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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
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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
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Favor considerar este documento como apuntes referenciales, corresponde a la versión de respaldo en pdf de una presentación que incluía elementos que contextualizan la información de forma diferente, la adaptación de este sitio web elimino dichos elementos y ademas cambia el formato de muchos textos e imágenes.
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Chronic Kidney Disease Management and caresachintutor
Chronic kidney disease (CKD) is defined as the presence of kidney damage or an estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 mt2, persisting for 3 months or more, irrespective of the cause.
- 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
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Thrombotic Microangiopathy (TMA) in Adults and Acute Kidney Injury - Dr. GawadNephroTube - Dr.Gawad
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Infection-related Glomerulonephritis (KDIGO 2021 Guidelines) - Dr. GawadNephroTube - 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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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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
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.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
11. Causes of CKD - EGYPT
DM
Hypertension
Chronic glomerulonephritis
Chronic pyelonephritis
CVD and its related risk factors
(e.g. obesity, smoking)
Analgesics abuse
Renal stones &
Obstructive uropathy
APKD
AKI
Many cases the cause is unknown
14. CKD Classification
What is GFR?
Glomerular
Filtration
Tubular
Reabsorption
Tubular
Secretion
Excretion
GFR:
The quantity of glomerular
filtrate formed in all nephrons of
both kidneys / min.
15. CKD Classification
What is GFR?
Glomerular
Filtration
Tubular
Reabsorption
Tubular
Secretion
Excretion
GFR:
The quantity of glomerular
filtrate formed in all nephrons of
both kidneys / min.
16. CKD Classification
How GFR is Estimated or Measured?
Estimation &/or Measurement of GFR
Exogenous
Filtration Markers
Inulin, iothalamate,
EDTA, diethylene
triamine pentaacetic
acid, iohexol
Endogenous
Filtration Markers
Creatinine Clearance
(CrCl)
eGFR equations
(age, sex, race, and
body size, in addition to
serum creatinine,
cystatin)
17. CKD Classification
How GFR is Estimated or Measured?
Estimation &/or Measurement of GFR
Exogenous
Filtration Markers
Inulin, iothalamate,
EDTA, diethylene
triamine pentaacetic
acid, iohexol
Endogenous
Filtration Markers
Creatinine Clearance
(CrCl)
eGFR equations
(age, sex, race, and
body size, in addition to
serum creatinine,
cystatin)
18. CKD Classification
How GFR is Estimated or Measured?
Estimation &/or Measurement of GFR
Exogenous
Filtration Markers
Endogenous
Filtration Markers
Inulin, iothalamate,
EDTA, diethylene
triamine pentaacetic
acid, iohexol
Creatinine Clearance
(CrCl)
eGFR equations
(age, sex, race, and
body size, in addition to
serum creatinine,
cystatin)
19. CKD Classification
How GFR is Estimated or Measured?
Estimation &/or Measurement of GFR
Exogenous
Filtration Markers
Endogenous
Filtration Markers
Complicated & Costy
eGFR is not Measured GFR
Inulin, iothalamate,
EDTA, diethylene
triamine pentaacetic
acid, iohexol
Creatinine Clearance
(CrCl)
eGFR equations
(age, sex, race, and
body size, in addition to
serum creatinine,
cystatin)
20. CKD Classification
How GFR is Estimated or Measured?
Cystatin C
• It is found in virtually all tissues and body fluids.
• It is a potent inhibitor of lysosomal proteinases (enzymes from a
special subunit of the cell that break down proteins)
• One of the most important extracellular inhibitors of cysteine
proteases (it prevents the breakdown of proteins outside the cell
by a specific type of protein degrading enzymes)
30. CKD Classification
KDIGO 2012
Albuminuria and
Proteinuria are corner
stones in classification
of all stages of CKD
beside eGFR
CGA
Classification
(Cause, GFR,
Albuminuria)
Also mention
the cause when
classifying CKD
31. CKD Classification
KDIGO 2012
Albuminuria and
Proteinuria are corner
stones in classification
of all stages of CKD
beside eGFR
The term micro or
macro albuminuria
no longer be used
CGA
Classification
(Cause, GFR,
Albuminuria)
Also mention
the cause when
classifying CKD
32. Why should proteinuria be added to
CKD Classification?
The Lancet, vol 375, Matshushita K, van de Velde M, Astor BC, et al.
33. How should proteinuria be
measured?
Test
Comments
Urine dipstick
semiquantitative
24-hour urine
collection
(PER, AER)
• cumbersome,
• often inaccurate or incomplete
PCR
• most useful for monitoring of proteinuria
• a first morning void is most reliable
ACR
• most useful for monitoring of albuminuria
• a first morning void is most reliable
35. What are the limitations of
albuminuria measurement?
