The document provides an overview of chronic kidney disease (CKD), including its definition as abnormal kidney function lasting more than three months, common causes like diabetes and hypertension, and management strategies. It discusses CKD classification based on glomerular filtration rate (GFR) and proteinuria, highlighting the limitations of estimation methods. Additionally, it covers complications arising from CKD such as anemia and mineral and bone disorders, emphasizing the importance of proper management and monitoring.

1. Chronic Kidney Disease
At a Glance
Mohammed Abdel Gawad
Nephrology Specialist
Kidney & Urology Center (KUC) - Alexandria
drgawad@gmail.com

4. CKD Definition, Diagnosis &
Classification
CKD Management

5. CKD Definition, Diagnosis &
Classification

6. What is the definition of CKD?
Abnormal
Kidney
or Kidney
structure
function
for
> 3 months
with
implications
for health.

7. What is the definition of CKD?
Abnormal
Kidney
or Kidney
structure
function
for
> 3 months
with
implications
for health.

8. What is the definition of CKD?
Abnormal
Kidney
or Kidney
structure
function
for
> 3 months
with
implications
for health.

9. Causes of CKD

10. Causes of CKD - USA

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

12. CKD Classification
What is GFR?

13. CKD Classification
What is GFR?
Glomerular
Filtration
Tubular
Reabsorption
Tubular
Secretion
Excretion

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)

21. CKD Classification
eGFR Equations

22. CKD Classification
eGFR Equations
The recommended equations by KDIGO 2012
to be used to eGFR

23. CKD Classification
eGFR Equations
Limitations
It depends on Cr serum level (affected by other factors)

24. CKD Classification
eGFR Equations
Limitations
It depends on serum Cystatin C (affected by other factors)

25. CKD Classification
eGFR Equations
Limitations
• Under or over-estimates GFR in certain GFR
ranges and age groups.
eGFR is not Measured GFR

26. CKD Classification
eGFR Equations
Limitations
eGFR equations are
not 100% accurate
in estimation of actual GFR.
eGFR is not Measured GFR

27. CKD Classification
KDIGO 2012

28. CKD Classification
KDIGO 2012

29. CKD Classification
KDIGO 2012
Albuminuria and
Proteinuria are corner
stones in classification
of all stages of CKD
beside eGFR

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

34. How should proteinuria be
measured?

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

38. CKD Definition, Diagnosis &
Classification
CKD Management

39. CKD Management

40. Management of
CKD Complications
Prevention of
CKD Progression
CKD Management

41. Management of
CKD Complications
CKD Management

42. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization

43. CKD Complications & Management
Anemia

44. Anemia in CKD
Back to Basics (1) – Erythropoietin Hormone
Hypoxia
M.Gawad. www.nephrotube.blogspot.com

45. Anemia in CKD
Back to Basics (1) – Erythropoietin Hormone
Hypoxia
90%
10%
Erythropoietin
M.Gawad. www.nephrotube.blogspot.com

46. Anemia in CKD
Back to Basics (1) – Erythropoietin Hormone
Hypoxia
90%
10%
Erythropoietin
M.Gawad. www.nephrotube.blogspot.com

47. Anemia in CKD
Back to Basics (1) – Erythropoietin Hormone
Increase RBCs formation
& Correct Hypoxia
Hypoxia
90%
10%
Erythropoietin
M.Gawad. www.nephrotube.blogspot.com

48. Anemia in CKD
Pathogenesis (1)
Decrease RBCs life span,
blood sampling, blood loss
during haemodialysis
Erythropoietin
deficiency
Increase RBCs formation
& Correct Hypoxia
Hematinic
deficiency
(back to
basics 2)
Hypoxia
90%
10%
Erythropoietin
• BM fibrosis (↑PTH)
• BM affected by
retained toxins
M.Gawad. www.nephrotube.blogspot.com

