This document discusses challenges in diagnosing and managing diabetic kidney disease. It emphasizes that renal problems in diabetic patients are not always due to diabetic nephropathy and may be caused by other conditions. A thorough evaluation is needed to determine the underlying cause, including considering patient history, type of diabetes, presence of retinopathy, characteristics of proteinuria and hematuria, rate of renal impairment, hypertension, and potential contributing factors. A renal biopsy may be warranted if the presentation is atypical or suggests an alternative diagnosis.
My Nephrology Registrar Seminar Talk from September 2013
Topics Covered
Pathogenesis of Diabetic Nephropathy
Other Renal Disease in Diabetes
Treatment of Diabetic Kidney Disease + The Joint Renal Diabetic Clinic
Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
- Recorded videos of this lecture:
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https://youtu.be/AtiaKPIdzAQ
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https://youtu.be/2cwyPcRDGEY
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My Nephrology Registrar Seminar Talk from September 2013
Topics Covered
Pathogenesis of Diabetic Nephropathy
Other Renal Disease in Diabetes
Treatment of Diabetic Kidney Disease + The Joint Renal Diabetic Clinic
Presentation given to our fellowship program about diabetic kidney disease.
2022 update discussing SGLT2i, MRA (e.g. finerenone), health economics and beyond
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/AtiaKPIdzAQ
Arabic Language version of this lecture is available at:
https://youtu.be/2cwyPcRDGEY
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- Recorded videos of this lecture:
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https://youtu.be/RaIP09m4XMY
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Insights from the FIGARO-DKD and FIDELIO-DKD trials - Dr. GawadNephroTube - Dr.Gawad
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Diabetes Mellitus Management in CKD (Clinical Tips) - Dr. GawadNephroTube - Dr.Gawad
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- English version of this lecture is available at:
https://youtu.be/XRD-QqGFP18
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- A new version of this lecture is available at: https://www.slideshare.net/MohammedGawad/thrombotic-microangiopathy-tma-in-adults-and-acute-kidney-injury-dr-gawad
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Insights from the FIGARO-DKD and FIDELIO-DKD trials - Dr. GawadNephroTube - Dr.Gawad
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Diabetes Mellitus Management in CKD (Clinical Tips) - Dr. GawadNephroTube - Dr.Gawad
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- English version of this lecture is available at:
https://youtu.be/XRD-QqGFP18
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https://youtu.be/c9PoavAtNKM
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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.
Diabetic nephropathy considered one of the most common complications of DM. This presentation answer the question are some diabetic patient immune to diabetic nephroapthy
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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- Video recording of this lecture in English language: https://youtu.be/gnlRvJ1TTr8
- Video recording of this lecture in Arabic language: https://youtu.be/KdVvfP7JIFI
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- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
- Video recording of this lecture in English language: https://www.youtube.com/watch?v=MA7nU5NWL2g&list=PLL7Q08IoVDSpg0VlGdvCHOHbXqMs0GFRe
- Video recording of this lecture in Arabic language: https://www.youtube.com/watch?v=FiWabzTPFqY&list=PLL7Q08IoVDSrVcm6SmppQyefL_Ub2-xGY
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- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
- Recorded video of this lecture is available at:
https://youtu.be/4MCu1C5xjvE
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Thrombotic Microangiopathy (TMA) in Adults and Acute Kidney Injury - Dr. GawadNephroTube - Dr.Gawad
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https://youtu.be/zrFm0hAZk2A
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- English version of this lecture is available at:
https://youtu.be/V3UGzJTwAWw
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https://youtu.be/hGLaUde2ue4
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- English version of this lecture is available at:
https://youtu.be/t7N2GSXhYwA
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https://youtu.be/WzFZym9hDtQ
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Infection-related Glomerulonephritis (KDIGO 2021 Guidelines) - Dr. GawadNephroTube - Dr.Gawad
- English version of this lecture is available at:
https://youtu.be/qItQlXUC2-Q
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- English version video of this lecture is available at:
https://youtu.be/z9P_1IiFR5I
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- English version of this lecture is available at:
https://youtu.be/lvcXwE0fb-w
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https://youtu.be/r-fG8bSCqZo
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- English version of this lecture is available at: https://youtu.be/_Efu52kZRS4
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- English version of this lecture is available at: https://youtu.be/WHu05hmExBY
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- Recorded videos of this lecture:
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- Recorded videos of this lecture:
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
The hemodynamic and autonomic determinants of elevated blood pressure in obes...
