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NEPHROTIC AND NEPHRITIC
SYNDROME
PRESENTER: UNISA A. KANU
SUPERVISOR: DR IRENE
LEARNING OBJECTIVES
 Understand and define nephrotic and nephritic
syndromes.
 Describe the initial investigations and management
of nephrotic and nephritic syndromes.
 Describe the complications of nephrotic and
nephritic syndromes.
GLOMERULONEPHRITIS
 Glomerulus – capillary loop with basement
membrane which allows passage of specific
molecules into the nephron
 Glomerulonephritis – inflammation/damage of the
glomerular basement membrane resulting in altered
function. Relatively uncommon cause of kidney
injury.
 Can present as nephrotic and/or nephritic
syndrome.
What is nephrotic syndrome?
• Increased permeability of the glomerulus leading to loss of
proteins into the tubules.
• Triad of:
 MASSIVE Proteinuria >3g/24hours
 Or spot urine protein: creatinine ratio >300-350mg/mmol
 Hypoalbuminaema <25g/L
 Oedema
• And often:
 Hypercholesterolemia/dyslipidaemia (total cholesterol
>10mmol/L)
PRESENTATION
 New-onset oedema
 Initially periorbital or peripheral
 Later genitals, ascites, anasarca
 Frothy urine
 Generalised symptoms – lethargy, fatigue, reduced
appetite
FURTHER POSSIBLE PRESENTATIONS...
 Oedema
 BP normal/raised
 Leukonychia
 Breathlessness:
 Pleural effusion, fluid overload, AKI
 DVT/PE/MI
 Eruptive xanthomata/ xanthalosmata
CAUSES OF NEPHROTIC SYNDROME
 Primary glomerulonephritis
 Minimal change disease (80% paeds cases)
 Focal segmental glomerulosclerosis (most common cause
in adults)
 Membranous glomerulonephritis
Systemic Causes
 Secondary glomerulonephritis
 Diabetic nephropathy
 Sarcoidosis
 Autoimmune: SLE, Sjogrens
 Infection: Syphilis, hepatitis B, HIV
 Amyloidosis
 Multiple myeloma
 Vasculitis
 Cancer
 Drugs: gold, penicillamine, captopril, NSAIDs
INVESTIGATIONS
 Urine dipstick and send to lab
 Urine microscopy
 Bloods – the usual ones, plus renal screen
 Immunoglobulins, electrophoresis (myeloma screen),
complement (C3, C4) autoantibodies (ANA, ANCA,
anti-dsDNA, anti-GBM)
 Renal ultrasound
 Renal biopsy (all adults)
 Children generally trial of steroids first
MANAGEMENT
 Conservative
 Monitor U&E, BP, fluid balance, weight
 Salt and fluid restriction
 Treat underlying cause
 Medical
 Diuretics
 ACE-inhibitors/ARBs
 Corticosteroids/immunosuppression
 Dialysis
 Anticoagulation
 Surgical
 Renal transplant
COMPLICATIONS
 Increased susceptibility to infection
 20% adult cases
 Due to reduced serum IgG, reduced complement activity,
reduced T cell function
 Thromboembolism
 40% adult cases
 Partly due to increased clotting factors and platelet
abnormalities
 Hyperlipidaemia
 due to hepatic lipoprotein synthesis to restore osmotic
pressure
Prognosis
 Varies
 With treatment, generally good prognosis
 Especially minimal change disease (1% progress to
ESRF)
 Without treatment, very poor prognosis
 Children under 5 or adults older than 30 = worse
prognosis
DIFFERENTIAL DIAGNOSIS FOR OEDEMA
 Congestive Cardiac Failure
 Raised JVP, pulmonary oedema, mild proteinuria
 Liver disease
 Hypoalbuminaemia, ascites/oedema
 What investigations can you do?
 You decide to send your patient to the renal clinic...
WHAT IS NEPHRITIC SYNDROME?
