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Semester 3 - urinary > 6. Nephritic and nephrotic conditions > Flashcards

6. Nephritic and nephrotic conditions Flashcards

1
Q

How can glomerular diseases be classified

A

Heridtary
Primary: disease process originates from the glomerulus
Secondary to systemic disease: systemic lupus erythematosus, diabetes mellitus, bacterial endocarditis

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2
Q

What do glomerular diseases result in?

A

inflammation of glomerulus - Glomerulonephritis

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3
Q

What 4 clinical structures within glomerulus are prone to damage?

A
  • Capillary endothelial cell lining
  • Glomerular basement membrane
  • Mesangium supporting the capillaries
  • Podocytes on the outer surface of the capillary
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4
Q

What if glomerular disease is long lasting or left untreated?

A

Progresses to CKD

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5
Q

What is characteristic of nephrotic syndrome?

A

Proteinuria (> 3.5g/day)

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6
Q

What are the secondary effects of proteinuria in nephrotic syndrome? Why do these occur?

A

Hypoalbuminaemia causing:

  • Oedema: lower capillary oncotic pressure
  • Hyperlipidaemia: due to increased hepatic lipoprotein synthesis, secondary to protein loss
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7
Q

What allows proteinuria in nephrotic syndrome?

A

Podocyte damage, leading to increased pore size and a disruption of glomerular basement membrane charge barrier, hence allowing albumin to exit

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8
Q

How is nephrotic syndrome managed?

A

• Oedema
– Diuretics, need large doses and may need to be i.v. if gut oedema
– Salt and fluid restriction
• ACE-Inhibitor
– Anti-proteinuric but caution if intravascularly deplete or if renal function deteriorating acutely
• Hypercholesterolaemia
– Atherogenic if long-term nephrotic
• Treat underlying condition
– e.g. steroids for MCD, underlying cause of disease (e.g.amyloid)
• Blood pressure control
• Anticoagulation if hypercoaguable (risk of thrombosis increases as albumin decreases)

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9
Q

Why may anticoagulation be required for management of nephrotic syndrome?

A

As albumin decreases, the risk of thrombosis increases

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10
Q

What is the triad of nephrotic syndrome?

A
  • Proteinuria
  • Hypoalbuminaemia
  • Oedema
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11
Q

What is nephritic syndrome usually accompanied by nephrotic syndrome and why?

A

high cholesterol as liver tries to compensate for hypalbuminaemia by producing more albumin and cholesterol made as a by product

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12
Q

What other features may be present with nephrotic syndrome>

A
  • BP often normal (can be low or high)
  • Creatinine may be normal
  • Proteinuria > 350 mg/ mmol alone = nephrotic range proteinuria
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13
Q

Which types of primary renal disease can cause nephrotic syndrome?

A
  • Minimal change disease
  • Membranous glomerulonephritis
  • Focal segmental glomerulosclerosis
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14
Q

Which types of secondary renal disease can cause nephrotic syndrome?

A
  • Systemic lupus erythematous
    Causing nephrotic syndrome but not glomerulonephritis:
  • Diabetes - most common cause
  • Amyloid
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15
Q

What is minimal change disease?

A

Most common cause of nephrotic syndrome in children under 6, resulting in damage and effacement of foot processes of podocytes

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16
Q

How does minimal change disease present?

A 
Foamy urine
facial and Periorbital swelling
peripheral and Pitting oedema
ascites
Possibly abdominal pain because of oedema in the gut mucosa (esp in children)
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17
Q

What causes nephrotic syndrome

A

podocyte damage leading to glomerular charge barrier disruption

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18
Q

How can you see the renal changes in minimal change disease?

A

Only on electron microscope, no significant changes visible under light microscope

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19
Q

How is minimal change disease treated?

A
  • Diuretics e.g. furosemide to help manage oedema
  • High-dose oral corticosteroids to reduce inflammation
  • May require additional supplements of vitamin das corticosteroids can reduce calcium absorption
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20
Q

How is the prognosis of minimal change disease?

A

Good in children, but many relapse after treatment

Variable w/ adults

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21
Q

What investigation can be done to confirm minimal change glomerulonephritis?

A

only way to confirm is renal biopsy but in children with nephrotic syndrome, minimal change is most likely diagnosis so risks of biopsy are generally considered to outweigh the potential diagnostic benefit.

22
Q

What is membranous glomerulonephritis?

A

Subepithelial deposition of immune complexes causes thickening of the basement membrane and subsequently larger fenestrations/filtration slits

23
Q

Causes of membranous glomerulonephritis

A 
Most idiopathic
Primary type - immune complexes
Infections - syphilis, malaria, hep B
Tumours
Drugs - heroin, mercury
SLE
24
Q

How is membranous glomerulonephritis treated?

A

Immunosuppressants

Treating underlying cause

25
Q

What causes primary FSGS?