Challenges in Diagnosis and Management of Diabetic Kidney Disease - Dr. Gawad
1. Challenges in Diagnosis and
Management of Diabetic Kidney
Disease
Mohammed Abdel Gawad
Nephrology Specialist
Kidney & Urology Center (KUC)
Alexandria – EGY
drgawad@gmail.com
14th Damanhour Nephrology Annual Conference
13/Nov/2014
2. Join Us
To download the lecture with full animations
contact me on
drgawad@gmail.com
5. IMPORTANT MESSAGE
Hematuria Proteinuria Rising creatinine
• Renal problems in diabetic patients are NOT
ALWAYS due to diabetic nephropathy and
even it may not be due to DM.
6. Renal & Urological Problems that may
be presented in Diabetics
Papillary necrosis
- Ischemic nephropathy
- Renal artery stenosis
- Drug induced
- Other ppt factors for AKI
Diabetic glomerulopathy
(diabetic nephropathy)
Autonomic neuropathy of the
bladder
UTI
Any other glomerular disease
not related to DM
7. Renal & Urological Problems that may
be presented in Diabetics
Papillary necrosis
- Ischemic nephropathy
- Renal artery stenosis
- Drug induced
- Other ppt factors for AKI
Diabetic glomerulopathy
(diabetic nephropathy)
Autonomic neuropathy of the
bladder
UTI
Any other glomerular disease
not related to DM
8. Renal & Urological Problems that may
be presented in Diabetics
Papillary necrosis
Always ask yourself: Is it DN?
- Ischemic nephropathy
- Renal artery stenosis
When to suspect other cause rather than DN?
- Drug induced
- Other ppt factors for AKI
Diabetic glomerulopathy
(diabetic nephropathy)
Autonomic neuropathy of the
bladder
UTI
Any other glomerular disease
not related to DM
When to biopsy?
9. Is it Diabetic Nephropathy?
You have to answer the following
1. What is the type of DM?
2. Is there an evidence of Diabetic retinopathy?
3. Proteinuria:
a. Is the evolution of proteinuria is typical (micro then macro)?
b. Is the range of proteinuria coincides with DN stage?
c. What is the rate of proteinuria progression?
4. Hematuria: Is it microscopic or macroscopic?
5. Rising Cr and decreasing GFR:
a. Is it related to proteinuria?
b. What is the rate of renal impairment progression?
6. Hypertension: refractory or not?
7. What is the drug history?
8. Is there any ppt factor for AKI?
10. Is it Diabetic Nephropathy?
You have to answer the following
1. What is the type of DM?
2. Is there an evidence of Diabetic retinopathy?
3. Proteinuria:
a. Is the evolution of proteinuria is typical (micro then macro)?
b. Is the range of proteinuria coincides with DN stage?
c. What is the rate of proteinuria progression?
4. Hematuria: Is it microscopic or macroscopic?
5. Rising Cr and decreasing GFR:
a. Is it related to proteinuria?
b. What is the rate of renal impairment progression?
6. Hypertension: refractory or not?
7. What is the drug history?
8. Is there any ppt factor for AKI?
12. Diabetic Nephropathy & Diabetic Retinopathy
Type 1 DM
Pre
(1 &2)
5y 15y 25y
Incipient (3)
(microalbuminuria
& HTN)
Overt (4)
(proteinuria,
nephrotic syndrome
and decreasing GFR)
ESRD (5)
At 5 years from onset of DM type 1,
nephropathy coincides with
retinopathy
So if nephropathy is evident in absence
of retinopathy in Type 1 DM
Search for other cause of
nephropathy rather that DM ±
Renal Biopsy
(especially if there is S&S of
other systemic disease)
Diabetic retinopathy is present in virtually
all patients with type 1 diabetes and
nephropathy *
* Girach A, Vignati L. Diabetic microvascular complications. J Diabetes Complications. 2006;20:228-237.
