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Dr Gabriel Guevara - 2024 Review
NephroticSyndrome
Definition
The term "nephrotic syndrome" refers to a distinct constellation of
clinical and laboratory features of kidney disease.
It is specifically defined by the presence of heavy proteinuria (protein
excretion greater than 3.5 g/24 hours), hypoalbuminemia (less than 3.5 g/
dL), and peripheral edema.
* Overview of heavy proteinuria and the nephrotic syndrome, UptoDate 2022
Pathophysiology
Etiology
Podocyte
effacement
Podocyte effacement
1.
2.
Pathophysiology - Clinical presentation
Podocyte
effacement
Proteinuria >3.5g/day
RAAS activation
Liver response
Hypoalbuminemia
Hypogammaglobulinemia
Anti-thrombin III def.
Edema
Immunede
fi
cient
Procoagulative state
HTN
MORE EDEMA
Hyperlipidemia
Hyperlipiduria
Fat oval bodies
Clinical presentation Summary
- Hyponatremia
- Albumin decrease
- Proteinuria >3.5g/d
- Hyperlipidemia
- Renal vein thrombosis
NAPHROTIC
- Orbital edema (lower limb)
- Thromboembolism
- Infection
- Coagulability
Etiology
Primary causes
Minimal Change Disease Membranous Nephropathy
Focal Segmental
Glomerulosclerosis
Idiopathic, URTI, NSAID, Hodgkin
Lymphoma
Hepatitis B, C, Syphilis, Gold,
Penicillamine
Heroine use, HIV and Sickle cell
disease
Mediated by Cytokines
Anti PLA 2 receptor antibodies,
Spike and dome appearance.
Hyalinosis and Sclerosis in the
glomerular structure
Etiology
Secondary causes
Diabetes
1. Uncontrolled
hyperglycaemia
2. Non enzymatic
Glycation of EA causing
Narrowing
3. Hyper
fi
ltration
4. Mesangial cell
release TGF Beta
5. Hyaline sclerosis of
glomerular structures
Kimmelstiel Wilson
Nodules
6. Decrease in GFR +
Podocyte effacement
Etiology
Secondary causes
Amyloidosis
• Chronic in
fl
ammatory
states
• Multiple myeloma
Diagnostics
1. Suspect
- NAPHROTIC
2. Urinalysis and Microscopy
Nephrotic syndrome Nephritic Syndrome
Protenuria >3.5g/d Proteinuria <3.5g/d
Fat oval body RBC cast ****
Lipiduria Sterile Pyuria (WBC)
Diagnostics
3. 24 hour urinary protein or UACR >3.5g/d
- 24 hour test needs more labour collecting urine for 24 h
- Urinary Albumin Creatinine Ratio doesn’t need to wait can be done in the spot
4. Serum albumin level
- Hypoalbuminemia <3.5g/dL
5. Lipid panel
- VLDL, LDL, TGL (Hyperlipidemia)
Nephrotic Syndrome!!!
Diagnostics
Look for the clues!!
- Children, HL, NSAID, URTI —————Minimal Change disease
- Hepatitis B, C, Syphilis, Gold penicillamine ——Membranous Neph.
- HIV, Heroin use, sickle cell disease ————Focal segmental Glomerulosclerosis
- Diabetes —————— Diabetic Nephropathy
- Rheumatoid arthritis, Multiple myeloma ————Amyloid associated Nephropathy
What is the cause?
Diagnostics
Corticosteroid trial
- If primary cause suspected (no diabetes no amyloidosis)
- If good response to it might be Minimal Change Disease
- No good response Biopsy
Biopsy
MCD MN FSGS Diabetic Nephropathy Amyloidosis
Light microscopy
NORMAL
Light Microscopy
thickened GBM
LM: Hyalunosis and
sclerosis segmental
LM: Kimmelstiel
wilson nodules
LM nodular sclerosis
Immuno
fl
uorescense
NORMAL
Immuno
fl
uorecense
Lights up!
IF: Normal
EM: Podocyte
e
ff
acement
CONGO RED STAIN
Electron Microscopy
PODOCYTE
EFFACEMENT
Electron microscopy
spike and dome
Electron microscopy
podocyte e
ff
acement
Management
1. Proteinuria
Low protein diet, ACE inhibitors or ARBS
2. Edema
Fluid restriction, sodium restriction and Loop diuretics
4. Hyperlipidemia
Low Fat diet and statins
5. Infections
Antibiotics
Management
6. Procoagulative state
Anticoagulation
TREATING THE CAUSE
If it is a secondary cause its only going to improve if we treat the underlying cause
If it is a primary cause:
1. Start with corticosteroids
2. If not good response (do biopsy) look for MN or FSGS
- Cyclophosphamide
- Rituximab - Tacrolimus
CKD RISK!!!!!
