The human amniotic membrane is a highly abundant and readily available tissue that may be useful for regenerative medicine and cell therapy. The amniotic membrane stem cells can differentiate into multiple cell lineages; they have low immunogenicity and anti-inflammatory functions. This research aims to examine the protocols for the isolation of human amniotic membrane stem cells, including their phenotypic characterization and in vitro potential for differentiation toward keratinocytes. Human placentas were obtained from selected cesarean-sectioned births. We isolated amniotic stem cells by trypsin and collagenase B digestion and centrifuged with Percoll. After monolayer expansion of adherent cells, the cells were characterized by immunocytology with octamer-binding transcription factor 4 and differentiated into keratinocytes by treating the cells with insulin, hydrocortisone, BMP-4, and vitamin C. Protocol for isolation of stem cells from amniotic membrane has high efficiency. Differentiation markers of stem cells into keratinocytes, such as vimentin, cytokeratin (CK) 14, and CK19, were determined by reverse transcription-polymerase chain reaction increase over time in culture. Stem cells isolated from the amniotic membrane can differentiate into keratinocytes. It has opened the prospect of using stem cells to regenerate skin and clinical applications.

Background: Kidney recipients often use a calcineurin inhibitor and a proliferation inhibitor after transplantation. The therapeutic drug monitoring for calcineurin inhibitor is more simple and feasible in clinical than proliferation inhibitor. In Vietnam, mycophenolic acid is a popular proliferation inhibitor used for transplantation patients. Although therapeutic mycophenolic acid monitoring is so important in treating kidney transplantation, the monitoring is still difficult to execute in Vietnam. Objectives: This study aimed to determine the MPA concentration on Vietnamese renal transplant recipients. Methods: This observational study was conducted on 35 adult kidney recipients to evaluate the MPA concentration at five sampling time points (predose, 1, 2, 3, and 6 hours) on day 3, day 10, and month 6 after transplantation. Results: Plasma MPA trough levels (C0) were 2.32 ± 1.47;1.58 ± 1.39; 2.29 ± 1.4 mg/L and the MPA-AUC0-12 h values were 50.1 ± 20.4; 41.9 ± 14.5; 60.3 ± 25.9 mg.h/L on day 3, day 10, and month 6. The number of patients who reached MPA-AUC0-12 h values of 30 - 60 mg.h/L was 18 (51.4%), 23 (65.7%) and 17 (51.5%) on day 3, day 10, and month 6, respectively. The number of patients who achieved the MPA C0 values of 1.5 - 2.5 mg/L was 15 (42.9 %), 14 (40%), and 10 (30.3%) on day 3, day 10, and month 6, respectively; and the linear correlation coefficients between AUC0-12 h and C0 were 0.652, 0.415, and 0.752, respectively. Conclusions: In renal transplant patients, the MPA-AUC0-12 h was lower on day 3 and day 10 post-transplantation than month 6 for the half dose of MMF or MPS. Therefore, MPA therapeutic drug level should be monitored usually in transplantation patients who use MPA.

Background: The transforming growth factor-beta 1 (TGF-β1) has been demonstrated as one of the main factors in the progression of fibrosis and sclerosis glomerular damages. Glomerulonephritis is one common cause of chronic kidney disease (CKD) with the promotion of inflammatory renal damage containing fibrosis and sclerosis glomerular. Objectives: This study aimed to evaluate the TGF-β1 level in CKD patients and compare it with the healthy control group. Methods: This cross-sectional case-control study was carried out on 212 subjects admitted to the Nghe An Friendship General Hospital in Vietnam from March 2018 to February 2020. The case group included 152 patients diagnosed with CKD caused by glomerulonephritis, and the control group included 60 healthy individuals. The TGF-β1 was determined in serum by ELISA method. Results: The serum TGF-β1 concentration of the healthy control group and CKD group was 13.45 ± 7.17 and 32.35 ± 11.74, respectively. The CKD group had a significantly higher TGF-β1 level than the control group (P < 0.05). The CKD group with the eGRP ≥ 60 mL/min/1.73 m2 group had a higher TGF-β1 level than the eGRP < 60 mL/min/1.73 m2 group, and the TGF-β1 level increased from stage 1 to stage 5 (P < 0.001). The TGF-β1 had a medium correlation to urea, creatinine, and hs-CRP. Conclusions: The concentration of TGF-β1 in the CKD group was higher than the control group so that it increased early from the first stage of the disease.

Background: Chronic kidney disease (CKD) is an increasingly common disease worldwide and has become a global health problem, especially in Vietnam. Cystatin C is a marker for the detection, classification, and prognosis of CKD. Cystatin C is filtered entirely through the glomerular membrane, reabsorbed, and metabolized completely in the renal tubules. In case of damage to the kidneys, glomerular filtration rate declines, and some substances increase in the blood, such as cystatin C. The concentration of cystatin C changes with damage to the renal system. Objectives: This study aimed to estimate the concentration of cystatin C and its variation in the different stages of CKD. Methods: A descriptive, cross-sectional study was conducted on 40 healthy individuals and 137 patients with CKD grade III, IV, and V in 103 Hospital. The concentration of cystatin C was estimated in all subjects. Results: Cystatin C plasma levels were significantly higher in the CKD group (9.17 ± 3.75 mg/L) than in the control group (0.82 ± 0.12 mg/L). Cystatin C plasma levels increased linearly with the serious kidney failure as the stage of CKD. Conclusions: Cystatin C is an effective marker for estimating kidney damage in CKD.