13. Diabetic Nephropathy & Diabetic Retinopathy
Type 2 DM Only 50% to 60% of proteinuric
patients with type 2 diabetes
suffer from retinopathy. **
Consequently, the absence of
retinopathy does not exclude
the diagnosis of DN in patients
with type 2 diabetes.
*
In type 2 DM the prevalence of
nondiabetic renal disease could
vary from 12 to 38% ***
* GIUSEPPE REMUZZI et al. N Engl J Med, Vol. 346, No. 15· April 11, 2002
** Wolf G, Müller N, Mandecka A, Müller UA. Clin Nephrol. 2007;68:81-86.
*** Huang F et al. Clin ephrol 2007, 67: 293-297.
**** Pham TT et al. Am J Nephrol. 2007;27:322-328.
14. Diabetic Nephropathy & Diabetic Retinopathy
Type 2 DM
± Renal
Biopsy
Only 50% to 60% of proteinuric
patients with type 2 diabetes
suffer from retinopathy. **
Consequently, the absence of
retinopathy does not exclude
the diagnosis of DN in patients
with type 2 diabetes.
*
In type 2 DM the prevalence of
nondiabetic renal disease could
vary from 12 to 38% ***
When to suspect other
cause****?
1- Younger patients with DM
2- Short duration of DM
3- Atypical presentation (atypical
proteinuria or hematuria, rapid rising
Cr ….. etc) or other ppt factors
(discussed later)
When to
suspect other
cause?
* GIUSEPPE REMUZZI et al. N Engl J Med, Vol. 346, No. 15· April 11, 2002
** Wolf G, Müller N, Mandecka A, Müller UA. Clin Nephrol. 2007;68:81-86.
*** Huang F et al. Clin ephrol 2007, 67: 293-297.
**** Pham TT et al. Am J Nephrol. 2007;27:322-328.
15. Is it Diabetic Nephropathy?
You have to answer the following
1. What is the type of DM?
2. Is there an evidence of Diabetic retinopathy?
3. Proteinuria:
a. Is the evolution of proteinuria is typical (micro then macro)?
b. Is the range of proteinuria coincides with DN stage?
c. What is the rate of proteinuria progression?
4. Hematuria: Is it microscopic or macroscopic?
5. Rising Cr and decreasing GFR:
a. Is it related to proteinuria?
b. What is the rate of renal impairment progression?
6. Hypertension: refractory or not?
7. What is the drug history?
8. Is there any ppt factor for AKI?
16. Diabetic Nephropathy & Proteinuria
Pre
(1 &2)
5y 15y 25y
Incipient (3)
(microalbuminuria
& HTN)
Overt (4)
(proteinuria,
nephrotic syndrome
and decreasing GFR)
ESRD (5)
If evolution of
proteinuria is atypical:
development of overt
proteinuria without
previous
microalbuminuria.
Search for other cause of nephropathy
rather that DM ± Renal Biopsy
(especially if there is S&S of other
systemic disease)
Costacou T, et al. Am J Kidney
Dis. 2007;50(5):721
17. Diabetic Nephropathy & Proteinuria
Pre
(1 &2)
5y 15y 25y
Incipient (3)
(microalbuminuria
& HTN)
Overt (4)
(proteinuria,
nephrotic syndrome
and decreasing GFR)
ESRD (5)
If evolution of
proteinuria is atypical:
development of overt
proteinuria without
previous
microalbuminuria.
Search for other cause of nephropathy
rather that DM ± Renal Biopsy
(especially if there is S&S of other
systemic disease)
Rate of proteinuria
progression is slow
If the onset of
proteinuria has
been sudden and
rapid
Costacou T, et al. Am J Kidney
Dis. 2007;50(5):721
18. Diabetic Nephropathy & Proteinuria
Pre
(1 &2)
5y 15y 25y
Incipient (3)
(microalbuminuria
& HTN)
Overt (4)
(proteinuria,
nephrotic syndrome
and decreasing GFR)
ESRD (5)
If evolution of
proteinuria is atypical:
development of overt
proteinuria without
previous
microalbuminuria.
