METHODS: This is a retrospective, single-centre study comprising 105 living kidney donor candidates from the year 2007 to 2020. By comparing against 51-Chromium ethylenediamine-tetraacetic acid (51Cr-EDTA), we analysed creatinine clearance for correlation, bias, precision and accuracy.
RESULTS: The study group had a mean age of 45.68 ± 10.97 years with a mean serum creatinine of 64.43 ± 17.68 µmol/L and a urine volume of 2.06 ± 0.83 L. Mean measured GFR from 51Cr-EDTA was 124.37 ± 26.83 ml/min/1.73m2 whereas mean creatinine clearance was 132.35 ± 38.18 ml/min/1.73m2. Creatinine clearance overestimated 51Cr-EDTA significantly with a correlation coefficient of 0.48 (p
MATERIAL AND METHODS: The mice were divided randomly into a control group (aqua bidest and mercury acetate) and an experimental group for this purpose. The experimental mice group was given orally nano Ca supplementation in three dose groups (9 mg, 18 mg, and 27 mg/200 g animal body weight) once a day for 21 consecutive days. The mice are then given mercury acetate (1300 µg/200 g animal body weight intraperitoneally) on the 21st day. One hour after giving the nano Ca supplement, the mice's blood was taken. Liver and kidney were autopsied two days later to check quantitative and qualitative changes caused by mercury concentrations in liver and kidney histopathologies.
RESULTS: The results demonstrated the importance of nano Ca supplementation before mercury acetate induction, which has been shown to reduce necrotic depletion and hepatocyte degeneration.
CONCLUSION: Nano Ca supplementation has decreased the concentration of Hg in the blood of mice so that it can be used as a potential health supplement to detoxify mercury toxins.
METHOD: A multi-centre cross-sectional survey was conducted in person among 409 kidney transplant recipients in six public hospitals in the Klang Valley, Malaysia. Catastrophic health expenditure is considered at 10% out-of-pocket payment from household income used for healthcare expenditure. The association of socioeconomic status with catastrophic health expenditure is determined via multiple logistic regression analysis.
RESULTS: 93 kidney transplant recipients (23.6%) incurred catastrophic health expenditures. Kidney transplant recipients in the Middle 40% (RM 4360 to RM 9619 or USD 1085.39 -USD 2394.57) and Bottom 40% (RM 9619 or > USD 2394.57) income group. Kidney transplant recipients in the Bottom 40% and Middle 40% income groups were more susceptible to catastrophic health expenditure at 2.8 times and 3.1 times compared to higher-income groups, even under the care of the Ministry of Health.
CONCLUSION: Universal health coverage in Malaysia cannot address the burden of out-of-pocket healthcare expenditure on low-income Kidney transplant recipients for long-term post-transplantation care. Policymakers must reexamine the healthcare system to protect vulnerable households from catastrophic health expenditures.
METHODS: An online systematic review of MEDLINE, Embase, PubMed, and the Cochrane Library from inception to January 7, 2022, was completed. Studies outlining the care of a patient with acrometastases of the hand were included. Data extracted included age, sex, site of primary tumor and metastasis, presence of other metastases, time from primary diagnosis to acrometastasis diagnosis, misdiagnosis, treatment, and survival.
RESULTS: Between 1889 and present, 871 lesions were described in 676 patients who met the inclusion criteria. There was no predilection for hand dominance or site of previous trauma. The mean age among patients was 59.5 (1.5-91) years, and male sex was more common (64.6%). The most common primary cancer source was the lung (39.2%), followed by the kidney (10.8%). The distal phalanx was the most frequently cited tumor location (33.7%). Mean survival after diagnosis of acrometastasis was 6.3 months (0.25-50) ± 11.5 months.
CONCLUSION: Acrometastasis remains an uncommon presentation of metastatic disease with poor prognosis. Treatment currently focuses on pain management and optimizing functional outcomes. Our review led to the development of 7 treatment recommendations when managing these patients.
Methods: A total of 63 unilateral nephrectomised male and female Wistar rats were divided into five groups. Group 1 (ShOPR): Rats as sham-operated group were subjected to surgical procedure without RIR. Group 2 (Isch): Rats underwent RIR (left kidney ischemia for 30 min followed by 48 h reperfusion). Group 3 (Zn+Isch): Rats were treated as group 2 but they received Zn sulphate (30 mg/kg) 1 h before induction of RIR. Group 4 (IPC+Isch): Rats were treated as group 2 but they underwent 1 min of ischemia followed by 3 min reperfusion as IPC, which was repeated for three times before induction of RIR. Group 5 (Zn+IPC+Isch): Rats were subjected to receive both Zn sulphate and IPC before induction of RIR. Urine samples were collected in the last 6 h of reperfusion, and finally biochemical and histological measurements were performed.
Results: The serum level of creatinine (Cr), normalised kidney weight (KW) and kidney tissue damage score (KTDS) increased by RIR alone significantly (P < 0.05). These parameters were attenuated statistically by Zn supplementation (P < 0.05). However, IPC alone or co-treatment of Zn and IPC did not improve the biochemical and histological markers altered by RIR injury.
Conclusion: Zn supplementation had a protective role against RIR while such protective effect was not observed by IPC alone or by co-treatment of Zn and IPC.
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.