This summary outlines the key findings of the EMPA-KIDNEY trial which evaluated the effect of empagliflozin treatment on kidney disease progression and cardiovascular outcomes in patients with chronic kidney disease (CKD). The randomized, double-blind trial involved over 6,600 patients with CKD across 8 countries. Patients received either empagliflozin 10mg or placebo daily. The primary outcome of kidney disease progression or cardiovascular death occurred in 13.1% of the empagliflozin group versus 16.9% of the placebo group, representing a 28% lower risk with empagliflozin. Secondary outcomes also favored empagliflozin treatment, including lower rates of hospitalization. The benefits were
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Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
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Cardiorenal Syndrome (Clinical Implications and Treatment Strategies) - Dr. G...NephroTube - Dr.Gawad
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Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
Diabetes Mellitus Management in CKD (Clinical Tips) - Dr. GawadNephroTube - Dr.Gawad
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Diabetes mellitus is a worldwide epidemic. Its prevalence is on a steep rise and is more pronounced in India making it the ‘diabetes capital of the world’. There is also a parallel increase in the prevalence of diabetic nephropathy and is now the single most common cause of end-stage kidney disease leading to significant morbidity and mortality as well as accounts for a tremendous burden on the health care costs. It is also shown that the presence of diabetes increases the risk and progression of non-diabetic kidney disease.
Comparative Study of Hscrp in Chronic Kidney Diseaseiosrphr_editor
Chronic kidney disease (CKD) is a global threat to health mainly in developing countries because therapy is expensive and lifelong. over 1 million people worldwide are on dialysis or with a functioning graft. Early detection of Chronic kidney disease (CKD) and its consequent complications can prevent its grave complications . It causes not only significant morbidity but also it causes high mortality. Because of increase in incidence of Diabetes mellitus, hypertension, obesity and an aging population there is increase in progression of chronic kidney disease to end stage renal disease (ESRD). . Cardiovascular disease (CVD) is the major cause of mortality in haemodialysis patients and so it has become imperative to have a screening programme at all levels to detect CKD at an early stage and to initiate specific therapy to reduce the progression of renal disease and also the burden of ESRD (1). High sensitive C-Reactive protein (Hs CRP) assay is useful for sensitive detection of inflammatory state (2,3). This study aims at estimating Hs CRP as a marker of inflammation in CKD patients...
(May 29th, 2024) Advancements in Intravital Microscopy- Insights for Preclini...Scintica Instrumentation
Intravital microscopy (IVM) is a powerful tool utilized to study cellular behavior over time and space in vivo. Much of our understanding of cell biology has been accomplished using various in vitro and ex vivo methods; however, these studies do not necessarily reflect the natural dynamics of biological processes. Unlike traditional cell culture or fixed tissue imaging, IVM allows for the ultra-fast high-resolution imaging of cellular processes over time and space and were studied in its natural environment. Real-time visualization of biological processes in the context of an intact organism helps maintain physiological relevance and provide insights into the progression of disease, response to treatments or developmental processes.
In this webinar we give an overview of advanced applications of the IVM system in preclinical research. IVIM technology is a provider of all-in-one intravital microscopy systems and solutions optimized for in vivo imaging of live animal models at sub-micron resolution. The system’s unique features and user-friendly software enables researchers to probe fast dynamic biological processes such as immune cell tracking, cell-cell interaction as well as vascularization and tumor metastasis with exceptional detail. This webinar will also give an overview of IVM being utilized in drug development, offering a view into the intricate interaction between drugs/nanoparticles and tissues in vivo and allows for the evaluation of therapeutic intervention in a variety of tissues and organs. This interdisciplinary collaboration continues to drive the advancements of novel therapeutic strategies.