Search for other cause of nephropathy
rather that DM ± Renal Biopsy
(especially if there is S&S of other
systemic disease)
If the onset of
proteinuria has
been sudden and
rapid
10-15 years
Overt proteinuria
in diabetes type 1
for <10 years
Rate of proteinuria
progression is slow
Costacou T, et al. Am J Kidney
Dis. 2007;50(5):721
19. DN without Albuminuria
Ischemic Nephropathy – Type 2 DM
Papillary necrosis
- Ischemic nephropathy
- Renal artery stenosis
- Drug induced
- Other ppt factors for AKI
Diabetic glomerulopathy
(diabetic nephropathy)
Autonomic neuropathy of the
bladder
UTI
Any other glomerular disease
not related to DM
20. HYPERperfusion/
Hyperfiltration
↑
Angiotensin II
Intraglomerular
Pressure
Hyperglycemia
Proteinuria
↓
Intraglomerular
Pressure
Atherosclerosis
J Am Soc Nephrol. 2003;14:3217-3232
22. DN without Albuminuria
Ischemic Nephropathy – Type 2 DM
• Renal ultrasound reveals small kidneys.
• Raised Serum Cr after administration of ACE-i
• Without albuminuria
Jamine P. Dwyer et al. DEMAND study. Cardiorenal Med, 2012;2:1-10
23. Jamine P. Dwyer et al. DEMAND study. Cardiorenal Med, 2012;2:1-10
24. DN without Albuminuria - Type 1 DM
• MARK E. MOLITCH. Diabetes Care 33:1536–1543, 2010
•Also same results are reported in:
•Caramori ML et al. Diabetes 52:1036-1040, 2003.
•Lane PH et al. Diabetes 41:581-586, 1992
•MacIsaac RJ et al. Diabetes Care 27:195-200,2004
25. Is it Diabetic Nephropathy?
You have to answer the following
1. What is the type of DM?
2. Is there an evidence of Diabetic retinopathy?
3. Proteinuria:
a. Is the evolution of proteinuria is typical (micro then macro)?
b. Is the range of proteinuria coincides with DN stage?
c. What is the rate of proteinuria progression?
4. Hematuria: Is it microscopic or macroscopic?
5. Rising Cr and decreasing GFR:
a. Is it related to proteinuria?
b. What is the rate of renal impairment progression?
6. Hypertension: refractory or not?
7. What is the drug history?
8. Is there any ppt factor for AKI?
26. Diabetic Nephropathy & Hematuria
Is it Micro or Macroscopic?
Hematuira in diabetic patient
Microscopic
hematuria is seen in
66% of patients with
DN *
Macroscopic hematuria
±
active nephritic urinary sediment
(acanthocytes and red cell casts)
Search for other cause of nephropathy
rather that DM ± Renal Biopsy
(especially if there is S&S of other systemic
disease)
Red blood cell casts have
also been described in
patients with diabetic
* Akimoto T, Ito C, Saito O, et al. Nephron Clin Pract. 2008; 109:c119-c126.
** Chong YB et al. Ren Fail. 2012;34(3):323-8. Epub 2012 Jan 17.
nephropathy **
27. Is it Diabetic Nephropathy?
You have to answer the following
1. What is the type of DM?
2. Is there an evidence of Diabetic retinopathy?
3. Proteinuria:
a. Is the evolution of proteinuria is typical (micro then macro)?
b. Is the range of proteinuria coincides with DN stage?
c. What is the rate of proteinuria progression?
4. Hematuria: Is it microscopic or macroscopic?
5. Rising Cr and decreasing GFR:
a. Is it related to proteinuria?
b. What is the rate of renal impairment progression?
6. Hypertension: refractory or not?
7. What is the drug history?
8. Is there any ppt factor for AKI?
28. Diabetic Nephropathy & Renal Impairment
Pre
(1 &2)
5y 15y 25y
Incipient (3)
(microalbuminuria
& HTN)
Overt (4)
(proteinuria,
nephrotic syndrome
and decreasing GFR)
ESRD (5)
If renal impairment is rapid
Search for other cause
Rate of renal
impairment
progression is slow
first, of course, renovascular
disease must be excluded
other cause of nephropathy
rather that DM ± Renal Biopsy
(especially if there is S&S of
other systemic disease)
29. Diabetic Nephropathy & Renal Impairment
Pre
(1 &2)
5y 15y 25y
Incipient (3)
(microalbuminuria
& HTN)
Overt (4)
(proteinuria,
nephrotic syndrome
and decreasing GFR)
ESRD (5)
Significant proteinuria without/with
non coinciding renal impairment
If renal impairment is rapid
Search for other cause
Rate of renal
impairment
progression is slow
first, of course, renovascular
disease must be excluded
other cause of nephropathy
rather that DM ± Renal Biopsy
(especially if there is S&S of
other systemic disease)