36. How does CKD present?
Asymptomatic Disease
Especially early despite the
accumulation of harmful
metabolites
Incidental finding of urine
abnormalities or raised creatinine
Is there a role for CKD Screening
Programs?
Whom to screen?
37. How does CKD present?
Asymptomatic Disease
Especially early despite the
accumulation of harmful
metabolites
Incidental finding of urine
abnormalities or raised creatinine
Is there a role for CKD Screening
Programs?
Whom to screen?
Non Specific S&S
42. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization
53. Anemia in CKD – Management
General Steps
Step 1:
Step 2:
Iron Status & Initial
Evaluation
ESA Therapy
54. Anemia in CKD – Management
Step1: Iron Status & Initial Evaluation
Step 1:
Iron Status & Initial
Evaluation
55. Anemia in CKD – Management
Step1: Iron Status & Initial Evaluation
Anemia of CKD?
Step 1:
Iron Status & Initial
Evaluation
• Normochromic Normocytic
• Hypochromic Microcytic
• Normochromic Macrocytic
56. Anemia in CKD – Management
Step1: Iron Status & Initial Evaluation
Anemia of CKD?
Step 1:
Iron Status & Initial
Evaluation
• Normochromic Normocytic
• Hypochromic Microcytic
• Normochromic Macrocytic
Presence of other type of anemia may point to
another cause rather than CKD (on top of CKD)
57. Anemia in CKD – Management
Step1: Iron Status & Initial Evaluation
+ other Investigations
• CHr
• CRP
• Occult blood in stool
• Blood film
Step 1:
Iron Status & Initial
Evaluation
58. Anemia in CKD – Management
Step 1: Iron Therapy
When to start?
TSAT is 30%
ferritin 500 ng/ml
59. Anemia in CKD – Management
Step 1: Iron Therapy
Oral vs IV iron?
Not on HD
On HD
Try oral iron
IV iron is mandatory
60. Anemia in CKD – Management
Step 1: Iron Therapy
Available IV iron therapy
Scott B. et al. American Journal of Hematology 76:74–78 (2004)
61. Anemia in CKD – Management
Step 1: Iron Therapy
Available IV iron therapy
So IV iron sensitivity test is always
required before IV dextran
Scott B. et al. American Journal of Hematology 76:74–78 (2004)
62. Anemia in CKD – Management
Step 1: Iron Therapy
What is the IV iron protocol in CKD patients?
Initial loading
(large) dose
Subsequent
maintenance
(small) doses
Follow up iron
profile (TSAT,
ferritin, CHr)
63. Anemia in CKD – Management
General Steps
Step 1:
Step 2:
Iron Status & Initial
Evaluation
ESA Therapy
64. Anemia in CKD – Management
General Steps
Step 2:
ESA Therapy
65. Anemia in CKD – Management
Step 2: ESA Therapy
Protocol
Initiation
Maintenance
66. Anemia in CKD – Management
Step 2: ESA Therapy
Protocol
Initiation
Maintenance
67. Anemia in CKD – Management
Step 2: ESA Therapy
Hb Target
10 – 11.5 g/dl
Individualization
(Some patients have improved
QOL with higher Hb level >
11.5g/dl)
In all adults not >13
68. Anemia in CKD – Management
Step 2: ESA Therapy
Available ESAs, dosing & route of administration
Initiation Dose
CKD ND
EPO
Darbepoetin alfa
Methoxy polyethylene
glycol-epoetin beta
Initiation Dose
CKD 5HD
20-50 units/kg 3 times/week
(I.V. dosage must be 20-30% higher than S.C. dosage)
0.45 g/kg every four
weeks
(S.C. or IV)
0.45 g/kg once weekly
or
0.75 g/kg once every two
weeks
(S.C. or IV)
0.6mcg (600ng)/kg every two weeks
(S.C. or IV)
69. Anemia in CKD – Management
Step 2: ESA Therapy
Available ESAs, dosing & route of administration
Initiation Dose
CKD ND
EPO
Darbepoetin alfa
Methoxy polyethylene
glycol-epoetin beta
Initiation Dose
CKD 5HD
20-50 units/kg 3 times/week
(I.V. dosage must be 20-30% higher than S.C. dosage)
0.45 g/kg every four
weeks
(S.C. or IV)
0.45 g/kg once weekly
or
0.75 g/kg once every two
weeks
(S.C. or IV)
0.6mcg (600ng)/kg every two weeks
(S.C. or IV)
70. Anemia in CKD – Management
Step 2: ESA Therapy
• What is the target Hb level for renal patients?
1. 11.5 - 13 g/dl.
2. 10 – 11.5 g/dl.
3. None of the above.
71. Anemia in CKD – Management
Step 2: ESA Therapy
• What is the target Hb level for renal patients?
1. 11.5 - 13 g/dl.
2. 10 – 11.5 g/dl.