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
Deep Behavioral Phenotyping in Systems Neuroscience for Functional Atlasing a...Ana Luísa Pinho
Functional Magnetic Resonance Imaging (fMRI) provides means to characterize brain activations in response to behavior. However, cognitive neuroscience has been limited to group-level effects referring to the performance of specific tasks. To obtain the functional profile of elementary cognitive mechanisms, the combination of brain responses to many tasks is required. Yet, to date, both structural atlases and parcellation-based activations do not fully account for cognitive function and still present several limitations. Further, they do not adapt overall to individual characteristics. In this talk, I will give an account of deep-behavioral phenotyping strategies, namely data-driven methods in large task-fMRI datasets, to optimize functional brain-data collection and improve inference of effects-of-interest related to mental processes. Key to this approach is the employment of fast multi-functional paradigms rich on features that can be well parametrized and, consequently, facilitate the creation of psycho-physiological constructs to be modelled with imaging data. Particular emphasis will be given to music stimuli when studying high-order cognitive mechanisms, due to their ecological nature and quality to enable complex behavior compounded by discrete entities. I will also discuss how deep-behavioral phenotyping and individualized models applied to neuroimaging data can better account for the subject-specific organization of domain-general cognitive systems in the human brain. Finally, the accumulation of functional brain signatures brings the possibility to clarify relationships among tasks and create a univocal link between brain systems and mental functions through: (1) the development of ontologies proposing an organization of cognitive processes; and (2) brain-network taxonomies describing functional specialization. To this end, tools to improve commensurability in cognitive science are necessary, such as public repositories, ontology-based platforms and automated meta-analysis tools. I will thus discuss some brain-atlasing resources currently under development, and their applicability in cognitive as well as clinical neuroscience.
This pdf is about the Schizophrenia.
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Comparing Evolved Extractive Text Summary Scores of Bidirectional Encoder Rep...University of Maribor
Slides from:
11th International Conference on Electrical, Electronics and Computer Engineering (IcETRAN), Niš, 3-6 June 2024
Track: Artificial Intelligence
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Multi-source connectivity as the driver of solar wind variability in the heli...Sérgio Sacani
The ambient solar wind that flls the heliosphere originates from multiple
sources in the solar corona and is highly structured. It is often described
as high-speed, relatively homogeneous, plasma streams from coronal
holes and slow-speed, highly variable, streams whose source regions are
under debate. A key goal of ESA/NASA’s Solar Orbiter mission is to identify
solar wind sources and understand what drives the complexity seen in the
heliosphere. By combining magnetic feld modelling and spectroscopic
techniques with high-resolution observations and measurements, we show
that the solar wind variability detected in situ by Solar Orbiter in March
2022 is driven by spatio-temporal changes in the magnetic connectivity to
multiple sources in the solar atmosphere. The magnetic feld footpoints
connected to the spacecraft moved from the boundaries of a coronal hole
to one active region (12961) and then across to another region (12957). This
is refected in the in situ measurements, which show the transition from fast
to highly Alfvénic then to slow solar wind that is disrupted by the arrival of
a coronal mass ejection. Our results describe solar wind variability at 0.5 au
but are applicable to near-Earth observatories.
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Richard's entangled aventures in wonderlandRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
5. EMPAGLIFLOZIN
1. SGLT 2 inhibitor.
2. Inhibits Sodium Glucose Co Transporter 2
in Proximal convoluted tubules.
3. Decrease renal reabsorption of Glucose.
4. Cause glycosuria.
5. It inhibits NHE3 activity and improves
renal salt and water handling.
6.
7. Chronic kidney disease (CKD) is often
progressive, with a decreased glomerular
filtration rate (GFR) and the presence of
albuminuria representing key risk factors for
the subsequent development of kidney failure.
Slowing CKD progression and avoiding
dialysis or kidney transplantation is highly
desirable.
8. Large, placebo-controlled trials involving
patients with diabetic kidney disease with
increased albuminuria have shown that renin–
angiotensin system (RAS) inhibitors, sodium–
glucose co-transporter 2 (SGLT2) inhibitors,
and the nonsteroidal mineralocorticoid
receptor antagonist finerenone all reduced the
risk of progression to kidney failure.