49. Anemia in CKD
Back to Basics (2) – RBCs Formation

50. Anemia in CKD
Back to Basics (2) – RBCs Formation

51. Anemia in CKD
Back to Basics (2) – RBCs Formation

52. Anemia in CKD
Pathogenesis (2) - Hematinic Deficiency

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

81. CKD Complications & Management
Mineral and bone disorder (MBD)

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

144. Mineral & Bone Disorder (MBD)
Management – Follow Up

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

147. Mineral & Bone Disorder (MBD)
Management

148. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization

149. CKD Complications & Management
Cardiovascular disease

150. Chronic Cardio-Renal Syndrome

151. Cardio-Kidney-Damage
El Nahas, KI 2010
Kidney International 78, 14-18 (July (1) 2010)

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

154. CKD Complications & Management
Malnutrition

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

158. CKD Complications & Management
Acidosis

159. CKD & Acidosis
Pathogenesis
Normal Acid Base

160. CKD & Acidosis
Pathogenesis
Normal Acid Base

161. CKD & Acidosis
Pathogenesis
Normal Acid Base
Reclamation
& formation
of HCO3

162. CKD & Acidosis
Pathogenesis
Normal Acid Base
Reclamation
& formation
of HCO3

163. CKD & Acidosis
Pathogenesis
CKD – Metabolic Acidosis
Reclamation
& formation
of HCO3

164. CKD & Acidosis
Pathogenesis
CKD – Metabolic Acidosis
Reclamation
& formation
of HCO3

165. CKD & Acidosis
Pathogenesis
CKD – Metabolic Acidosis
Reclamation
& formation
of HCO3

166. CKD & Acidosis
Pathogenesis
CKD – Metabolic Acidosis
Reclamation
& formation
of HCO3

167. CKD & Acidosis
Pathogenesis

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

170. CKD Complications & Management
Drug Dosing

171. CKD & Drug Dosing

172. CKD Complications & Management
Mineral and bone disorder (MBD)
Anemia
Cardiovascular disease
Acidosis
Drug Dosing
Malnutrition
Infection &
Immunization

173. CKD Complications & Management
Infection &
Immunization

174. Infection & Immunization

175. Management of
CKD Complications
Prevention of
CKD Progression
CKD Management

176. Prevention of
CKD Progression
CKD Management

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

180. Glycemic Control in CKD
Target HbA1c

181. Glycemic Control in CKD
Target HbA1c

182. Glycemic Control in CKD
Target HbA1c

183. Glycemic Control in CKD
Target HbA1c

184. Glycemic Control in CKD
Target HbA1c

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

190. Blood Pressure Control in CKD
Life Style

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

208. Diet
Recommendations

209. Diet - Phosphorus Intake

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)

213. Diet - Protein Intake
Recommended Intake

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

221. Study A
585 patient
mGFR of 25-55 ml/min/1.73 m2
DPIs
1.11 g/kg/day
LDPIs
0.73 g/kg/day

222. 585 patient
mGFR of 25-55 ml/min/1.73 m2
DPIs
1.11 g/kg/day
LDPIs
0.73 g/kg/day
GFR Decline
Study A

223. Study B
255 patients
mGFR 13-24 ml/min/1.73 m2
LDPIs
0.69 g/kg/day
LDPIs + KA
0.46 g/kg/day

224. Study B
255 patients
mGFR 13-24 ml/min/1.73 m2
LDPIs
0.69 g/kg/day
LDPIs + KA
0.46 g/kg/day

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.

231. High protein diet
Ann Intern Med. 2003;138:460-467.

232. High protein diet
Ann Intern Med. 2003;138:460-467.

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

241. Hyperuricemia
When to start therapy?

242. Hyperuricemia
When to start therapy?

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

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%

249. Timing of Initiation of RRT
Dialysis

250. Timing of Initiation of RRT
Transplantation

251. CKD NOC 2014
Registration is opened
Contact: enquiries@globalkidneyacademy.co.uk

252. Thank You
Gawad