Don’t forget Individualization
3. None of the above.
72. Anemia in CKD – Management
Step 2: ESA Therapy
ESA Hyporesponsivness
Treat
Ix
Hyporesponsivness
to ESA therapy
73. Anemia in CKD – Management
Step 2: ESA Therapy
ESA Hyporesponsivness
• CHr
• CRP
• Occult blood in stool
• Blood film
Treat
Ix
Hyporesponsivness
to ESA therapy
74. Anemia in CKD – Management
Step 2: ESA Therapy
• CHr
• CRP
• Occult blood in stool
• Blood film
Hb Response
ESA Hyporesponsivness
Plateau Effect
Due to Fe ↓ 2nry
to ESA
administration
Treat
Time
Ix
Hyporesponsivness
to ESA therapy
75. Anemia in CKD – Management
Step 2: ESA Therapy
ESA Side Effects
Influenza-like
syndrome
(affecting 5 %)*
Unknown
etiology**
Respond to antiinflammatory
drugs**
*Bennett WM. J Am Soc Nephrol 1991; 1:990.
** Buur T etal. Clin Nephrol 1990; 34:230.
76. Anemia in CKD – Management
Step 2: ESA Therapy
ESA Side Effects
Influenza-like
syndrome
(affecting 5 %)*
Hypertension
Unknown
etiology**
Respond to antiinflammatory
drugs**
*Bennett WM. J Am Soc Nephrol 1991; 1:990.
** Buur T etal. Clin Nephrol 1990; 34:230.
77. Anemia in CKD – Management
Step 2: ESA Therapy
ESA Side Effects
Influenza-like
syndrome
(affecting 5 %)*
Hypertension
Unknown
etiology**
Pure red cell
aplasia (PCR)
Respond to antiinflammatory
drugs**
Human serum albumin is used as a stabilizing
agent in many EPO preparations, although
polysorbate was used with Eprex which
stimulate the formation of EPO-Ab
*Bennett WM. J Am Soc Nephrol 1991; 1:990.
** Buur T etal. Clin Nephrol 1990; 34:230.
78. Anemia in CKD – Management
Step 2: ESA Therapy
ESA Side Effects
Influenza-like
syndrome
(affecting 5 %)*
Hypertension
Unknown
etiology**
Pure red cell
aplasia (PCR)
Respond to antiinflammatory
drugs**
Human serum albumin is used as a stabilizing
agent in many EPO preparations, although
polysorbate was used with Eprex which
stimulate the formation of EPO-Ab
*Bennett WM. J Am Soc Nephrol 1991; 1:990.
** Buur T etal. Clin Nephrol 1990; 34:230.
79. Anemia in CKD – Management
Blood Transfusion
When managing chronic anemia, we recommend avoiding,
when possible, red cell transfusions to minimize the general
risks related to their use.
In patients eligible for organ transplantation, we specifically
recommend avoiding, when possible, red cell transfusions to
minimize the risk of allosensitization.
Benefits of red cell transfusions may outweigh the risks in patients
in whom:
1. ESA therapy is ineffective (e.g., hemoglobinopathies, bone
marrow failure, ESA resistance)
2. The risks of ESA therapy may outweigh its benefits (e.g.,
previous or current malignancy, previous stroke)
80. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization
82. Mineral & Bone Disorder (MBD)
General Definition
PTH – Vit D – Ca – Pi Axis
Mineral and bone disorder (MBD)
83. Mineral & Bone Disorder (MBD)
General Definition
PTH – Vit D – Ca – Pi Axis
Mineral and bone disorder (MBD)
84. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (1) : PTH – Vit D – Ca – Pi Axis
PTH
Increase
serum Pi
Increase
serum Ca
M.Gawad. www.nephrotube.blogspot.com
85. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (1) : PTH – Vit D – Ca – Pi Axis
PTH
Increase
serum Pi
Increase
serum Ca
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
Decrease
serum Pi
86. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (1) : PTH – Vit D – Ca – Pi Axis
PTH Action:
increase serum Ca and
decrease serum Pi
PTH
So low serum Ca & high
serum Pi will stimulate
PTH release & vise verca
Increase
serum Pi
Increase
serum Ca
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
Decrease
serum Pi
87. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (1) : PTH – Vit D – Ca – Pi Axis
Vit D
PTH
Increase
serum Pi
Calcidiol
25-OH-D
Increase
serum Ca
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
Decrease
serum Pi
88. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (1) : PTH – Vit D – Ca – Pi Axis
Vit D
PTH
Increase
serum Pi
Calcidiol
25-OH-D
α1 hydroxylase
Increase
serum Ca
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
Decrease
serum Pi
89. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (1) : PTH – Vit D – Ca – Pi Axis
Vit D
PTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
Increase
serum Pi
Increase
serum Ca
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
Decrease
serum Pi
90. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (1) : PTH – Vit D – Ca – Pi Axis
Vit D
PTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
Increase
serum Pi
Increase
serum Ca
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
Decrease
serum Pi
91. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (1) : PTH – Vit D – Ca – Pi Axis
Vit D
Increase Ca
& Pi
reabsorption
Calcidiol
25-OH-D
PTH
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
Increase
serum Pi
Increase
serum Ca
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
Decrease
serum Pi
92. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (1) : PTH – Vit D – Ca – Pi Axis
Active vit D
Action:
Vit D
Increase Ca
& Pi
reabsorption
Calcidiol
25-OH-D
PTH
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
increase serum Ca & Pi
Increase
serum Pi
Increase
serum Ca