30. Is it Diabetic Nephropathy?
You have to answer the following
1. What is the type of DM?
2. Is there an evidence of Diabetic retinopathy?
3. Proteinuria:
a. Is the evolution of proteinuria is typical (micro then macro)?
b. Is the range of proteinuria coincides with DN stage?
c. What is the rate of proteinuria progression?
4. Hematuria: Is it microscopic or macroscopic?
5. Rising Cr and decreasing GFR:
a. Is it related to proteinuria?
b. What is the rate of renal impairment progression?
6. Hypertension: refractory or not?
7. What is the drug history?
8. Is there any ppt factor for AKI?
31. Diabetic Nephropathy & Refractory HTN
Refractory hypertension (and fluid
retention) in diabetic patients is highly
suggestive for renovascular disease
32. Is it Diabetic Nephropathy?
You have to answer the following
1. What is the type of DM?
2. Is there an evidence of Diabetic retinopathy?
3. Proteinuria:
a. Is the evolution of proteinuria is typical (micro then macro)?
b. Is the range of proteinuria coincides with DN stage?
c. What is the rate of proteinuria progression?
4. Hematuria: Is it microscopic or macroscopic?
5. Rising Cr and decreasing GFR:
a. Is it related to proteinuria?
b. What is the rate of renal impairment progression?
6. Hypertension: refractory or not?
7. What is the drug history?
8. Is there any ppt factor for AKI?
33. Diabetic Nephropathy & Drugs
ACEi & ARBs
> 30% reduction in GFR
within 2-3 months after
initiation
Suspect renovascular
disease
34. Diabetic Nephropathy & Drugs
Diabetics kidneys are at
high risk to be affected
by nephrotoxic drugs
NSAIDs Contrast
Any other nephrotoxic
drug
35. Is it Diabetic Nephropathy?
You have to answer the following
1. What is the type of DM?
2. Is there an evidence of Diabetic retinopathy?
3. Proteinuria:
a. Is the evolution of proteinuria is typical (micro then macro)?
b. Is the range of proteinuria coincides with DN stage?
c. What is the rate of proteinuria progression?
4. Hematuria: Is it microscopic or macroscopic?
5. Rising Cr and decreasing GFR:
a. Is it related to proteinuria?
b. What is the rate of renal impairment progression?
6. Hypertension: refractory or not?
7. What is the drug history?
8. Is there any ppt factor for AKI?
36. ppt factors for AKI in Diabetics
They are the same as any high risk population
1. Dehydration (fluid loss, hyperglycemia, decrease fluid
intake).
2. UTI.
3. Drugs.
4. Cardiac problem.
5. Septicemia.
6. Surgery.
37. To Conclude
When to suspect other Cause(s) of Renal
Disease rather than DN? (Is it DN?) – Step 1
Step 1:
Renal US
Evidence of
chronic
changes
No need for
biopsy
No evidence
of chronic
changes
Go to Step 2
Overall, renal biopsy is indicated only in a
small minority of diabetic patients.
38. To Conclude
When to suspect other Cause(s) of Renal Disease
rather than DN? (Is it DN?) – Step 2
Suspect other cause rather that DN if:
Diabetic retinopathy - Absent in Type 1
- Absent in type 2 +
1- Short duration of DM
2- Atypical presentation or other ppt factors
Proteinuria & Nephrotic syndrome
(Don’t forget DN without
albuminuria)
- Development of overt proteinuria without previous microalbuminuria
- Overt proteinuria in diabetes type 1 for <10 years
- If the onset of proteinuria has been sudden and rapid
- Resistant Nephrotic Syndrome
Hematuria Macroscopic hematuria & active urinary sediment
(Don’t forget casts are described in DN also)
Rising Cr and decreasing GFR - If renal impairment is rapid
- If significant proteinuria without renal impairment
Hypertension Refractory HTN
Drug history - ACEi & ARBs: > 30% reduction in GFR within 2-3 months after initiation
- NSAIDs & Contrast
- Others
ppt factor for AKI Dehydration, UTI, Drugs, Cardiac problem, Septicemia, Surgery.