PATHOPHYSIOLOGY
 Thin glomerular basement membrane with pores that
allow protein and blood into the tubule.
 Clinical syndrome defined by:
 Haematuria/ red cell casts
 Hypertension (mild)
 Oliguria
 Uraemia
 Proteinuria (<3g/24 hours)
SIGNS AND SYMPTOMS
 Haematuria (E.g. cola coloured)
 Proteinuria
 Hypertension
 Oliguria
 Flank pain
 General systemic symptoms
 Post-infectious = 2-3 weeks after strep-throat/URTI
What are your differentials?
 Malignancy (older patients)
 UTI
 Trauma
 What bedside investigation would you like to do?
 You decide to refer to the renal clinic...
Causes
 Post-infectious glomerulonephritis
 Primary
 IgA Nephropathy (Berger's disease)
 Rapidly progressive glomerulonephritis
 Proliferative glomerulonephritis
 Secondary glomerulonephritis
 Henoch-Schonlein purpura
 Vasculitis
INVESTIGATIONS
 Urine dipstick and send sample to lab
 Urine microscopy – red cell casts
 Bloods – the usual plus renal screen
 Immunoglobulins, electrophoresis, complement (C3, C4)
autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM);
blood culture; ASOT (anti-streptolysin O titre)
 Renal ultrasound
 Renal biopsy
Red Cell Casts
Management
 Conservative
 Monitor U&E, BP, fluid balance, weight
 Salt and fluid restriction
 Treat underlying cause
 Medical
 Diuretics
 Treat hypertension
 Corticosteroids/immunosuppression
 Dialysis
 Surgical
 Renal transplant
PROGNOSIS
 Varies
 Post-infectious usually self-resolving (95% recover
renal function)
 Others are a bit more nasty
EXAMPLE CASE
ANY QUESTIONS?
SUMMARY
 Nephrotic syndrome = MASSIVE proteinuria
 Nephritic syndrome = haematuria/red cell casts
 May be a mixed presentation
 New oedema? Dipstick that urine!
 Haematuria? Exclude malignancy!
THANK YOU

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Nephrotic presentation.ppt9999999999999999999999999999999999999

  • 1. NEPHROTIC AND NEPHRITIC SYNDROME PRESENTER: UNISA A. KANU SUPERVISOR: DR IRENE
  • 2. LEARNING OBJECTIVES  Understand and define nephrotic and nephritic syndromes.  Describe the initial investigations and management of nephrotic and nephritic syndromes.  Describe the complications of nephrotic and nephritic syndromes.
  • 3.
  • 4. GLOMERULONEPHRITIS  Glomerulus – capillary loop with basement membrane which allows passage of specific molecules into the nephron  Glomerulonephritis – inflammation/damage of the glomerular basement membrane resulting in altered function. Relatively uncommon cause of kidney injury.  Can present as nephrotic and/or nephritic syndrome.
