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Coronavirus disease 2019 (COVID-19) in kidney transplant recipients is a subject of much debate and became of interest to nephrologists amidst the pandemic. The main concerns are the influence of the chronic use of immunosuppressive drugs, the viral-related risk of acute rejection, and the long-term outcome of allograft function. This single-center prospective study included kidney transplant recipients with COVID-19 infection. Patients were maintained on immunosuppressive regimens. The severity of disease was defined as oxygen saturation < 94%, the need for hospitalization and/or hemodialysis, the occurrence of acute kidney injury (AKI), and mortality. Seventeen patients (54.8%) required hospital admission, four patients needed hemodialysis (12.9%), twelve patients (38.7%) had AKI, and three patients died (9.7%). Oxygen saturation < 94% showed a positive correlation with the presence of diabetes (p value 0.031) and a negative correlation with the maintenance steroid dose (p value 0.046). A negative correlation existed between the need for hemodialysis and average Cyclosporin level (p value 0.019) and between the need for hospitalization and average Tacrolimus level (p value 0.046). Severity of disease was associated with the presence of lymphopenia (p value 0.042), the cumulative steroid dose (p value 0.001), increased serum levels of LDH (p value 0.010), Ferritin (p value 0.020), AST (p value 0.047), and ALT (p value 0.006) and D-dimer levels more than 0.5 mg/L (p value 0.038). This study highlighted that the immunocompromised state of renal transplant recipients may not be regarded as a disadvantage in the setting of COVID-19 infection. Studies on a larger scale are needed to validate these results.

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End-stage renal disease is a major health problem with many complications. Previous studies emphasized the relationship of cardiovascular disease and mortality among these patients to dysregulated phosphate homeostasis. Even after successful renal transplantation, the risk is not eliminated. Several factors seem to interplay to regulate serum phosphorus levels after renal transplantation. Fibroblast growth factor-23 (FGF-23) is a hormone with the major function of inhibiting the reabsorption of phosphate by the renal tubules. Parathormone reduces the reabsorption of phosphate from the proximal tubule of the kidney. The aim of our study was to explore the changes that occurred in FGF-23 and intact parathyroid hormone (iPTH) levels in a cohort of Egyptian patients undergoing renal transplantation and to examine the effect of these factors on posttransplant serum phosphorus levels. The study was carried out prospectively on 37 candidates for live-donor renal transplantation. Serum levels of calcium, phosphorus, iPTH, and FGF-23 were measured before and 6 months after renal transplantation. Statistically significant differences were detected in serum calcium, phosphorus, FGF-23, and iPTH before and 6 months after transplantation (P < 0.001, P < 0.001, P < 0.001, and P < 0.001, respectively). The results also showed a statistically significant correlation between FGF-23 levels and phosphorus levels before transplantation. The interplay between FGF-23 and iPTH has an impact on posttransplant serum phosphorus levels.

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OBJECTIVES: Several biological markers have been studied for the differentiation of infection from disease activity in systemic lupus erythematosus (SLE) patients with discrepant results. We aimed to evaluate the role of serum presepsin, hs-CRP, procalcitonin (PCT), and copeptin (CPP) in differentiating bacterial infections from disease activity in SLE patients. METHODS: This study is a cross-sectional observational study in which 94 Egyptian patients were recruited from June 2017 to January 2018. Our patients were divided into two groups: group (1) included 48 patients with active SLE hospitalized with any sort of lupus activity and group (2) included 46 patients with active SLE admitted with a proven bacterial infection. Hs-CRP, presepsin, PCT, and CPP were measured using enzyme-linked immune sorbent assay technique. RESULTS: Hs-CRP, presepsin, PCT, and CPP were highly significantly higher among group (2) patients compared to group (1) patients (p < 0.001). Serum presepsin expressed higher specificity than hs-CRP (87.5% vs 60.4%) but the same sensitivity (80.4%) in the detection of bacterial infection in SLE patients. Serum PCT expressed higher specificity than hs-CRP (100% vs 60.4%) but lower sensitivity (73.9% vs 80.4%). Serum CPP expressed higher specificity than hs-CRP (65.9% vs 60.4%) but lower sensitivity (65.9% vs 80.4%). CONCLUSION: Our study suggests that increased serum levels of hs-CRP, presepsin and PCT levels are useful in differentiating bacterial infections from disease activity in SLE patients. Serum CPP could be used as an adjunct with more specific inflammatory biomarkers in making better diagnostic judgments. KEY POINTS: • The increased serum levels of hs-CRP, presepsin and PCT levels are useful in differentiating bacterial infections from disease activity in SLE patients. • Serum Presepsin expressed higher specificity than hs-CRP but the same sensitivity in the detection of bacterial infection in SLE patients. • Serum CPP expressed higher specificity than hs-CRP but lower sensitivity.

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INTRODUCTION: Medication Regimen complexity is an important issue of patients care that needs to be addressed. The aim of this study is the safe reduction of regimens complexities. The effect of this intervention on glycemic control was assessed in this study. METHODS: Seventy eight patients were recruited to the study. The entry criteria were non optimal glycemic, non-adherence (as demonstrated by indirect tools), and polypharmacy. The only intervention was the safe reduction of medication regimen complexity. This was done in view of the best practice guidelines; to ensure that all comorbidities are treated with the optimum number of medications for the optimum duration. There was no change to hypoglycemic regimen. All patients, whose hypoglycemic regimen has changed after the recruitment, were excluded. The primary outcome measure was the change in HbA1c three months after the intervention. RESULTS: Reducing medications regimen complexities led to a significant improvement of HbA1c in the after phase compared to the before phase (mean HbA1c in the before phase was 7.7 ± 0.43% compared to 6.93 ± 0.4% in the after phase. Mean reduction in the HbA1c was 0.77 ± 0.23%, p values < 0.001). CONCLUSION: Medications regimen complexity constitutes a burden for patients with diabetes. Reducing such regimens might improve glycemic control in those patients. Further studies are needed to confirm this favourable effect on the glycemic control.

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