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Chronic Kidney Disease (CKD) - At a Glance - Dr. Gawad
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.
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Overview of CKD, its definition, diagnosis, and initial management strategies.
Overview of CKD, its definition, diagnosis, and initial management strategies.
CKD is characterized by abnormalities in kidney structure or function for over 3 months.
Major causes of CKD in the USA and Egypt, including diabetes, hypertension, and other risk factors.
Classification of CKD using GFR metrics and methods for measuring GFR via various markers.
Details on eGFR equations recommended by KDIGO, including limitations affecting their accuracy.
Overview of KDIGO classification involving albuminuria and its significance in CKD.
Discussion on why measuring proteinuria is vital for CKD classification and management.Asymptomatic nature of early CKD and potential screening programs for at-risk populations.Overview of CKD, its definition, diagnosis, and initial management strategies.Comprehensive management strategies for CKD complications including minerals and anemia.
Focuses on managing anemia in CKD, including treatment protocols and available therapies.
Introduction to Mineral and Bone Disorder, key definitions and underlying pathophysiology.
Pathogenesis details of Mineral and Bone Disorder related to CKD including lab abnormalities.
Management strategies for mineral and bone disorders including drug options and follow-ups.
Discussion on complications of CKD including cardiovascular issues, malnutrition, and infections.
Strategies including glycemic control, blood pressure, and proteinuria management to prevent progression. Focus on dietary recommendations and debates concerning protein intake in CKD patients.
End of presentation notes thanking the audience and providing contact information for follow-up.
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- 1. Chronic Kidney Disease Ata Glance Mohammed Abdel Gawad Nephrology Specialist Kidney & Urology Center (KUC) - Alexandria [email protected]
- 4. CKD Definition, Diagnosis& Classification CKD Management
- 5. CKD Definition, Diagnosis& Classification
- 6. What is thedefinition of CKD? Abnormal Kidney or Kidney structure function for > 3 months with implications for health.
- 7. What is thedefinition of CKD? Abnormal Kidney or Kidney structure function for > 3 months with implications for health.
- 8. What is thedefinition of CKD? Abnormal Kidney or Kidney structure function for > 3 months with implications for health.
- 9.
- 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.
- 13. CKD Classification What isGFR? Glomerular Filtration Tubular Reabsorption Tubular Secretion Excretion
- 14. CKD Classification What isGFR? 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 isGFR? 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 GFRis 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 GFRis 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 GFRis 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 GFRis 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 GFRis 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.
- 22. CKD Classification eGFR Equations Therecommended equations by KDIGO 2012 to be used to eGFR
- 23. CKD Classification eGFR Equations Limitations Itdepends on Cr serum level (affected by other factors)
- 24. CKD Classification eGFR Equations Limitations Itdepends 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 eGFRequations are not 100% accurate in estimation of actual GFR. eGFR is not Measured GFR
- 27.
- 28.
- 29. CKD Classification KDIGO 2012 Albuminuriaand Proteinuria are corner stones in classification of all stages of CKD beside eGFR
- 30. CKD Classification KDIGO 2012 Albuminuriaand 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 Albuminuriaand 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 proteinuriabe added to CKD Classification? The Lancet, vol 375, Matshushita K, van de Velde M, Astor BC, et al.
- 33. How should proteinuriabe 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 proteinuriabe measured?
- 35. What are thelimitations of albuminuria measurement?
- 36. How does CKDpresent? 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 CKDpresent? 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.