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
Decrease
serum Pi
93. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : PTH – Vit D – Ca – Pi Axis
Vit D
Increase Ca
& Pi
reabsorption
Calcidiol
25-OH-D
PTH
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
Increase
serum Pi
Increase
serum Ca
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
Decrease
serum Pi
94. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : PTH – Vit D – Ca – Pi Axis
Vit D
PTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
95. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : PTH – Vit D – Ca – Pi Axis
Vit D
PTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
96. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : PTH – Vit D – Ca – Pi Axis
Vit D
2ry hyperPTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
PTH
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
97. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : PTH – Vit D – Ca – Pi Axis
Bone Disease
Fractures
Bone pain
Marrow fibrosis
Erythropoietin resistance
Vit D
2ry hyperPTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
PTH
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
98. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : Tertiary Hyperparathyroidism
PTH
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
99. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : Tertiary Hyperparathyroidism
PTH
Persistent
untreated
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
100. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : Tertiary Hyperparathyroidism
Persistent parathyroid
stimulation
PTH
Persistent
untreated
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
101. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : Tertiary Hyperparathyroidism
Persistent parathyroid
stimulation
Formation of
parathyroid adenoma
PTH
Persistent
untreated
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
102. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : Tertiary Hyperparathyroidism
Persistent parathyroid
stimulation
Formation of
parathyroid adenoma
PTH
Persistent
untreated
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
103. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (1) : Tertiary Hyperparathyroidism
Persistent parathyroid
stimulation
Formation of
parathyroid adenoma
Increase
serum Pi & Ca
PTH
Persistent
untreated
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
M.Gawad. www.nephrotube.blogspot.com
104. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Summary
PTH
Ca
Pi
ALK
Phosphatase
Secondary
Hyperparathyroidism
↑
↓
↑
↑
Tertiary
Hyperparathyroidism
↑↑↑
↑
↑↑
↑
105. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (2): FGF 23
Vit D
2ry hyperPTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
PTH
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
106. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (2): FGF 23
Vit D
2ry hyperPTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
PTH
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
107. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (2): FGF 23
Fibroblast Growth Factor 23
(FGF 23)
Vit D
2ry hyperPTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
PTH
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
108. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Back to Basics (2): FGF 23
Fibroblast Growth Factor 23
(FGF 23)
Vit D
2ry hyperPTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
PTH
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
109. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (2): FGF 23
Fibroblast Growth Factor 23
(FGF 23)
in CKD
Vit D
PTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
110. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (2): FGF 23
Fibroblast Growth Factor 23
(FGF 23)
in CKD
Vit D
PTH
Calcidiol
25-OH-D
Calcitriol
1,25-(OH)2-D
α1 hydroxylase
Still ↑ Pi
serum level
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
111. Mineral & Bone Disorder (MBD)
Lab Abnormalities
Pathogenesis (2): FGF 23
in CKD
Persistent very high
level of FGF 23 in CKD
Vit D
Calcidiol
25-OH-D
Fibroblast Growth Factor 23
(FGF 23)
Calcitriol
1,25-(OH)2-D
Strong independent
predictor of
mortality in CKD
α1 hydroxylase
Still ↑ Pi
serum level
PTH
Decrease
serum Ca
Increase
serum Pi
Increase Ca
reabsorption
Increase Pi
excretion
112. Mineral & Bone Disorder (MBD)
General Definition
PTH – Vit D – Ca – Pi Axis
Mineral and bone disorder (MBD)
113. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
Back to Basics – TMV Classification System
Turnover
High
Normal
Low
Mineralization
Normal
Abnormal
Volume
High
Normal
Low
114. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
Spectrum
iPTH
< 50 pg/ml
Low turn over
bone disease
iPTH
150-300 pg/ml
Normal bone
formation
iPTH
> 300 pg/ml
High turn over
bone disease
(Ostetis fibrosa
cystica)
Mixed lesion
KEITH A et al. July 20, 1995. Vol. 333 No. 3
115. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
High turn over - Osteitis Fibrosa Cystica
Increased bone resorption and formation
Increased numbers of osteoclasts and osteoblasts
iPTH
150-300 pg/ml
Increased of woveniPTH and peritrabecular
bone,
fibrosis.