“The good physician treats the disease: the
great physician treats the patient who has the
disease”
- Sir William Osler
Thanks for your attention!

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Nephrotic syndrome by Dr Gabriel Guevara

  • 1. Dr Gabriel Guevara - 2024 Review NephroticSyndrome
  • 2. Definition The term "nephrotic syndrome" refers to a distinct constellation of clinical and laboratory features of kidney disease. It is specifically defined by the presence of heavy proteinuria (protein excretion greater than 3.5 g/24 hours), hypoalbuminemia (less than 3.5 g/ dL), and peripheral edema. * Overview of heavy proteinuria and the nephrotic syndrome, UptoDate 2022
  • 4. Pathophysiology - Clinical presentation Podocyte effacement Proteinuria >3.5g/day RAAS activation Liver response Hypoalbuminemia Hypogammaglobulinemia Anti-thrombin III def. Edema Immunede fi cient Procoagulative state HTN MORE EDEMA Hyperlipidemia Hyperlipiduria Fat oval bodies
  • 5. Clinical presentation Summary - Hyponatremia - Albumin decrease - Proteinuria >3.5g/d - Hyperlipidemia - Renal vein thrombosis NAPHROTIC - Orbital edema (lower limb) - Thromboembolism - Infection - Coagulability
  • 6. Etiology Primary causes Minimal Change Disease Membranous Nephropathy Focal Segmental Glomerulosclerosis Idiopathic, URTI, NSAID, Hodgkin Lymphoma Hepatitis B, C, Syphilis, Gold, Penicillamine Heroine use, HIV and Sickle cell disease Mediated by Cytokines Anti PLA 2 receptor antibodies, Spike and dome appearance. Hyalinosis and Sclerosis in the glomerular structure
  • 7. Etiology Secondary causes Diabetes 1. Uncontrolled hyperglycaemia 2. Non enzymatic Glycation of EA causing Narrowing 3. Hyper fi ltration 4. Mesangial cell release TGF Beta 5. Hyaline sclerosis of glomerular structures Kimmelstiel Wilson Nodules 6. Decrease in GFR + Podocyte effacement
  • 8. Etiology Secondary causes Amyloidosis • Chronic in fl ammatory states • Multiple myeloma
  • 9. Diagnostics 1. Suspect - NAPHROTIC 2. Urinalysis and Microscopy Nephrotic syndrome Nephritic Syndrome Protenuria >3.5g/d Proteinuria <3.5g/d Fat oval body RBC cast **** Lipiduria Sterile Pyuria (WBC)
  • 10. Diagnostics 3. 24 hour urinary protein or UACR >3.5g/d - 24 hour test needs more labour collecting urine for 24 h - Urinary Albumin Creatinine Ratio doesn’t need to wait can be done in the spot 4. Serum albumin level - Hypoalbuminemia <3.5g/dL 5. Lipid panel - VLDL, LDL, TGL (Hyperlipidemia) Nephrotic Syndrome!!!
  • 11. Diagnostics Look for the clues!! - Children, HL, NSAID, URTI —————Minimal Change disease - Hepatitis B, C, Syphilis, Gold penicillamine ——Membranous Neph. - HIV, Heroin use, sickle cell disease ————Focal segmental Glomerulosclerosis - Diabetes —————— Diabetic Nephropathy - Rheumatoid arthritis, Multiple myeloma ————Amyloid associated Nephropathy What is the cause?
  • 12. Diagnostics Corticosteroid trial - If primary cause suspected (no diabetes no amyloidosis) - If good response to it might be Minimal Change Disease - No good response Biopsy
  • 13. Biopsy MCD MN FSGS Diabetic Nephropathy Amyloidosis Light microscopy NORMAL Light Microscopy thickened GBM LM: Hyalunosis and sclerosis segmental LM: Kimmelstiel wilson nodules LM nodular sclerosis Immuno fl uorescense NORMAL Immuno fl uorecense Lights up! IF: Normal EM: Podocyte e ff acement CONGO RED STAIN Electron Microscopy PODOCYTE EFFACEMENT Electron microscopy spike and dome Electron microscopy podocyte e ff acement
  • 14. Management 1. Proteinuria Low protein diet, ACE inhibitors or ARBS 2. Edema Fluid restriction, sodium restriction and Loop diuretics 4. Hyperlipidemia Low Fat diet and statins 5. Infections Antibiotics
  • 15. Management 6. Procoagulative state Anticoagulation TREATING THE CAUSE If it is a secondary cause its only going to improve if we treat the underlying cause If it is a primary cause: 1. Start with corticosteroids 2. If not good response (do biopsy) look for MN or FSGS - Cyclophosphamide - Rituximab - Tacrolimus CKD RISK!!!!!
  • 16. “The good physician treats the disease: the great physician treats the patient who has the disease” - Sir William Osler
  • 17. Thanks for your attention!