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Euglycemic diabetic ketoacidosis is a rare, acute, and life-threatening complication of diabetes mellitus associated with several risk factors such as infection, surgery, pregnancy, fasting, alcohol intake, acute vascular events (acute coronary syndrome or stroke), and the use of sodium–glucose cotransporter 2 (SGLT2) inhibitors. It is characterized by euglycemia, high-anion-gap metabolic acidosis, and ketoacidosis. Herein, we report two patients who used SGLT2 inhibitors before surgery and presented with severe metabolic acidosis after surgery. Subsequently, one patient required intubation, and both patients received two cycles of hemodialysis despite normal renal parameters. This was done to correct the metabolic acidosis, which led to early recovery.

Background: Patients with end-stage renal disease need renal replacement therapy, including hemodialysis, peritoneal dialysis, and kidney transplant (KT), to live a relatively normal life. Compared with other dialysis modalities, KT remains the choice for better survival. Objectives: This study aimed to report the KT outcomes at our center and investigate risk factors for graft and patient survival. Methods: This is a retrospective chart review of 72 KT recipients cared for at our center between July 1, 2004, and June 30, 2017. Delayed graft function (DGF) was defined as the need for dialysis within 1 week after KT. The primary outcome is death after KT. The secondary outcome is graft failure, which is defined as a return to dialysis while the patient is alive. Patient death with functional graft was censored during the survival analysis. Results: Among the patients, 17 KT recipients had primary diabetic nephropathy (23.6%) with a mean age of 47.4 ± 11.8 years. Furthermore, 13 patients returned to dialysis and 12 died during the study period, with malignancy being the leading cause of death (n = 4). The 1-, 3-, and 5-year graft survival rates were 94.3%, 90.4%, and 85.4%, respectively. The 1, 3-, and 5-year patient survival rates were 97.1%, 92.1%, and 85.7%, respectively. A total of 24 patients (33%) encountered DGF after KT. Patients with DGF had significantly poorer graft survival than those without DGF (P = 0.002 by log-rank test). Cox-proportional hazard analysis revealed that only DGF increased the risk of graft failure (hazard ratio (HR) = 6.52, 95% confidence interval (CI): 1.4629.2), and age predicted patient survival (HR = 1.09, 95% CI: 1.021.17). Conclusion: This study showed that patients with DGF had significantly poor graft survival. Patient's age was the only prognostic factor for patient survival in our cohort.

Despite the continuous progression in dialysis medicine, mortality and the burden of cardiovascular disease (CVD) among hemodialysis patients are still substantial. Substantial evidence suggests that proinflammatory (CD16+) monocytes contribute to the development of atherosclerosis. A cohort of 136 stable hemodialysis patients (follow-up: 6.25 year) was assessed to investigate the association between the proportion of CD16+ monocytes for all-cause and CVD mortalities. The CD16+ monocytes were associated with both mortalities after adjusting for a preexisting CVD history. Compared to the reference group (CD16+ monocytes within [15.6–18.6], the first and second quartile), patients with CD16+ monocytes above the highest quartile level (>21.5) had an adjusted hazard ratio (HR) of 30.85 (95% confidence interval [CI]: 7.12–133.8) for CVD mortality and 5.28 (2.07–13.49) for all-cause mortality, and those with CD16+ monocytes below the lowest quartile ≤15.6), had significantly elevated death risks after 3.5-year follow-up (HR [95% CI]: 10.9 [2.42–48.96] and 4.38 [1.45–13.24] for CV and all-cause mortalities, respectively). The hemodialysis patients with CD16+ monocyte level in a low but mostly covering normal range also portended a poor prognosis. The findings shed some light for nephrologists on future prospects of early recognizing immune dysfunction and improving early intervention outcomes.

BACKGROUND: Substantial evidence suggests that increased oxidative stress in hemodialysis (HD) patients may contribute to cardiovascular complications. Oxidative modifications of human serum albumin (HSA), the largest thiol pool in plasma, alter its biological properties and may affect its antioxidant potential in HD patients. METHODS: We conducted a long-term follow-up study in a cohort of normoalbuminemic HD patients to examine the impact of redox state of serum albumin on patients' survival by measuring the human nonmercaptoalbumin (HNA) fraction of HSA. RESULTS: After adjusting for potential demographic, anthropometric, and clinical confounders, a positive association of HNA level with the risk of death from cardiovascular disease (CVD) and all-cause mortality was observed in normoalbuminemic HD patients. Using stratified analysis, we found a stronger association between HNA level and the risk of death from CVD and all-cause mortality in patients with pre-existing CVD. CONCLUSIONS: Serum HNA level is a positive predictor of mortality in normoalbuminemic HD patients, especially among those with pre-existing CVD. Increased oxidative stress resulting from biological changes in serum albumin levels could contribute to accelerated atherosclerosis and the development of cardiovascular disease in HD patients.

