinary metabolic evaluation in stone-formers.
METHODS: 30 urinary stone-formers out of an initial 62 recruited provided a complete 24-hour urine and early morning spot urine samples for metabolic evaluation. Pearson correlation and Bland and Altman Test were used to assess the correlations and agreements.
RESULTS: Significant correlations were established between the 24-hour urinary solute excretions and the corresponding early morning spot urine solute/creatinine ratios for calcium, magnesium, urate, potassium, oxalate, citrate, and the Differential Gibb's free energy value of calcium oxalate DG(CaOx) values. However, all these solute/creatinine measurements between the 24-hour and early morning spot urine samples were judged to be not within the acceptable limits based on the estimated "limit of agreement" by the Bland and Altman Test of Agreement. Diurnal circadian rhythm and postprandial excretion surge are thought to be responsible for the disagreements.
CONCLUSIONS: Thus, the early morning spot urine is not suitable to be used interchangeably to replace the 24-hour urine collection in the evaluation of urinary metabolic abnormalities in stone-formers. A good correlation does not translate to an agreement between the 2 measurements.
Vitamin E deficiency has been found to impair bone calcification. This study was done to determine the effects of vitamin E deficiency and supplementation on parathyroid hormone, i.e. the hormone involved in bone regulation. Female Sprague-Dawley rats were divided into 4 groups: 1) normal rat chow (RC), 2) vitamin E deficiency (VED), vitamin E deficient rats supplemented with 3) 60 mg/kg alpha-tocotrienol (ATT) and 4) 60 mg/kg (alpha-tocopherol (ATF). Treatment was carried out for 3 months. Vitamin E deficiency caused hypocalcaemia during the first month of the treatment period, increased the parathyroid hormone level in the second month and decreased the bone calcium content in the 4th lumbar bone at the end of the treatment. Vitamin E supplementation (ATT and ATF) failed to improve these conditions. The bone formation marker, osteocalcin, and the bone resorption marker, deoxypyridinoline did not change throughout the study period. In conclusion vitamin E deficiency impaired bone calcium homeostasis with subsequent secondary hyperparathyroidism and vertebral bone loss. Replacing the vitamin E with pure ATF or pure ATT alone failed to correct the changes seen.