< 50 pg/ml
Low turn over
bone disease
Normal bone
formation
iPTH
> 300 pg/ml
High turn over
bone disease
(Ostetis fibrosa
cystica)
Mixed lesion
KEITH A et al. July 20, 1995. Vol. 333 No. 3
116. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
High turn over - Osteitis Fibrosa Cystica
117. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
High turn over - Osteitis Fibrosa Cystica
118. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
High turn over - Osteitis Fibrosa Cystica
Salt & Pepper
Appearance
119. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
High turn over - Osteitis Fibrosa Cystica
Rugger jersey Spine
120. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
High turn over - Osteitis Fibrosa Cystica
121. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
High turn over - Osteitis Fibrosa Cystica
122. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
High turn over - Osteitis Fibrosa Cystica
Clinically
Bone fractures
Bone pain and discomfort
Metastatic calcification
123. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
Low turn over – Adynamic Bone Disease
iPTH
< 50 pg/ml
Low turn over
bone disease
iPTH
150-300 pg/ml
iPTH
> 300 pg/ml
low or
Normal bone absent bone formation
High turn over
formation
bone disease
paucity of bone-forming osteoblasts and
(Ostetis fibrosa
bone-resorbing osteoclasts.
cystica)
Mixed lesion
KEITH A et al. July 20, 1995. Vol. 333 No. 3
124. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
Low turn over – Adynamic Bone Disease
What is the cause??
1- In the past it was attributed to
Al toxicity
2- Over treated
hyperparathyroidism
iPTH
< 50 pg/ml
Low turn over
bone disease
iPTH
150-300 pg/ml
iPTH
> 300 pg/ml
low or
Normal bone absent bone formation
High turn over
formation
bone disease
paucity of bone-forming osteoblasts and
(Ostetis fibrosa
bone-resorbing osteoclasts.
cystica)
Mixed lesion
KEITH A et al. July 20, 1995. Vol. 333 No. 3
125. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
Low turn over – Adynamic Bone Disease
What is the cause??
1- In the past it was attributed to
Al toxicity
2- Over treated
hyperparathyroidism
iPTH
< 50 pg/ml
Low turn over
bone disease
Laboratory??
Low PTH
Low ALK Phosphatase
High Ca & Pi
iPTH
High incidence
> 300 pg/ml
iPTHtissue
of
150-300 pg/ml
calcification
low or
Normal bone absent bone formation
High turn over
formation
bone disease
paucity of bone-forming osteoblasts and
(Ostetis fibrosa
bone-resorbing osteoclasts.
cystica)
Mixed lesion
KEITH A et al. July 20, 1995. Vol. 333 No. 3
126. Mineral & Bone Disorder (MBD)
Bone Abnormalities – Renal Osteodystrophy
Spectrum
S Moe et al. Kidney International (2006) 69, 1945–1953
127. Mineral & Bone Disorder (MBD)
General Definition
PTH – Vit D – Ca – Pi Axis
Mineral and bone disorder (MBD)
128. Mineral & Bone Disorder (MBD)
Ca-Phosphate Product
PTH – Vit D – Ca – Pi Axis
↑ Ca X Pi
Deposition of Ca & Pi
1- Vascular, articular, and extra-articular soft
tissue
2- Pruritis (deposition under skin)
129. Mineral & Bone Disorder (MBD)
Vascular & Soft tissue Classification
PTH – Vit D – Ca – Pi Axis
130. Mineral & Bone Disorder (MBD)
Management – Biochemical Targets
131. Mineral & Bone Disorder (MBD)
Management – Drugs Used
1- Phosphate binders.
2- Vit D and Vit D analogues.
3- Cinacalcet.
132. Mineral & Bone Disorder (MBD)
Management – Drugs
1- Phosphate binders.
2- Vit D and Vit D analogues.
3- Cinacalcet.
133. Mineral & Bone Disorder (MBD)
Management – Drugs
Phosphate Binders
134. Mineral & Bone Disorder (MBD)
Management – Drugs
Phosphate Binders
135. Mineral & Bone Disorder (MBD)
Management – Drugs
Phosphate Binders
136. Mineral & Bone Disorder (MBD)
Management – Drugs Used
1- Phosphate binders.
2- Vit D and Vit D analogues.
3- Cinacalcet.
137. Mineral & Bone Disorder (MBD)
Management – Drugs Used
1- Phosphate binders.
2- Vit D and Vit D analogues.
3- Cinacalcet.
138. Mineral & Bone Disorder (MBD)
Management – Drugs
Vitamin D & Vit D Analogues
139. Mineral & Bone Disorder (MBD)
Management – Drugs
Vitamin D & Vit D Analogues
Liver
140. Mineral & Bone Disorder (MBD)
Management – Drugs
Vitamin D & Vit D Analogues
141. Mineral & Bone Disorder (MBD)
Management – Drugs Used
1- Phosphate binders.