- 40. Management of CKD Complications Preventionof CKD Progression CKD Management
- 41. Management of CKD Complications CKDManagement
- 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 Backto Basics (1) – Erythropoietin Hormone Hypoxia M.Gawad. www.nephrotube.blogspot.com
- 45. Anemia in CKD Backto Basics (1) – Erythropoietin Hormone Hypoxia 90% 10% Erythropoietin M.Gawad. www.nephrotube.blogspot.com
- 46. Anemia in CKD Backto Basics (1) – Erythropoietin Hormone Hypoxia 90% 10% Erythropoietin M.Gawad. www.nephrotube.blogspot.com
- 47. Anemia in CKD Backto 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 Backto Basics (2) – RBCs Formation
- 50. Anemia in CKD Backto Basics (2) – RBCs Formation
- 51. Anemia in CKD Backto 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 & BoneDisorder (MBD) General Definition PTH – Vit D – Ca – Pi Axis Mineral and bone disorder (MBD)
- 83. Mineral & BoneDisorder (MBD) General Definition PTH – Vit D – Ca – Pi Axis Mineral and bone disorder (MBD)
- 84. Mineral & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (MBD) Lab Abnormalities Summary PTH Ca Pi ALK Phosphatase Secondary Hyperparathyroidism ↑ ↓ ↑ ↑ Tertiary Hyperparathyroidism ↑↑↑ ↑ ↑↑ ↑
- 105. Mineral & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (MBD) General Definition PTH – Vit D – Ca – Pi Axis Mineral and bone disorder (MBD)
- 113. Mineral & BoneDisorder (MBD) Bone Abnormalities – Renal Osteodystrophy Back to Basics – TMV Classification System Turnover High Normal Low Mineralization Normal Abnormal Volume High Normal Low
- 114. Mineral & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (MBD) Bone Abnormalities – Renal Osteodystrophy High turn over - Osteitis Fibrosa Cystica
- 117. Mineral & BoneDisorder (MBD) Bone Abnormalities – Renal Osteodystrophy High turn over - Osteitis Fibrosa Cystica
- 118. Mineral & BoneDisorder (MBD) Bone Abnormalities – Renal Osteodystrophy High turn over - Osteitis Fibrosa Cystica Salt & Pepper Appearance
- 119. Mineral & BoneDisorder (MBD) Bone Abnormalities – Renal Osteodystrophy High turn over - Osteitis Fibrosa Cystica Rugger jersey Spine
- 120. Mineral & BoneDisorder (MBD) Bone Abnormalities – Renal Osteodystrophy High turn over - Osteitis Fibrosa Cystica
- 121. Mineral & BoneDisorder (MBD) Bone Abnormalities – Renal Osteodystrophy High turn over - Osteitis Fibrosa Cystica
- 122. Mineral & BoneDisorder (MBD) Bone Abnormalities – Renal Osteodystrophy High turn over - Osteitis Fibrosa Cystica Clinically Bone fractures Bone pain and discomfort Metastatic calcification
- 123. Mineral & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (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 & BoneDisorder (MBD) Bone Abnormalities – Renal Osteodystrophy Spectrum S Moe et al. Kidney International (2006) 69, 1945–1953
- 127. Mineral & BoneDisorder (MBD) General Definition PTH – Vit D – Ca – Pi Axis Mineral and bone disorder (MBD)
- 128. Mineral & BoneDisorder (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 & BoneDisorder (MBD) Vascular & Soft tissue Classification PTH – Vit D – Ca – Pi Axis
- 130. Mineral & BoneDisorder (MBD) Management – Biochemical Targets
- 131. Mineral & BoneDisorder (MBD) Management – Drugs Used 1- Phosphate binders. 2- Vit D and Vit D analogues. 3- Cinacalcet.
- 132. Mineral & BoneDisorder (MBD) Management – Drugs 1- Phosphate binders. 2- Vit D and Vit D analogues. 3- Cinacalcet.
- 133. Mineral & BoneDisorder (MBD) Management – Drugs Phosphate Binders
- 134. Mineral & BoneDisorder (MBD) Management – Drugs Phosphate Binders
- 135. Mineral & BoneDisorder (MBD) Management – Drugs Phosphate Binders
- 136. Mineral & BoneDisorder (MBD) Management – Drugs Used 1- Phosphate binders. 2- Vit D and Vit D analogues. 3- Cinacalcet.
- 137. Mineral & BoneDisorder (MBD) Management – Drugs Used 1- Phosphate binders. 2- Vit D and Vit D analogues. 3- Cinacalcet.
- 138. Mineral & BoneDisorder (MBD) Management – Drugs Vitamin D & Vit D Analogues
- 139. Mineral & BoneDisorder (MBD) Management – Drugs Vitamin D & Vit D Analogues Liver
- 140. Mineral & BoneDisorder (MBD) Management – Drugs Vitamin D & Vit D Analogues
- 141. Mineral & BoneDisorder (MBD) Management – Drugs Used 1- Phosphate binders. 2- Vit D and Vit D analogues. 3- Cinacalcet.
- 142. Mineral & BoneDisorder (MBD) Management – Drugs Used 1- Phosphate binders. 2- Vit D and Vit D analogues. 3- Cinacalcet.
- 143. Mineral & BoneDisorder (MBD) Management – Drugs Cinacalcet
- 144. Mineral & BoneDisorder (MBD) Management – Follow Up
- 145. Mineral & BoneDisorder (MBD) Management – Follow Up Therapeutic decisions must base on trends rather than on a single laboratory value.
- 146. Mineral & BoneDisorder (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 & BoneDisorder (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.
