METHODS: Mice were dosed intraperitoneally with mefenamic acid either as a single dose (100 or 200 mg/kg in 10% Dimethyl sulfoxide/Palm oil) or as single daily doses for 14 days (50 or 100 mg/kg in 10% Dimethyl sulfoxide/Palm oil per day). Venous blood samples from mice during the dosing period were taken prior to and 14 days post-dosing from cardiac puncture into heparinized vials. Plasma blood urea nitrogen (BUN) and creatinine activities were measured.
RESULTS: Single dose of mefenamic acid induced mild alteration of kidney histology mainly mild glomerular necrosis and tubular atrophy. Interestingly, chronic doses induced a dose dependent glomerular necrosis, massive degeneration, inflammation and tubular atrophy. Plasma blood urea nitrogen was statistically elevated in mice treated with mefenamic acid for 14 days similar to plasma creatinine.
CONCLUSION: RESULTS from this study suggest that mefenamic acid as with other NSAIDs capable of producing nephrotoxicity. Therefore, the study of the exact mechanism of mefenamic acid induced severe nephrotoxicity can be done in this animal model.
METHODS: Retrospective data on serum calcium and infusion rates was collected from 2011-2015. The relationship between peak calcium efflux (PER) and time was determined using a scatterplot and linear regression. A comparison between regimens was made based on treatment efficacy (hypocalcaemia duration, total infusion amount and time) and calcium excursions (outside target range, peak and trough calcium) using bar charts and an unpaired t-test.
RESULTS: Fifty-one and 34 patients on the original and new regimens respectively were included. Mean PER was lower (2.16 vs 2.56 mmol/h; P = 0.03) and occurred earlier (17.6 vs 23.2 h; P = 0.13) for the new regimen. Both scatterplot and regression showed a large correlation between PER and time (R-square 0.64, SE 1.53, P
METHODS: Articles were found in the Medline database using the key words "paediatrics", "urine screening", "proteinuria", "haematuria" and "population". The Asian countries which had carried out population-based urinary screening of the paediatric population included Taiwan, Japan and Korea. One study was found on urinary screening in a select population in Malaysia. Preliminary results of the urinary screening of school children in Singapore are presented and compared with the results found in the above-mentioned countries.
RESULTS: Overall, the proportion of children found to have urinary abnormalities ranged from less than 0.1% of the population screened to almost 50% of a select cohort referred from the screening programmes for the evaluation of urinary abnormalities. In the pilot Singapore school screening programme, the prevalence of clinically significant proteinuria was 1.25 per 1000 children screened. Multivariate analysis showed that low body weight was associated with a 1.8-fold greater risk for proteinuria. The major cause of haematuria and proteinuria in those studies where renal biopsies were performed was glomerulonephritis. The Taiwanese experience also showed a reduction in the incidence of end-stage renal failure diagnosed in children after the onset of urine screening.
CONCLUSION: These studies showed that urinary screening programmes in school children allow the early detection of disease. The cost-benefit ratio for specific populations should be determined before the implementation of such programmes.