Systemic disease S&S of other systemic disease
Red and green colored indications are not listed in KDOQI Guidelines for Diabetes & CKD
39. Pathology
Pathology - Nodular
Kimmelstiel Wilson nodules
Pathognomonic for diabetes
But reported in only 10% to 50% of
biopsy specimens in both type 1
and type 2 diabetes.
40. Pathology
Pathology - Nodular
Kimmelstiel Wilson nodules
Pathognomonic for diabetes
But reported in only 10% to 50% of
biopsy specimens in both type 1
and type 2 diabetes.
41. Pathology
Pathology - Nodular Pathology - Diffuse
Kimmelstiel Wilson nodules - MORE FREQUENT than the nodular lesion
- Correlates with the clinical manifestations
of worsening renal function
42. Pathology
DN
Other
Pathology
DN
+ Other Pathology
LM/IF/EM whenever possible,
especially if there is high suspicion of other pathology
47. Primary outcome was a composite of nonfatal myocardial
infarction, nonfatal stroke, or death from cardiovascular causes
ACCORD Group. N Engl J Med. 2008;358:2545-2559.
48. 22% increase in mortality from any cause and
did not significantly reduce major CV events
Primary outcome was a composite of nonfatal myocardial
infarction, nonfatal stroke, or death from cardiovascular causes
ACCORD Group. N Engl J Med. 2008;358:2545-2559.
50. Diabetic Kidney Disease
Management
Glycemic
Control
Hypertension
Other Strategies
Proteinuria &
Progression
Aldosterone
Breakthrough
Emerging Therapy
51. Diabetic Kidney Disease
Management
Hypertension
BP Target?
Which Class?
ACE-i/ARBS fit for all?
ACE-I + ARBS?
52. Diabetic Kidney Disease
Management
Hypertension
BP Target?
Which Class?
ACE-i/ARBS fit for all?
ACE-I + ARBS?
53.
54. There was also a trend for increased adverse cardiovascular
outcomes, including all-cause mortality, with diastolic blood
pressures below 85 mmHg
Pohl MA et al. J Am Soc Nephrol. 2005;16:3027-3037.
57. Diabetic Kidney Disease
Management
Hypertension
BP Target?
Which Class?
ACE-i/ARBS fit for all?
ACE-I + ARBS?
58. Which Anti-HTN Class?
• The overall effect of BP lowering may be more important than
the type of antihypertensive used.
• Antihypertensive therapies, regardless of agent used:
– reduce UAE
– delay progression of nephropathy
– improve survival in both type 1 and type 2 diabetic patients with DN
Ismail N et al. Kidney Int. 1999;55:1-28.
Mogensen CE. J Intern Med. 2003;254:45-66.
• RAS blockade with ACE inhibitors or ARBs confers preferential
renoprotection that is independent of BP reduction.
Microalbuminuria Captopril Study Group. Diabetologia. 1996;39:587-593.
EUCLID Study Group. Lancet. 1997;349:1787-1792.
Ann Intern Med. 2001;134:370-379.
Lewis EJ et al. N Engl J Med. 1993;329:1456-1462.
Parving HH et al. N Engl J Med. 2001;345:870-878.
Viberti G, Wheeldon NM. Circulation. 2002;106:672-678.
Brenner BM et al. N Engl J Med. 2001;345:861-869.
Lewis EJ et al. N Engl J Med. 2001;345:851-860.
Barnett AH et al. N Engl J Med. 2004;351:1952-1961.
59. ACE-i / ARBs Renoprotection in DN
HYPERperfusion/
Hyperfiltration
↑
Angiotensin II
Intraglomerular
Pressure
Hyperglycemia
Proteinuria
J Am Soc Nephrol. 2003;14:3217-3232
60. ACE-i / ARBs Renoprotection in DN
HYPERperfusion/
Hyperfiltration
Hyperglycemia Angiotensin II
ACE-I
& ARBs
↓
Intraglomerular
Pressure
J Am Soc Nephrol. 2003;14:3217-3232
61.