9. The EMPA-KIDNEY trial was designed to
assess the effect of once-daily empagliflozin
treatment on the progression of kidney
disease and cardiovascular disease and to
examine the safety profile of the drug in a
wide range of patients with CKD.
10. METHODS
TRIAL DESIGN
The EMPA KIDNEY trial (study of heart
kidney protection with empagliflozin) was an
international, randomized, parallel-group
double –blind, placebo-controlled, clinical trial
of Empagliflozin.
11. TRIAL PARTICIPANTS
This trial was conducted at 241 centers in eight
countries after approval by Regulatory
authorities, as well as ethics committee. The trial
was designed and led by a steering committee
that included representatives from the central
coordinating office at the University of Oxford.
12. INCLUSION CRITERIA
1. Eligible patients were adults with a race-
adjusted eGFR of at least 20 but less than 45 ml
per minute per 1.73 m2 , regardless of the level
of albuminuria, or with an eGFR of at least 45
but less than 90 ml per minute per 1.73 m2 with
a urinary albumin-to-creatinine ratio of at least
200 at the screening visit.
15. TRIAL PROCEDURE
All eligible patients entered a pre-
randomization run-in phase and were provided
with a 15-week supply of once-daily placebo
tablets. During this time, local investigators
reviewed screening data, assessed current RAS
inhibitor use, and approved potential patients
for later randomization.
16. Patients were randomly assigned to receive
empagliflozin (10 mg once daily) or
matching placebo.
17. At each follow-up visit, patients provided
information on their kidney status (i.e., any
dialysis treatment or receipt of a kidney
transplant), adherence to the assigned trial
regimen (including reasons for stopping)
and any serious adverse effect.
19. STATISTICAL ANALYSIS
All the analyses were performed according
to the intention-to-treat principle and
included data from all patients who had
undergone randomization, including data
collected from the time of the formal
interim analysis to the final follow-up visit.
20. RESULTS
•Recruitment and follow up
From February 2019 through 2021, a
total of 8544 potential participants
attended a screening visit.
21. 6609 underwent randomization. At the time
of randomization, the mean age of the
patients was 63.8 years, 33.2% of the patients
were women, and 54% did not have diabetes.
8184 patients (95.8%) entered the pre-
randomization run-in phase.
22. The mean (±SD) eGFR was 37.3±14.5 ml
per minute per 1.73 m2 , and 34.5% of the
patients had an eGFR of less than 30 ml per
minute per 1.73 m2.
The median urinary ACR was 329, and
48.3% of the patients had ACR of 300 or
less.
23.
24.
25.
26. PRIMARY OUTCOMES
Progression of kidney disease or death
from cardiovascular causes occurred in
13.1% in Empagliflozin group and
16.9% in placebo group (hazard ratio
0.72; 95% CI, 0.64 to 0.83, p<0.001).
27. SECONDARY OUTCOMES
1. The rate of first and subsequent
hospitalizations from any cause was lower in
the empagliflozin group than in the placebo
group (24.8 vs. 29.2 hospitalizations per 100
patient-years; hazard ratio, 0.86; 95% CI, 0.78
to 0.95; P=0.003)
28. 2. No significant effect was observed with
respect to hospitalization for heart failure or
death from cardiovascular causes (composite
outcome).
3. The hazard ratio for the comparison of
empagliflozin with placebo with respect to
progression of kidney disease was 0.71 (95%
CI, 0.62 to 0.81)
29. 4. The hazard ratio for death from
cardiovascular causes was 0.84 (95% CI, 0.60
to 1.19).
5. The hazard ratio for the composite
outcome of ESKD or death from
cardiovascular causes was 0.73 (95% CI, 0.59
to 0.89).
30. TERTIARY AND EXPLORATORY
OUTCOMES
1. The benefits of empagliflozin treatment
were consistent among patients with or
without diabetes and regardless of the eGFR
at randomization. There was some evidence
that the proportional risk reduction may have
been larger among patients with higher
urinary albumin-to-creatinine ratios.