A

Idiopathic

26
Q

What causes secondary FSGS?

A

Sickle cell disease
HIV
Heroin abuse
Kidney hyperfusion

27
Q

How is FSGS treated?

A

Steroids

28
Q

What is focal segmental glomerulosclerosis?

A

Sclerosis of segments of some but not all glomeruli

29
Q

Briefly describe the pathophysiology of FSGS

A

Podocytes damaged
Proteins build up in glomerulus
Hyalinosis
Sclerosis

30
Q

What type of condition is diabetic nephropathy?

A

nephrotic condition

31
Q

Describe the pathophysiology of diabetic nephropathy

A
  • Excess glucose in blood binds to proteins. Especially at efferent arteriole.
  • Hyaline atherosclerosis – obstructs blood flow
  • Initially ↑GFR
  • Over time mesangial cells secrete more structural matrix
  • Thickening of BM
  • ↓GFR
32
Q

What is the treatment of diabetic nephropathy?

A

Hypertension, good glycemic control, ACE inhibitors, angiotensin receptor blockers

33
Q

What is nephritic syndrome?

A

inflammation disrupting glomerular basement membrane

34
Q

What is nephritic syndrome characterized by?

A

Triad of haematuria(microscopic or macroscopic), reduced GFR (so oliguria) and hypertension

35
Q

What are some other features of nephritic syndrome, other than the classic triad?

A
  • Often some proteinuria but less than nephrotic syndrome
  • Disruption of the endothelium results in inflammatory response & damage to the glomerulus
  • Onset may be acute or rapidly progressive (RPGN)
  • Rapidly Progressive / Crescentic GN - a fulminant form of nephritic syndrome
  • Fluid retention – seen as facial oedema
  • Uraemia
  • Patients may also complain of loin pain, headaches and general malaise
36
Q

What are some common causes of nephritic syndrome?

A
  • Goodpasture’s (Anti GMB)
  • Rapidly progressive GN
  • IgA Nephropathy (Berger’s Disease)
  • Post-streptococcal GN
37
Q

What is Berger’s disease?

A

IgA deposited in the mesangium, causing sclerosis of the damaged segment

38
Q

What is the most common primary glomerular disease which causes recurrent haematuria?

A

IgA Nephropathy/Berger’s disease

39
Q

What will be raised in berger’s disease

A

Hypertension and IgA levels raised

40
Q

How is Berger’s disease treated?

A

Controlling BP
Antihypertensives
Steroids

41
Q

What will 20% of patients with Berger’s disease go onto develop?

A

Advanced CKD

42
Q

What is rapidly progressive glomerulonephritis?

A

AKA crescentric glomerulonephritis

Inflammation in the glomerulus, leading to loss of renal function within days to weeks

43
Q

Describe the pathology in rapidly progressive glomerulonephritis

A

Severe glomerular injury, leading to leakage of fibrin and macrophages, and the proliferation of epithelial cells into crescent shaped masses which reduced the glomerular blood supply

44
Q

How is rapidly progressive glomerulonephritis treated? Give examples of the medications required

A

High dose steroids e.g. prednisolone
Immunosuppressants e.g. cyclophosphamide, rituximab
Plasma exchange - removing immune complexe

45
Q

What is post-streptococcal glomerulonephritis?

A

Nephrotic syndrome arising 1-3 weeks following the group A beta-haemolytic streptococcal infection of tonsils, pharynx or skin

46
Q

How is post-streptococcal glomerulonephritis treated?

A

Antibiotics for remaining infection

47
Q

What is the prognosis for post-streptococcal glomerulonephritis?

A

Excellent in children

60% of adults recover completely, rest develop hypertension or renal impairment

48
Q

What is Goodpasture’s syndrome?

A

Inflammation due to antibodies against type IV collagen in glomerular basement membrane, resulting in progressive glomerulonephritis, acute renal failure and lung haemorrhage

49
Q

Why is the lung affected in Goodpasture’s syndrome?

A

Has similar type of collagen to which the antibodies are against

50
Q

What is the treatment of Goodpasture’s syndrome? What is the prognosis like without treatment?

A

Treated with plasma exchange to remove antibodies and corticosteroids for the inflammation
Poor prognosis without treatment

51
Q

What can be a sign of proteinuria? Is this always a sign of it?

A

Frothy urine

Can be frothy for other reasons e.g. high volume of urine expelled quickly

52
Q

How is nephritic syndrome managed?

A

• Blood pressure control / reduction of proteinuria
– ACE-I or AIIR first line if renal function allows
– Salt restrict
• Treatment of oedema
– As for nephrotic syndrome if adequate renal function
• Disease specific treatments
– Generally immunosuppressants
– e.g. RPGN – prednisolone, cyclophosphamide or rituximab +/- plasma exchange
• Cardiovascular risk management
– Stop smoking, statin etc
• Dialysis (often short-term)

Semester 3 - urinary (33 decks)

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