Aristolochic acid (AA) is a component of Chinese medicinal herbs, including asarum and aristolochia and has been used in Traditional Chinese Medicine for a long time. Recent studies found that AA has a cytotoxic effect resulting in nephropathy. These studies indicated that AA-induced cytotoxicity is associated with increases in oxidative stress and caspase-3 activation. The present study further demonstrated that AA mainly elevates the H2O2 ratio, leading to increases in oxidative stress. Furthermore, the results indicated that AA induces cell death can via caspase-dependent and -independent pathways. It is desirable to identify means of inhibiting AA-induced renal damage; therefore, the present study applied an anti-oxidative nutrient, vitamin C, to test whether it can be employed to reduce AA-induced cell cytotoxicity. The results showed that vitamin C decreased AA-induced H2O2 levels, caspase-3 activity and cytotoxicity in renal tubular cells. In conclusion, the present study was the first to demonstrate that AA-induced increases of the H2O2 ratio resulted in renal tubular cell death via caspase-dependent and -independent pathways, and that vitamin C can decrease AA-induced increases in H2O2 levels and caspase-3 activity to attenuate AA-induced cell cytotoxicity. [ABSTRACT FROM AUTHOR]

Retinoic acid (RA), vitamin D and 12-O-tetradecanoyl phorbol-13-acetate (TPA) can induce HL-60 cells to differentiate into granulocytes, monocytes and macrophages, respectively. Similar to RA and vitamin D, ascorbic acid also belongs to the vitamin family. High-dose ascorbic acid (>100 µM) induces HL-60 cell apoptosis and induces a small fraction of HL-60 cells to express the granulocyte marker, CD66b. In addition, ascorbic acid exerts an anti-oxidative stress function. Oxidative stress is required for HL-60 cell differentiation following treatment with TPA, however, the effect of ascorbic acid on HL-60 cell differentiation in combination with TPA treatment remains to be fully elucidated. The aim of the present study was to investigate the cellular effects of ascorbic acid treatment on TPA-differentiated HL-60 cells. TPA-differentiated HL-60 cells were used for this investigation, this study and the levels of cellular hydrogen peroxide (H2O2), caspase activity and ERK phosphorylation were determined following combined treatment with TPA and ascorbic acid. The results demonstrated that low-dose ascorbic acid (5 µM) reduced the cellular levels of H2O2 and inhibited the differentiation of HL-60 cells into macrophages following treatment with TPA. In addition, the results of the present study further demonstrated that low-dose ascorbic acid inactivates the ERK phosphorylation pathway, which inhibited HL-60 cell differentiation following treatment with TPA. [ABSTRACT FROM AUTHOR]

Human glioblastoma multiforme is one of the most aggressive malignant brain tumor types, and the mean survival time of patients with a brain tumor is <2 years when traditional therapies are administered. Thus, numerous studies have focused on the development of novel treatments for brain tumors. Frog ribonucleases, such as Onconase and Rana catesbeiana ribonuclease (RC-RNase), exert antitumor effects on various tumor cells, including cervical cancer, breast cancer, hepatoma, leukemia, pancreatic cancer and prostate cancer cells. In addition, frog Onconase has been applied as a treatment in clinical trials. However, the antitumor effects of frog ribonucleases on brain tumors are unclear. Previous studies have indicated that RC-RNase demonstrates a decreased cytotoxic effect in normal cells compared with Onconase. Therefore, the present study investigated the ability of RC-RNase to exert antitumor activities on human glioblastoma. It was found that RC-RNase inhibits the growth of the human glioblastoma DBTRG, GBM8901 and GBM8401 cells. In addition, the present study revealed that RC-RNase induces caspase-9/-3 activity and triggers the apoptotic cell death pathway in human glioblastoma cells. Notably, it was also demonstrated that RC-RNase effectively inhibits the growth of human glioblastoma tumors in a nude mouse model. Overall, the present study indicates that RC-RNase may be a potential agent for the treatment of human glioblastoma. [ABSTRACT FROM AUTHOR]

