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- Clinical Physiology of the Kidneys
-
1. Molecular basis of genetic renal diseases 1
- Dr. Paul Jennings
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2. Molecular basis of genetic renal diseases 2
- Dr. Paul Jennings
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3. Assessment of renal function
- Dr. Jochen Raimann
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4. Isolated microhematuria and proteinuria in adults
- Dr. Eva Seiringer
-
5. Intradialytic oxygen saturation
- Dr. Lili Chan
-
6. Pervasive sensing in chronic kidney disease
- Ms. Maggie Han
- Ms. Schantel Williams
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7. The genetic basis of kidney cancer
- Dr. W. Marston Linehan
- Glomerular Disorders
-
8. Focal segmental glomerulosclerosis
- Prof. Moin Saleem
- Tubular Interstitial Disorders
-
9. What’s new for IgA nephropathy part 1: epidemiology and pathogenesis
- Prof. Maurizio Salvadori
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10. What’s new for IgA nephropathy part 2: clinical presentation, diagnosis, prognosis, treatment
- Prof. Maurizio Salvadori
-
11. Renal complications of sickle cell disease
- Dr. Claire Sharpe
- Acute Kidney Injury
- Chronic Kidney Disease
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13. Pathophysiology of acute renal failure
- Dr. Viviane Calice-Silva
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14. Anaemia in chronic kidney disease
- Prof. Iain Macdougall
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15. Kidney disease and pregnancy: a new era?
- Dr. Kate Bramham
- Renal Cell Carcinoma
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16. The genetics and genomics of familial renal carcinoma
- Prof. Eamonn Maher
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17. Immune checkpoint blockade in renal cell carcinoma
- Prof. David McDermott
- Pharmacology and the Kidney
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19. Toxicology of the kidney
- Prof. Lawrence Lash
- Proteomics and the Kidney
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20. Proteomics in diabetic kidney disease
- Prof. Peter Rossing
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21. Urinary proteomics in kidney and cardiovascular disease
- Prof. Harald Mischak
- Pediatric Nephrology
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22. Continuous renal replacement therapy (CRRT) in children
- Prof. Timothy E. Bunchman
- Archived Lectures *These may not cover the latest advances in the field
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23. Proteomics in kidney disease: clinical considerations
- Prof. Peter Rossing
Printable Handouts
Navigable Slide Index
- Introduction
- Disclosures
- Global incidence of diabetes
- Screening for CKD in people living with diabetes
- Proteinuria-based prevention of DM nephropathy
- Hypothesis-driven search for biomarkers
- suPAR and association with complications in type 1 DM CVD and arterial stiffness (PWV)
- suPAR and association with complications in type 1 DM albuminuria and autonomic neuropathy
- Results – Cox models and rIDI
- Pathway-focused proteomics approach
- Unbiased (open) search for new markers
- From albuminuria to profile-omics
- Proteomic utility in DKD
- Urinary proteomics identifies cathepsin D as a biomarker of rapid eGFR decline in type 1 diabetes
- Cathepsin D mRNA and tubulointerstitial damage
- KRIS
- KRIS: response to intervention
- CE-MS proteomic technique: high separation power and sensitive detection
- Proteomic CKD biomarker discovery
- CKD-biomarkers and their regulation
- Proteomic profile: T1DM +/- DN
- Prediction
- Monitoring treatment efficacy: candesartan in T2DM and DN
- Responder prediction
- The Priority trial
- Clinical characteristics at baseline in high and low risk patients
- Persistent microalbuminuria: high-risk vs. low risk
- Progression to CKD 3 (eGFR<60 ml/min/1.73m2): high-risk vs. low-risk
- Spironolactone or placebo in high-risk individuals
- Renal trials in type 2 DM
- Dapagliflozin improves CKD273 in type 2 diabetes with albuminuria
- Cost effectiveness of urinary proteomics: depends on baseline risk
- Personalised treatment in the future
- PROMINENT (proposal)
- Linking kidney and cardiovascular complications in diabetes
- Conclusions
- Thank you
Topics Covered
- Biomarkers
- Proteomics
- Diabetes
- Chronic Kidney Disease
- Proteinuria
- Albuminuria
- Nephropathy
- suPAR
- Kidney Risk Inflammatory Signature (KRIS)
- Candesartan
- The Priority trial
- Spironolactone
- Dapagliflozin
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Rossing, P. (2023, March 30). Proteomics in diabetic kidney disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 21, 2024, from https://doi.org/10.69645/QIZQ7762.Export Citation (RIS)
Publication History
Financial Disclosures
- Professor Rossing has received the following: Consultancy and/or speaking fees (to his institution) from Astellas, AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, MSD, Novo Nordisk and Sanofi Aventis, Research grants from AstraZeneca Bayer and Novo Nordisk.
A selection of talks on Clinical Practice
Transcript
Please wait while the transcript is being prepared...
0:00
Hello, I'm Peter Rossing,
I'm a Professor at University
of Copenhagen in Denmark and
also Head of
complications researchers
Steno Diabetes Copenhagen.
I'm going to talk about
proteomics in diabetic
kidney disease.
0:16
First, I'll share
my disclosures.
I worked with different
pharmaceutic companies
in relation to clinical trials.
Some of them are
relevant for today,
but most of them are not.
0:28
Diabetes is a major
problem globally.
Currently, 463 million
people are estimated to
have diabetes in 2019.
And this was expected to
rise to more than
700 million in 2045.
These numbers are rising
all over the world.
Approximately 90
percent of those with
diabetes have type two diabetes.
With more people
having diabetes,
more people are at risk for
kidney disease due to diabetes.
It's estimated that
approximately 40 percent of
those with diabetes have
some degree of chronic
kidney disease.
With more people
having diabetes,
more people have
chronic kidney disease.
Diabetes is actually
unfortunately,
so far the leading cause of
kidney failure around
most of the world.
1:19
We need to look out for
chronic kidney disease
or diabetic kidney disease
in people having diabetes.
As there are no symptoms,
this has to rely on
systematic screening.
Therefore, the American
Diabetes Association
and K-deal and
organization issuing
guidelines for treatment
of people with
chronic kidney disease have
made a consensus guidelines
saying we need to treat and
screen everybody for kidney
disease on a yearly basis.
If there's signs
of kidney damage,
that is increased albumin
creatinine ratio or
impaired kidney function that
is estimated glomerular
filtration rate,
or a combination
of this, well then
we need start intervention if
these impairments in
albuminuria or GFR
can be confirmed and are
sustained for more
than three months.
This has become
particularly important
because we have now today
more treatment
opportunities than
we've had in the past
than just during
very recent times
more treatment opportunities
have become apparent.