2- Vit D and Vit D analogues.
3- Cinacalcet.
142. Mineral & Bone Disorder (MBD)
Management – Drugs Used
1- Phosphate binders.
2- Vit D and Vit D analogues.
3- Cinacalcet.
143. Mineral & Bone Disorder (MBD)
Management – Drugs
Cinacalcet
145. Mineral & Bone Disorder (MBD)
Management – Follow Up
Therapeutic decisions must base on trends rather than on
a single laboratory value.
146. Mineral & Bone Disorder (MBD)
Management – Follow Up
Therapeutic decisions must base on trends rather than on
a single laboratory value.
It is reasonable to base the frequency of monitoring on the
presence and magnitude of abnormalities, and the rate of
progression of CKD and also to monitor for trends and
treatment efficacy and side-effects
148. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization
152. Heart & Kidney
For good cardiac condition
there must be a good
renal condition.
For good renal condition
there must be a good
cardiac condition.
153. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization
155. CKD & Malnutrition
Why CKD patients are malnourished?
Decreased intake; loss of appetite
Chronic inflammation:
malnutrition-inflammationatherosclerosis (MIA) syndrome
Resistance to anabolic hormones
such as insulin and GH
Decreased absorption
Cytokines release and
complement activation
during haemodialysis
Metabolic acidosis
Diet restriction: e.g., low
phosphate diet may lead to protein
malnourishment
156. CKD & Malnutrition
How can I minimize and treat malnutrition in CKD?
Prevention of
low-protein or low-calorie diets
Correction of underlying infections or
inflammatory processes
Correction of anemia
Control of metabolic acidosis
Optimization of dialysis
157. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization
168. CKD & Acidosis
Management
When is the drug to be used?
Oral HCO3 (unless contraindicated)
When to start HCO3 therapy?
When serum HCO3 < 22 mmol/L
What is the therapy target?
Maintain serum HCO3 within normal
169. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization
172. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization
177. Why it is important to delay CKD progression?
Prevention of
CKD Progression
Matshushita K et al. The Lancet, vol 375, p. 2073-2081, 2010,
Kidney International. Levey AS, de Jong PE, Coresh J, et al.
178. How to prevent CKD progression?
Glycemic control
BP control &
Proteinuria
Diet
Hyperuricemia
Hyperlipidemia
Prevention of
CKD Progression
179. How to prevent CKD progression?
Glycemic control
Prevention of
CKD Progression
185. How to prevent CKD progression?
Glycemic control
BP control &
Proteinuria
Diet
Hyperuricemia
Hyperlipidemia
Prevention of
CKD Progression
186. How to prevent CKD progression?
BP control &
Proteinuria
Prevention of
CKD Progression
187. Blood Pressure Control in CKD
Why to treat HTN in CKD?
HTN is a precipitating & initiating factor of CKD
El Nahas, KI 2010
Kidney International 78, 14-18 (July (1) 2010)
188. Blood Pressure Control in CKD
Why to treat HTN in CKD?
HTN is a prognostic marker for CKD progression
Bakris et al. American Journal of Kidney Diseases, Vol 36, No 3 (September), 2000: pp 646-661
189. Proteinuria & CKD
Why Proteinuria is an important issue?
Relationship Between Baseline Proteinuria and
Subsequent GFR Decline
J Am Soc Nephrol. 2003;14:3217-3232
191. Blood Pressure & Proteinuria Control in CKD
When to start anti-HTN therapy?
When to start?
192. Blood Pressure & Proteinuria Control in CKD
When to start anti-HTN therapy?
When to start?
193. Blood Pressure & Proteinuria Control in CKD
When to start anti-HTN therapy?
When to start?
194. Blood Pressure & Proteinuria Control in CKD
When to start anti-HTN therapy?
There is insufficient evidence to recommend combining an
ACE-I with ARBs to prevent progression of CKD.
When to start?
195. Blood Pressure & Proteinuria Control in CKD
When to start anti-HTN therapy?
There is insufficient evidence to recommend combining an
ACE-I with ARBs to prevent progression of CKD.
196. Blood Pressure & Proteinuria Control in CKD
Mechanism of action of ACE-I & ARBs?
Afferent Arteriole
Efferent Arteriole
M.Gawad. www.nephrotube.blogspot.com
197. Blood Pressure & Proteinuria Control in CKD
Mechanism of action of ACE-I & ARBs?
In HTN & CKD
Afferent Arteriole
↑
Intraglomerular
Pressure
Efferent Arteriole
M.Gawad. www.nephrotube.blogspot.com
198. Blood Pressure & Proteinuria Control in CKD
Mechanism of action of ACE-I & ARBs?
In HTN & CKD
Afferent Arteriole
↑
Intraglomerular
Pressure
Efferent Arteriole
M.Gawad. www.nephrotube.blogspot.com
199. Blood Pressure & Proteinuria Control in CKD
Mechanism of action of ACE-I & ARBs?