Aim: The CD40–CD40L system has been implicated in the pathogenesis of atherothrombotic complications in cardiovascular disease. The aim of this study was to determine the relationship between plasma soluble CD40 ligand (sCD40L) and symptomatic coronary heart disease (CHD) in end-stage renal disease (ESRD) patients on maintenance haemodialysis (HD). Methods: This cross-sectional study included 57 HD patients, 31 of whom had symptomatic CHD. Lipid profile, markers of endothelial activation such as sCD40L, and both inflammatory and oxidative stress markers were measured and analyzed. Results: The sCD40L concentration was significantly higher in HD patients than in controls (1.34 ± 0.53 vs 0.86 ± 0.12 ng/mL, P < 0.01). Plasma concentration of sCD40L ( P < 0.01), soluble vascular adhesion molecule-1 (sVCAM-1; P < 0.01) and high-sensitivity CRP (hsCRP; P < 0.01) were higher in HD patients with symptomatic CHD than in those without CHD. In addition, we also found that oxidative stress biomarkers such as nitrotyrosine (NT), malonaldehyde (MDA) and protein carbonyl (PC) were significantly elevated in patients with symptomatic CHD compared to those without. There was a strong overall positive relationship between sCD40L concentration and sVCAM-1 ( r = 0.54, P < 0.001), MDA ( r = 0.365, P < 0.01), NT ( r = 0.293, r < 0.05) and log-transformed triglycerides ( r = 0.275, P < 0.05). Conclusion: Circulating concentrations of sCD40L were elevated in HD patients with symptomatic CHD. This study suggests that CD40–CD40L may play a potentially important role in the atherosclerotic complications of HD patients. [ABSTRACT FROM AUTHOR]

Background: Peripheral arterial disease (PAD) is a leading cause of morbidity in haemodialysis (HD) patients. Recent evidence suggests that adiponectin, an adipose-derived cytokine, may play a role in atherosclerosis. However, the association between plasma levels of the adiponectin and the ankle-brachial index (ABI), an indicator of the presence and severity of PAD, has not been thoroughly studied in HD patients. Methods: The present cross-sectional study attempted to examine the relationship between plasma adiponectin and PAD in a cohort of 136 chronic HD patients. The ABI was used as an estimate of the presence of PAD. Plasma adiponectin, high-sensitivity C-reactive protein ( hsCRP), tumour necrosis factor-α and lipid profiles were measured. Logistic regression was used to estimate the association between presence of PAD and adiponectin as well as other potential risk factors. Results: Plasma levels of adiponectin were significantly lower among patients with evidence of PAD than among those without (8.51 ± 5.75 vs 17.15 ± 11.53; P < 0.001). Univariate analysis showed a positive correlation between ABI values and plasma adiponectin levels ( r = 0.369, P < 0.001), high-density lipoprotein cholesterol levels, diastolic blood pressure, Kt/V and serum phosphate. On the other hand, negative correlations between ABI and log-transformed triglyceride, hsCRP, fasting blood sugar, girth circumference and white blood cell counts were noted. Using logistic regression, plasma adiponectin was found to be associated with PAD independently of classical risk factors for atherosclerosis. In addition, models that incorporated plasma adiponectin were significantly better at predicting PAD than models limited to classical confounding factors. Conclusion: We conclude that there was a significant inverse correlation between plasma adiponectin levels and the presence of PAD in dialysis patients. This suggests that plasma adiponectin level may have a role in the atherosclerotic process of PAD. [ABSTRACT FROM AUTHOR]

AbstractBackground:Recent evidence suggests that oxidative stress may be an instigator of the metabolic syndrome, and adiponectin, an adipocyte-derived polypeptide, may modulate oxidative stress, ameliorating the atherosclerotic process. Aim:Oxidative stress is increased in hemodialysis (HD) patients. We hypothesize that a relationship between plasma levels of adiponectin and markers of inflammation and oxidative stress exists. Methods and Results:In 124 HD patients, plasma adiponectin levels and three separate oxidative stress markers, tumor necrosis factor-? as well as high-sensitivity C-reactive protein (hsCRP) were determined. Plasma adiponectin was significantly and negatively correlated with serum hsCRP (r = –0.247, p = 0.008) and plasma malondialdehyde (MDA) levels (r = –0.326; p < 0.001). Multiple regression analyses suggested that plasma MDA, serum HDL cholesterol levels and logarithmically transformedhsCRP were the variables independently associated with plasma adiponectin levels. Conclusion:Plasma adiponectin was significantly associated with plasma MDA, serum HDL cholesterol levels and serum hsCRP levels. Our results suggest the possibility that plasma adiponectin may play a role in alleviating oxidative stress in HD patients.Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]