Background: Renal dysfunction is one of the major causes of in-hospital mortality in STEMI patients. In this study, we evaluated the combined predictive value of eGFR by CKD-EPI equation and shock index for in-hospital mortality and other adverse clinical outcomes in Egyptian patients with STEMI. Results: A total of 450 STEMI patients were divided into 2 groups according to their eGFR with a cutoff value of 60 ml/min/1.73 m 2 and compared as regards mortality, major bleeding, reinfarction, development of heart failure, stroke, and atrial fibrillation during the period of admission. Univariate analysis was performed to define significant factors that affected mortality; then, significant factors were subjected to a multivariate logistic regression. Patients with eGFR < 60 ml/min/1.73 m 2 had higher rates of mortality (P < 0.0005) and atrial fibrillation (P = .006) during the hospital admission. A multivariate logistic regression model showed the predictors of mortality were factors SI (OR = 28.56, 95% CI 8-101.97, P < 0.0001), cardiac troponin (OR = 2.89, 95% CI 1.08-7.77, P = 0.03), age (OR = 1.07, 95% CI 1.02-1.2, P = 0.002), and eGFR (OR = 0.98, 95% CI 0.96-0.99, P = 0.04). Conclusions: Estimated GFR < 60 ml/min/1.73 m 2 in STEMI patients is associated with higher rate of mortality. Estimated GFR, age, shock index, and cardiac troponin were the most significant predictors of mortality in STEMI patients
Background Disordered Treg counts and function have been observed in patients with SARS-Cov-2 and are thought to contribute to disease severity. In hemodialysis patients, scarce data are available on the Treg response to SARS-CoV-2 or its relation to the clinical presentation. Methods A cross-sectional study included one hundred patients divided into three groups, thirty SARS-CoV-2-infected hemodialysis patients (COV-HD), and thirty confirmed SARSCoV-2 infected patients (COV), and forty non-infected hemodialysis patients (HD). Flow cytometric analysis of CD4, CD25, FoxP3, and CD39+ Tregs was done for all patients and tested for correlation to in-hospital mortality, clinical, radiological severity indices. Results COV-HD and COV patients had significantly lower Treg cell count than HD patients (Median value of 0.016 cell/ μl vs 0.28 cell/ μl, respectively- P: 0.001). COV-HD patients had higher CD39+ Tregs (median value of 0.006 cell/ μl vs 0.002 cell/ μl, respectively- P: 0.04). COV-HD patients had significantly lower hospital stay (median value of 3 vs 13 days, P:0.001), ICU admission rates (26.5% vs 46.7%, P:0.005) and in-hospital mortality (20.7% versus 43.3%, P:0.003) than COV patients. Treg and CD39 expressing Treg counts were not correlated to severity indices in both groups. A high neutrophil to lymphocyte ratio is strongly correlated to disease severity in COV-HD patients. Conclusions This study provides evidence of T-cell, particularly T-regulatory cell decline in SARS-CoV-2 and suggests that hemodialysis per se does not distinctively impact the T-cell response. COV-HD patients exhibited a higher CD39+ Treg count and a better clinical profile, however, larger studies are needed to extrapolate on these findings.
Introduction: With the evolution of SARS-CoV-2 pandemic, it was believed to be a direct respiratory virus. But, its deleterious effects were observed on different body systems, including kidneys. Aim of Work: In this review, we tried as much as we can to summarize what has been discussed in the literature about the relation between SARS-CoV-2 infection and kidneys since December, 2019.Methods: Each part of the review was assigned to one or two authors to search for relevant articles in three databases (Pubmed, Scopus, and Google scholar) and collected data were summarized and revised by two independent researchers. Conclusion:The complexity of COVID-19 pandemic and kidney could be attributed to the direct effect of SARS-CoV-2 infection on the kidneys, different clinical presentation, difficulties confronting dialysis patients, restrictions of the organ transplant programs, poor outcomes and bad prognosis in patients with known history of kidney diseases who got infected with SARS-CoV-2.
Background and Aims Impaired autophagy in the kidney resulted in podocyte loss and massive proteinuria in diabetic nephropathy. Improvement of autophagy by activation of mTORC1 and reduction of AMPK and Sirt1 may be a novel therapeutic option for the suppression of diabetic nephropathy. Method This experimental work was carried out on 48 adult male Sprague dawely rats. The total duration of the study was 10 weeks. All investigation and intervention were carried out at 3 time points, 3 weeks, 6 weeks, 10 weeks. The rats were randomly divided into healthy control group (n = 12) and 3 induced diabetic groups (n = 12 each), the three groups were the non-treated, treated with rapamycin and treated with rapamycin and metformin. To study autophagy, we use electron microscopy and immunohistochemical staining of kidney tissue with LC3 antibody Results Diabetic rats treated with rapamycin alone or rapamycin and metformin showed lower level of proteinuria and almost normal serum creatinine through all intervals of the study. Also, their Kidney tissue showed increased autophagosomes and high expression of LC3 compared to diabetic rats. There are no significant differences between both treated groups in terms of induction of autophagy during the experiment period. Conclusion we concluded that using a small dose of rapamycin for short duration in early diabetic rats is beneficial in halting the course of diabetic nephropathy, adding metformin to rapamycin aiming to potentiate its effect on autophagy seems to be less beneficial.
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