In HTN & CKD
Afferent Arteriole
↑
Intraglomerular
Pressure
Efferent Arteriole
ACE-I &
ARBs
M.Gawad. www.nephrotube.blogspot.com
200. Blood Pressure & Proteinuria Control in CKD
Mechanism of action of ACE-I & ARBs?
In HTN & CKD
Afferent Arteriole
↑
Intraglomerular
Pressure
Efferent Arteriole
ACE-I &
ARBs
M.Gawad. www.nephrotube.blogspot.com
201. Blood Pressure & Proteinuria Control in CKD
Mechanism of action of ACE-I & ARBs?
In HTN & CKD
Afferent Arteriole
↓
Intraglomerular
Pressure
Efferent Arteriole
ACE-I &
ARBs
M.Gawad. www.nephrotube.blogspot.com
202. Blood Pressure & Proteinuria Control in CKD
Mechanism of action of ACE-I & ARBs?
In HTN & CKD
Afferent Arteriole
↓
Intraglomerular
Pressure
Efferent Arteriole
ACE-I &
ARBs
M.Gawad. www.nephrotube.blogspot.com
203. Blood Pressure & Proteinuria Control in CKD
When to start anti-HTN therapy??
When to start?
What is the target of BP in CKD?
204. Blood Pressure & Proteinuria Control in CKD
What is the target of BP in CKD?
205. Blood Pressure & Proteinuria Control in CKD
What is the target of BP in CKD?
206. How to prevent CKD progression?
Glycemic control
BP control &
Proteinuria
Diet
Hyperuricemia
Hyperlipidemia
Prevention of
CKD Progression
207. How to prevent CKD progression?
Prevention of
CKD Progression
Diet
210. Diet - Phosphorus Intake
Drugs & HD are not sufficient
alone for Pi reduction
Diet has an important role in
Pi reduction
211. Diet - Protein Intake
Recommended Intake
Protein Intake
GFR < 30 ml/min
in diabetics (2C) & non diabetics (2B)
Protein intake
0.8 g/kg/day
Adults with CKD at risk of
progression
Avoid high protein
intake
(>1.3 g/kg/day) (2C)
212. Diet - Protein Intake
Recommended Intake
Protein Intake
GFR < 30 ml/min
in diabetics (2C) & non diabetics (2B)
Protein intake
0.8 g/kg/day
Adults with CKD at risk of
progression
Avoid high protein
intake
(>1.3 g/kg/day) (2C)
214. Diet - Protein Intake
Why to restrict protein intake?
Reduction of accumulation of
metabolic waste products &
uremic toxins
The role of dietary protein
restriction in slowing progression
of CKD is more controversial
215. Dose low protein diet slow CKD
progression?
What is the available evidence?
Think Critically
216. Dose low protein diet slow CKD
progression?
What is the available evidence?
When criticizing an evidence about low
protein diet & CKD progression, check
the following points
Number of
patients in
the study
Duration of
the study
follow up
Controlling of
other risk
factors
The duration
of causative
factor of CKD
How renal
function is
assessed?
217. Dose low protein diet slow CKD
progression?
What is the available evidence?
There is no convincing
or conclusive evidence
that long-term protein
restriction delays the
progression of CKD.
218. Kasiske BL et al. Am J Kidney Dis 1998; 31: 954–961.
219. Kasiske BL et al. Am J Kidney Dis 1998; 31: 954–961.
220. Compared the effects of LPD and BP control on the progression of CKD in over 800 subjects
Mean follow-up was 2.2 years
Study A
Study B
585 patient
mGFR of 25-55 ml/min/1.73 m2
255 patients
mGFR 13-24 ml/min/1.73 m2
DPIs
1.11 g/kg/day
LDPIs
0.73 g/kg/day
LDPIs
0.69 g/kg/day
LDPIs + KA
0.46 g/kg/day
GFR loss was estimated by the slope of 125I-iothalamate clearance
225. A follow-up study of the original MDRD Study followed those
subjects recruited to Study B until the year 2000
Study B
mGFR 13-24 ml/min/1.73 m2
LDPIs
0.69 g/kg/day
LDPIs + KA
0.46 g/kg/day
226. A follow-up study of the original MDRD Study followed those
subjects recruited to Study B until the year 2000
Study B
mGFR 13-24 ml/min/1.73 m2
LDPIs
0.69 g/kg/day
LDPIs + KA
0.46 g/kg/day
227. Compared the effects of LPD and BP control on the progression of CKD in over 800 subjects
Mean follow-up was 2.2 years
Study A
Study B
585 patient
mGFR of 25-55 ml/min/1.73 m2
255 patients
mGFR 13-24 ml/min/1.73 m2
Usual DPIs
1.11 g/kg/day
LDPIs
0.73 g/kg/day
LDPIs
0.69 g/kg/day
LDPIs + KA
0.46 g/kg/day
GFR loss was estimated by the slope of 125I-iothalamate clearance
228. Compared the effects of LPD and BP control on the progression of CKD in over 800 subjects
Mean follow-up was 2.2 years
Study A
Study B
No significant differences in GFR decline, measured by
585 patient
255 patients
mGFR of 25-55 ml/min/1.73 m2
125I-iothalamate clearance every 4 mGFR 13-24 ml/min/1.73 m2
months, were found
between the diet groups in either study.