  • 5. What is nephrotic syndrome? • Increased permeability of the glomerulus leading to loss of proteins into the tubules. • Triad of:  MASSIVE Proteinuria >3g/24hours  Or spot urine protein: creatinine ratio >300-350mg/mmol  Hypoalbuminaema <25g/L  Oedema • And often:  Hypercholesterolemia/dyslipidaemia (total cholesterol >10mmol/L)
  • 6. PRESENTATION  New-onset oedema  Initially periorbital or peripheral  Later genitals, ascites, anasarca  Frothy urine  Generalised symptoms – lethargy, fatigue, reduced appetite
  • 7. FURTHER POSSIBLE PRESENTATIONS...  Oedema  BP normal/raised  Leukonychia  Breathlessness:  Pleural effusion, fluid overload, AKI  DVT/PE/MI  Eruptive xanthomata/ xanthalosmata
  • 8. CAUSES OF NEPHROTIC SYNDROME  Primary glomerulonephritis  Minimal change disease (80% paeds cases)  Focal segmental glomerulosclerosis (most common cause in adults)  Membranous glomerulonephritis
  • 9. Systemic Causes  Secondary glomerulonephritis  Diabetic nephropathy  Sarcoidosis  Autoimmune: SLE, Sjogrens  Infection: Syphilis, hepatitis B, HIV  Amyloidosis  Multiple myeloma  Vasculitis  Cancer  Drugs: gold, penicillamine, captopril, NSAIDs
  • 10. INVESTIGATIONS  Urine dipstick and send to lab  Urine microscopy  Bloods – the usual ones, plus renal screen  Immunoglobulins, electrophoresis (myeloma screen), complement (C3, C4) autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM)  Renal ultrasound  Renal biopsy (all adults)  Children generally trial of steroids first
  • 11. MANAGEMENT  Conservative  Monitor U&E, BP, fluid balance, weight  Salt and fluid restriction  Treat underlying cause  Medical  Diuretics  ACE-inhibitors/ARBs  Corticosteroids/immunosuppression  Dialysis  Anticoagulation  Surgical  Renal transplant
  • 12. COMPLICATIONS  Increased susceptibility to infection  20% adult cases  Due to reduced serum IgG, reduced complement activity, reduced T cell function  Thromboembolism  40% adult cases  Partly due to increased clotting factors and platelet abnormalities  Hyperlipidaemia  due to hepatic lipoprotein synthesis to restore osmotic pressure
  • 13. Prognosis  Varies  With treatment, generally good prognosis  Especially minimal change disease (1% progress to ESRF)  Without treatment, very poor prognosis  Children under 5 or adults older than 30 = worse prognosis
  • 14. DIFFERENTIAL DIAGNOSIS FOR OEDEMA  Congestive Cardiac Failure  Raised JVP, pulmonary oedema, mild proteinuria  Liver disease  Hypoalbuminaemia, ascites/oedema  What investigations can you do?  You decide to send your patient to the renal clinic...
  • 15. WHAT IS NEPHRITIC SYNDROME?
  • 16. PATHOPHYSIOLOGY  Thin glomerular basement membrane with pores that allow protein and blood into the tubule.  Clinical syndrome defined by:  Haematuria/ red cell casts  Hypertension (mild)  Oliguria  Uraemia  Proteinuria (<3g/24 hours)
  • 17. SIGNS AND SYMPTOMS  Haematuria (E.g. cola coloured)  Proteinuria  Hypertension  Oliguria  Flank pain  General systemic symptoms  Post-infectious = 2-3 weeks after strep-throat/URTI
  • 18. What are your differentials?  Malignancy (older patients)  UTI  Trauma  What bedside investigation would you like to do?  You decide to refer to the renal clinic...
  • 19. Causes  Post-infectious glomerulonephritis  Primary  IgA Nephropathy (Berger's disease)  Rapidly progressive glomerulonephritis  Proliferative glomerulonephritis  Secondary glomerulonephritis  Henoch-Schonlein purpura  Vasculitis
  • 20. INVESTIGATIONS  Urine dipstick and send sample to lab  Urine microscopy – red cell casts  Bloods – the usual plus renal screen  Immunoglobulins, electrophoresis, complement (C3, C4) autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM); blood culture; ASOT (anti-streptolysin O titre)  Renal ultrasound  Renal biopsy
  • 22. Management  Conservative  Monitor U&E, BP, fluid balance, weight  Salt and fluid restriction  Treat underlying cause  Medical  Diuretics  Treat hypertension  Corticosteroids/immunosuppression  Dialysis  Surgical  Renal transplant
  • 23. PROGNOSIS  Varies  Post-infectious usually self-resolving (95% recover renal function)  Others are a bit more nasty
  • 26. SUMMARY  Nephrotic syndrome = MASSIVE proteinuria  Nephritic syndrome = haematuria/red cell casts  May be a mixed presentation  New oedema? Dipstick that urine!  Haematuria? Exclude malignancy!