31. 2. The rate of annual decrease in the eGFR in
the placebo group was constant. In the
empagliflozin group, there was an acute
decrease in the eGFR when the trial regimen
was started; the rate of annual decline slowed
after this initial decrease.
32. 3. Overall, the between-group
difference in the eGFR slope from
randomization to the final follow-up
visit was 0.75 ml per minute per 1.73
m2 (95% CI, 0.54 to 0.96) per year,
favoring empagliflozin.
33. 4. With respect to the decline in eGFR there
was a between-group difference of 1.37 ml per
minute per 1.73 m2 (95% CI, 1.16 to 1.59) per
year.
5.No significant effects of empagliflozin were
observed with respect to any specific cause of
death, major cardiovascular events (hazard
ratio, 0.93; 95% CI, 0.76 to 1.12.
34. Safety Outcomes and Adverse Events
1. Ketoacidosis occurred in 6 patients in the
empagliflozin group and in 1 patient in the
placebo group.
2. Lower-limb amputations occurred in 28
patients in the empagliflozin group and in 19
patients in the placebo group.
35. 3. The incidences of serious urinary tract
infection, hyperkalemia, acute kidney injury,
serious or symptomatic dehydration, liver injury,
and bone fracture were broadly similar in the
two groups.
4. There was no apparent evidence that
empagliflozin treatment increased the incidence
of serious adverse events overall.
36. The geometric mean urinary albumin-
to-creatinine ratio was 19% lower in
the empagliflozin group than in the
placebo group (95% CI, 15 to 23).
37.
38. DISCUSSION
1. In this population of patients with a wide
range of GFRs, levels of albuminuria, and
causes of CKD, empagliflozin led to a risk of
progression of kidney disease or death from
cardiovascular causes that was 28% lower
than that with placebo, with no major safety
concerns.
39. 2. The risk of hospitalization for any
cause was 14% lower in the
empagliflozin group than in the
placebo group.
40. 3. The EMPA-KIDNEY trial adds
substantially to the existing evidence by
showing consistent benefits among 3569
patients (54.0%) without diabetes and,
separately, among 2282 patients (34.5%) with
an eGFR of less than 30 ml per minute per
1.73 m2.
41. 4. The effect of SGLT2 inhibition on the
progression of kidney disease or death
from cardiovascular causes that was seen
in the current trial is quantitatively
similar to that seen in two other large,
placebo-controlled trials involving
patients with CKD.
42. 5. An accepted surrogate for progression
of kidney disease, showed that
empagliflozin slowed the rate of long-term
eGFR decline among patients with a
urinary albumin-to-creatinine ratio of less
than 300 at baseline (including patients
with a urinary albumin-to-creatinine ratio
of <300).
43. STRENGTH OF TRIAL
Key strengths of this trial were:
1. Its large size and broad eligibility
criteria,
2. The high level of adherence to the
trial regimen,
3. And almost complete follow-up of all
patients.
44. LIMITATIONS
The trial has certain limitations,
including the lower-than-expected
number of cardiovascular events, which
reduced the statistical power for the
assessment of the secondary and tertiary
cardiovascular outcomes.
45. Among a broad range of patients with
CKD who were at risk for disease
progression, including a large number of
patients without diabetes, with an eGFR
of less than 30 ml per minute per 1.73 m2,
and with a low albumin-to-creatinine
ratio,
46. EMPAGLIFLOZIN treatment led to a
lower risk of progression of kidney
disease or death from cardiovascular
causes than placebo.
47. REFFERENCE
1. Fox CS, Matsushita K, Woodward M, et al. Associations of
kidney disease measures with mortality and end-stage renal
disease in individuals with and without diabetes: a meta-
analysis. Lancet 2012; 380:1662-73
2. Webster AC, Nagler EV, Morton RL, Masson P. Chronic
kidney disease. Lancet 2017;389:1238-52
3. EMPA-KIDNEY Collaborative Group. Design, recruitment,
and baseline characteristics of the EMPA-KIDNEY trial.
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