Usual DPIs
1.11 g/kg/day
LDPIs
0.73 g/kg/day
LDPIs
0.69 g/kg/day
LDPIs + KA
0.46 g/kg/day
GFR loss was estimated by the slope of 125I-iothalamate clearance
229. 4 small RCTs examining the effect of dietary protein
restriction (0.6-0.8 g/kg/day) on CKD progression in
adult patients with early (stages 2-3) CKD. (1-4)
(1) Hansen HP et al. Kidney International. 2002; 62: 220-228.
(2) Pijls LT et al. Journal of Clinical Nutrition. 2002; 56: 1200 - 1207.
(3) Meloni C et al. Journal of Renal Nutrition. 2002; 12: 96 - 101.
(4) Meloni et al. Journal of Renal Nutrition. 2004; 14: 208 - 213.
230. 4 small RCTs examining the effect of dietary protein
restriction (0.6-0.8 g/kg/day) on CKD progression in
adult patients with early (stages 2-3) CKD. (1-4)
None of the trials demonstrated a significant effect
of dietary protein restriction on CKD progression,
(except in a subgroup of 89 patients with nondiabetic early CKD). (4)
(1) Hansen HP et al. Kidney International. 2002; 62: 220-228.
(2) Pijls LT et al. Journal of Clinical Nutrition. 2002; 56: 1200 - 1207.
(3) Meloni C et al. Journal of Renal Nutrition. 2002; 12: 96 - 101.
(4) Meloni et al. Journal of Renal Nutrition. 2004; 14: 208 - 213.
233. Diet - Protein Intake
What to take care from?
Reverse Epidemiology
(U-shaped Curve)
234. Diet - Protein Intake
What to take care from?
Reverse Epidemiology
(U-shaped Curve)
Recommended
Protein intake
leads to reduction of
accumulation of
uremic toxins
235. Diet - Protein Intake
What to take care from?
Reverse Epidemiology
(U-shaped Curve)
Insufficient
protein intake
may lead to loss
of lean body
mass, and
malnutrition
Recommended
Protein intake
leads to reduction of
accumulation of
uremic toxins
236. Diet - Protein Intake
What to take care from?
Reverse Epidemiology
(U-shaped Curve)
Insufficient
protein intake
may lead to loss
of lean body
mass, and
malnutrition
Excess dietary
protein
leads to the
accumulation of
uremic toxins &
decrease GFR
Recommended
Protein intake
leads to reduction of
accumulation of
uremic toxins
M.Gawad. www.nephrotube.blogspot.com
237. Always talk with your
patient about
MALNUTRITION
and its bad consequences
238. Low Protein Diet Evidence
What We Miss?
Large RCT for both
diabetics & non diabetics,
for long time for follow, up
after controlling all
precipitating parameters
with recommended targets
239. How to prevent CKD progression?
Glycemic control
BP control &
Proteinuria
Diet
Hyperuricemia
Hyperlipidemia
Prevention of
CKD Progression
240. How to prevent CKD progression?
Prevention of
CKD Progression
Hyperuricemia
243. How to prevent CKD progression?
Glycemic control
BP control &
Proteinuria
Diet
Hyperuricemia
Hyperlipidemia
Prevention of
CKD Progression
244. How to prevent CKD progression?
Prevention of
CKD Progression
Hyperlipidemia
245.
246. Newly CKD
Lipid profile:
Total chloesterol
LDL
HDL
TG
Detect 2ry causes:
– smoking status
– alcohol consumption
– blood pressure
– body mass index or other measure of obesity
– fasting blood glucose
– renal function
- Nephrotic Syndrome
– liver function (transaminases)
No need for follow up
– thyroid-stimulating hormone (TSH) if dyslipidaemia is present.
- Medications
247. When to treat?
Life style is
mandatory in all
stratigies
if on dialysis
if on statin or
statin/ezetimibe
if not on dialysis
if not on statin or
statin/ezetimibe
Age: 18-49
Age: ≥50
Start Statins if:
Continue
Dont initiate
- known coronary
disease (myocardial
infarction or
coronary
revascularization)
GFR <60
GFR ≥60
Statin or
statin/ezetimibe
Statins
- diabetes mellitus
- prior ischemic
stroke
- estimated 10-year
incidence of coronary
death or non-fatal
myocardial infarction
> 10%