- 151. Cardio-Kidney-Damage El Nahas, KI2010 Kidney International 78, 14-18 (July (1) 2010)
- 152. Heart & Kidney Forgood 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 WhyCKD 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 Howcan 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 NormalAcid Base
- 160. CKD & Acidosis Pathogenesis NormalAcid Base
- 161. CKD & Acidosis Pathogenesis NormalAcid Base Reclamation & formation of HCO3
- 162. CKD & Acidosis Pathogenesis NormalAcid 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.
- 168. CKD & Acidosis Management Whenis 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 & DrugDosing
- 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.
- 175. Management of CKD Complications Preventionof CKD Progression CKD Management
- 176. Prevention of CKD Progression CKDManagement
- 177. Why it isimportant 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 preventCKD progression? Glycemic control BP control & Proteinuria Diet Hyperuricemia Hyperlipidemia Prevention of CKD Progression
- 179. How to preventCKD progression? Glycemic control Prevention of CKD Progression
- 180. Glycemic Control inCKD Target HbA1c
- 181. Glycemic Control inCKD Target HbA1c
- 182. Glycemic Control inCKD Target HbA1c
- 183. Glycemic Control inCKD Target HbA1c
- 184. Glycemic Control inCKD Target HbA1c
- 185. How to preventCKD progression? Glycemic control BP control & Proteinuria Diet Hyperuricemia Hyperlipidemia Prevention of CKD Progression
- 186. How to preventCKD progression? BP control & Proteinuria Prevention of CKD Progression
- 187. Blood Pressure Controlin 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 Controlin 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 WhyProteinuria is an important issue? Relationship Between Baseline Proteinuria and Subsequent GFR Decline J Am Soc Nephrol. 2003;14:3217-3232
- 190. Blood Pressure Controlin 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 preventCKD progression? Glycemic control BP control & Proteinuria Diet Hyperuricemia Hyperlipidemia Prevention of CKD Progression
- 207. How to preventCKD progression? Prevention of CKD Progression Diet
- 208.
- 209. Diet - PhosphorusIntake
- 210. Diet - PhosphorusIntake Drugs & HD are not sufficient alone for Pi reduction Diet has an important role in Pi reduction
- 211. Diet - ProteinIntake 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 - ProteinIntake 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 - ProteinIntake Recommended Intake
- 214. Diet - ProteinIntake 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 proteindiet slow CKD progression? What is the available evidence? Think Critically
- 216. Dose low proteindiet 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 proteindiet 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 etal. Am J Kidney Dis 1998; 31: 954–961.
- 219. Kasiske BL etal. Am J Kidney Dis 1998; 31: 954–961.
- 220. Compared the effectsof 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 mGFRof 25-55 ml/min/1.73 m2 DPIs 1.11 g/kg/day LDPIs 0.73 g/kg/day
- 222. 585 patient mGFR of25-55 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 mGFR13-24 ml/min/1.73 m2 LDPIs 0.69 g/kg/day LDPIs + KA 0.46 g/kg/day
- 224. Study B 255 patients mGFR13-24 ml/min/1.73 m2 LDPIs 0.69 g/kg/day LDPIs + KA 0.46 g/kg/day
- 225. A follow-up studyof 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 studyof 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 effectsof 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 effectsof 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 RCTsexamining 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 RCTsexamining 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 AnnIntern Med. 2003;138:460-467.
- 232. High protein diet AnnIntern Med. 2003;138:460-467.
- 233. Diet - ProteinIntake What to take care from? Reverse Epidemiology (U-shaped Curve)
- 234. Diet - ProteinIntake What to take care from? Reverse Epidemiology (U-shaped Curve) Recommended Protein intake leads to reduction of accumulation of uremic toxins
- 235. Diet - ProteinIntake 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 - ProteinIntake 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 withyour patient about MALNUTRITION and its bad consequences
- 238. Low Protein DietEvidence 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 preventCKD progression? Glycemic control BP control & Proteinuria Diet Hyperuricemia Hyperlipidemia Prevention of CKD Progression
- 240. How to preventCKD progression? Prevention of CKD Progression Hyperuricemia
- 241. Hyperuricemia When to starttherapy?
- 242. Hyperuricemia When to starttherapy?
- 243. How to preventCKD progression? Glycemic control BP control & Proteinuria Diet Hyperuricemia Hyperlipidemia Prevention of CKD Progression
- 244. How to preventCKD progression? Prevention of CKD Progression Hyperlipidemia
- 246. Newly CKD Lipid profile: Totalchloesterol 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? Lifestyle 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 Initiationof RRT Dialysis
- 250. Timing of Initiationof RRT Transplantation
- 251. CKD NOC 2014 Registrationis opened Contact: [email protected]
- 252.