62. Renal Response to ACE-i
Serum creatinine concentration may increase up
to 30% after an ACE inhibitor is started.
This rise in creatinine is associated with
long-term renoprotection
ACE inhibitor should not necessarily be
stopped in these patients
Bakris GL et al. Arch Intern Med.2000;160:685-693.
63. Enhance ACE-i/ARBs Action
The antiproteinuric effect of RAS
blockade is enhanced by
low-sodium diet
(<2 g/day)
combination of a loop diuretic
or a thiazide diuretic
64. Diabetic Kidney Disease
Management
Hypertension
BP Target?
Which Class?
ACE-i/ARBS fit for all?
ACE-I + ARBS?
66. ACE-i / ARBs in DN
HYPERperfusion/
Hyperfiltration
Hyperglycemia Angiotensin II
HYPOperfusion/
Ischemia
Atherosclerosis
ACE-I
& ARBs
↓
Intraglomerular
Pressure
Angiotensin II
↑
Intraglomerular
Pressure
Important Auto-regulatory
mechanism to maintain GFR
ACE-I & ARBs are
dangerous in this case
71. The VA NEPHRON-D study was in fact terminated
early because of the unfavorable patient-risk
benefit ratio.
VA NEPHRON-D Investigators. N Engl J Med. 2013;369:1892-1903.
74. Smoking cessation
Dieting
Weight reduction
N Engl J Med 2008;358:580-91.
Phisitkul K et al. Am J Kidney Dis. 2003;41:319-327.
Ritz E et al. Metab. 2000;26(suppl 4):54-63.
76. Relation between Proteinuria and
disease progression in DN
Patients who progressed to
severely increased albuminuria
had the highest rate of loss of
GFR
J Am Soc Nephrol. 2003;14:3217-3232
Perkins BA et al. Kidney Int. 2010;77(1):57.
Caramori ML, Fioretto P, Mauer M. Diabetes. 2003;52(4):1036.
MacIsaac RJ et al. Diabetes Care. 2006;29(7):1560.
Perkins BA et al. J Am Soc Nephrol. 2007;18(4):1353.
77. Relation between Proteinuria and
disease progression in DN
The degree of albuminuria is not
always necessarily linked to disease
progression in patients with diabetic
nephropathy
Some patients may progress to
advanced disease although these
patients had either stable
moderately increased albuminuria
or regression to normal albuminuria.
Patients who progressed to
severely increased albuminuria
had the highest rate of loss of
GFR
The rate of loss of GFR was
lower in patients with
regression to normal
albuminuria compared with
patients with stable moderately
increased albuminuria
Perkins BA et al. Kidney Int. 2010;77(1):57.
Caramori ML, Fioretto P, Mauer M. Diabetes. 2003;52(4):1036.
MacIsaac RJ et al. Diabetes Care. 2006;29(7):1560.
Perkins BA et al. J Am Soc Nephrol. 2007;18(4):1353.
79. Aldosterone Breakthrough
Screening for aldosterone
breakthrough
(evidence is not strong enough to
support screening)
Hollenberg NK. Kidney Int. 2004;66:1-9.
Microalbuminuria Captopril Study Group. Diabetologia. 1996;39:587-593.
79
In a subset of patients despite
ACE inhibitor and ARB therapy
Plasma aldosterone levels are
elevated (aldosterone
breakthrough)
Aldosterone promotes tissue
inflammation and fibrosis with
faster decline in GFR
Aldosterone blockade with close
monitoring of serum potassium levels may
represent optimal therapy for patients
who show aldosterone breakthrough
during treatment with an ACE inhibitor or
an ARB and who no longer show maximal
antiproteinuric effects with these agents
82. Management Home Messages
• HbA1C% should be individualized
• Lower BP target (< 120mmHg) increases mortality
• The overall effect of BP lowering may be more important than the type of
antihypertensive used
• RAS blockade with ACE inhibitors or ARBs confers preferential
renoprotection that is independent of BP reduction.
• Take care of ACE-i/ARBs with ischemic nephropathy
• Don’t combine ACE-I with ARBs
• Multitarget treatment is mandatory (diet, weight loss, smoking …etc)