Effect of sodium-glucose transporter 2 inhibitor empagliflozin on proteinuria and kidney function progression in patients with non-diabetic glomerulonephritis: a pilot superiority randomized controlled trial.

BACKGROUND: Amelioration of proteinuria is one of main treatment targets in patients with glomerulonephritis, yet the remission rates are suboptimal. AIM OF THE STUDY: To examine the effect of the sodium-glucose transporter 2 inhibitor (empagliflozin) on proteinuria and kidney function progression, in patients with glomerulonephritis not due to diabetic kidney diseases. SUBJECTS AND METHODS: Fifty patients were recruited. The entry criteria were diagnosis of glomerulonephritis, and proteinuria (proteinuria ≥ 500 mg/g) in spite of the use of the maximal tolerated dose of RAAS blocking agents together with specific immunosuppression treatment regimens. Group 1 (Empagliflozin arm): 25 patients who received 25 mg of empagliflozin once daily for 3 months as add-on to their regular treatment protocol (RAAS blockers and immunosuppression). Group 2 (Placebo arm): 25 patients treated with RAAS blockers and immunosuppression. The primary efficacy endpoints were the change in creatinine eGFR, and proteinuria 3 months after starting treatment. RESULTS: Progression of proteinuria was lower with empagliflozin as compared to placebo (odds ratio, 0.65; 95% CI, 0.55 to 0.72, p = 0.002). Decline in eGFR was lower with empagliflozin as compared to placebo; however, this was statistically not significant (odds ratio, 0.84; 95% CI, 0.82 to 1.2, p = .31). The percentage change in proteinuria was greater with empagliflozin as compared to placebo (median, - 77 (- 97-105) vs - 48 (- 80-117). CONCLUSION: Empagliflozin has a favorable effect on amelioration of proteinuria in patients with glomerulonephritis. Empagliflozin has tendency to preserve kidney function in patients with glomerulonephritis as compared to placebo; however, longer term studies are required.

Genetic Variations among Different Variants of G1-like Avian Influenza H9N2 Viruses and Their Pathogenicity in Chickens.

Since it was first discovered, the low pathogenic avian influenza (LPAI) H9N2 subtype has established linages infecting the poultry population globally and has become one of the most prevalent influenza subtypes in domestic poultry. Several different variants and genotypes of LPAI H9N2 viruses have been reported in Egypt, but little is known about their pathogenicity and how they have evolved. In this study, four different Egyptian LPAI H9N2 viruses were genetically and antigenically characterized and compared to representative H9N2 viruses from G1 lineage. Furthermore, the pathogenicity of three genetically distinct Egyptian LPAI H9N2 viruses was assessed by experimental infection in chickens. Whole-genome sequencing revealed that the H9N2 virus of the Egy-2 G1-B lineage (pigeon-like) has become the dominant circulating H9N2 genotype in Egypt since 2016. Considerable variation in virus shedding at day 7 post-infections was detected in infected chickens, but no significant difference in pathogenicity was found between the infected groups. The rapid spread and emergence of new genotypes of the influenza viruses pinpoint the importance of continuous surveillance for the detection of novel reassortant viruses, as well as monitoring the viral evolution.

Vitamin D Deficiency in Egyptian Systemic Lupus Erythematosus Patients: How Prevalent and Does It Impact Disease Activity?

BACKGROUND: The emerging role of vitamin D in immunology and autoimmune disorders has been a worldwide interest in the last decade. Systemic lupus erythematosus (SLE) patients are particularly at a delicate position predisposing them to suffer from vitamin D deficiency due to the multiple risk factors accompanying the disease. Whether vitamin D deficiency is also involved as a risk factor for developing SLE and affecting its course is a considerable concern. OBJECTIVES: The objective of this study was to estimate the prevalence of vitamin D deficiency in SLE patients and its relation to disease. MATERIALS AND METHODS: In our observational cross-sectional study, serum levels of vitamin D [25(OH)D] in 60 SLE patients and 30 age- and sex-matched healthy controls were assessed and estimated for deficiency and insufficiency at 10 and 30 ng/mL, respectively. Disease activity was evaluated by SLE disease activity index (SLEDAI), irreversible organ damage by Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SLICC/ACR DI), and severity by Severity of Disease Index. Fatigue was measured by visual analog scale. RESULTS: Significantly lower levels of 25(OH)D were found in SLE patients (17.6 ± 6.9 ng/mL) in comparison to controls (79.0 ± 28.7 ng/mL), with a statistically high significant difference (t = -11.2, P < 0.001). High prevalence of vitamin D insufficiency and deficiency was detected as 73.3% and 23.3%, respectively. Vitamin D had a highly significant negative correlation with SLEDAI (r = -0.495, P < 0.001), SLICC (r = -0.431, P < 0.05), and fatigue (r = -0.436, P < 0.05). CONCLUSION: Vitamin D deficiency and insufficiency were found to be prevalent in SLE patients in our study and related to disease activity and fatigue. If needed, routine screening and consequent repletion of vitamin D are recommended in SLE patients. Restoring adequate vitamin D levels in SLE patients should be more explored as a potential yet simple measure to their usual management to improve their condition.