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Medicine (Year 5) > Renal (Glomerulonephritis) > Flashcards

Renal (Glomerulonephritis) Flashcards

1
Q

Nephritis and glomerulonephritis

A

Nephritis describes damage to the kidneys due to inflammation.

Glomerulonephritis describes nephritis involving the glomerulus.

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2
Q

structure of the glomerulus

A

Ultrafiltration occurs at the glomerulus. Liquid and small molecules need to pass through 3 layers to enter the nephron tubules:

1) The capillary endothelium:

  • Allows fluid, plasma proteins, and large substances through
  • Does not allow red or white blood cells and some proteins through

2) The glomerular basement membrane:
- Allows fluid and solutes through
- Does not allow intermediate-large substances including some proteins through

3) The epithelium of the Bowman’s capsule (made of podocytes):

  • Allows fluid and small solutes through
  • Does not allow large molecules such as proteins through

These three layers filter the blood with each layer preventing increasingly large substances from passing through into the nephron tubule. Overall, cells (such as red blood cells or white blood cells) and large proteins are not passed through.

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3
Q

nephritic vs nephrotic sydrome : location of disorder

A

1) Nephritic syndrome describes the signs and symptoms generally seen due to dysfunction of the capillary endothelium. This usually refers to severe and acute presentations of glomerulonephritis.

2) Nephrotic syndrome describes the signs and symptoms generally seen due to the dysfunction of podocytes. It is less associated with inflammation.

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4
Q

summary of nephritis vs nephrotic syndrome

A

Nephrotic syndrome
Active urine sediments with or without renal insufficiency, with nephrotic range proteinuria (>3g in 24hrs)

  • Diabetes
  • Minimal changes disease
  • Membranous
  • FSGS (focal segmental glomerular sclerosis)
    amyloid

Nephritic syndrome
Active urine sediments with or without renal insufficiency, with mild proteinuria – blood in urine

  • IgA nephropathy
  • Lupus
  • Mesangial proliferative glomerulonephritis
  • Vasculitis
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5
Q

Nephrotic syndrome overview

A

Damage and dysfunction of the podocytes can lead to a loss of protein in the urine. As mentioned above, the podocytes are the ‘last line’ of filtration where large molecules such as proteins are prevented from entering the nephron tubule. Nephrotic syndrome is defined as:

  • Proteinuria (>3.5 g/24hr)
  • Hypoalbuminaemia
  • Oedema

Other features that may also be seen include:

  • Hyperlipidaemia
  • Hypercoagulability
  • Immunodeficiency
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6
Q
A
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7
Q

presentation of nephrotic syndrome

A
  • Swollen e.g. periorbital and oedema
  • Proteinuria >3 g in 24s hours
  • Low serum albumin
  • Hyperlipidaemia
  • Hypercoagulable state
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8
Q

cause of nephrotic syndrome

A

In children
- 90% minimal change disease

In adults
- Minimal change
- Membranous nephropathy
- Focal segmental glomerulosclerosis (35%)
- Membranoproliferative glomerulonephritis
- Amyloid

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9
Q

Pathophysiology of minimal change

A

Where podocyte become effaced -> losing the ability to control the amount of protein leaked into the urine

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10
Q

management of nephrotic syndrome

A

Oedema

  • Diuretics, need large doses and may need to be I.v. if gut oedema
  • Salt and fluid retention

ACE-i

  • Anti-proteinuria but caution if intravascularly deplete or if renal function deteriorating acutely

Hypercholesterolaemia

  • Atherogenic if long-term nephrotic
  • Life style advice and statins

Treat underlying condition

  • Steroids for Minimal change disorder, underlying cause of disease
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11
Q

Diabetic nephropathy (DN)

A

describes a chronic reduction in kidney function associated with diabetes mellitus. It is characterised by proteinuria and a progressive reduction in the estimated glomerular filtration rate (eGFR). It generally occurs around 5-10 years after the onset of diabetes mellitus and can lead to chronic kidney disease (CKD).

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12
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A
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13
Q

screening for diabetic nephropathy

A

Since the predominant feature in DN is proteinuria, and many patients may be asymptomatic, all patients with both type 1 or type 2 diabetes mellitus should be screened annually with a urinary albumin:creatinine ratio (ACR). An ACR ≥3 mg/mmol is considered clinically significant.

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14
Q

management of diabetic nephropathy

A
  • Optimise control of diabetes mellitus
  • If ACR ≥3 mg/mmol: ACE inhibitor or angiotensin-II receptor blocker (ARB): slows progression
  • If ACR ≥30 mg/mmol: ACE inhibitor/ARB and offer dapagliflozin if relevant eGFR thresholds are met
  • Consider adding dapagliflozin to ACE inhibitor/ARB if ACR between 3-30 mg/mmol and relevant eGFR thresholds are met
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15
Q

Minimal change disease (MCD)

A

is the most common form of nephrotic syndrome in children. Its exact pathogenesis is unclear and immunofluorescence and light microscopy testing on biopsies showed no or minimal changes, hence MCD’s name. However, with electron microscopy, a diffuse loss of podocytes is seen, explaining proteinuria and the development of nephrotic syndrome.

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16
Q

RF MCD

A
  • Leukaemia – MCD is associated with leukaemia
  • Hodgkin’s lymphoma (HL) – MCD is associated with HL and may be the initial presenting symptom in some
  • Recent viral illness – a dysregulated immune system is thought to play a role in MCD
17
Q

management of MCD

A

Most cases are responsive to steroids, therefore oral corticosteroids are first-line. Other options include:

Cyclophosphamide or ciclosporin if corticosteroids are ineffective

18
Q

investigations for MCD

A

urinalysis
- proteinuria
- no signif haematuria

Urine microscopya nd culutre
- to rule out UTI

UEs
- urea and creatinine gernally normal
- eGFR normal

Serum albumin
- low

Serum lipids
- hypercholesterol

C3 and C4
- to rule out immune complex glomerulonephritis

LFT
- to rule out liver disease

Renal US
- structural abnormality

Kidney biopsy
- not generally performed in childer because MCD is so likely

19
Q

complications of MCD

A

Infection:
Due to urinary loss of immunoglobulins or immunosuppressive treatment

Thrombosis:
Due to the loss of antithrombin III in the urine

20
Q

treatment for most causes of nephrotic syndrome

A
  • steroids
  • blood pressure management
21
Q

nephritic syndrome overview

A

Inflammation leads to damage to the capillary endothelium. As mentioned above, this layer prevents the leakage of red blood and white blood cells into the nephron tubules. Nephritic syndrome is defined as:

Active urine sediments e.g. blood with or without renal insufficiency with mild proteinuria <3 g per 24 hr

A triad of:

  • Haematuria
  • Reduction in GFR (renal impairment / oliguria)
  • Hypertension

Other features

  • 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
22
Q

causes of nephritic syndrome

A
  • Anti-glomerular basement membrane disease (Goodpastures syndrome)
  • IgA nephropathy (most common form)
  • Post streptococcal glomerulonephritis
  • Lupus
  • Mesangial proliferative glomerulonephritis
  • Vasculitis e.g. Granulomarosis with polyangiitis
23
Q

Management of nephritic syndrome

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)
24
Q

IgA nephropathy

A

Also known as Berger’s disease, IgA nephropathy describes the clinical manifestations of immunoglobulin A (IgA)-containing immune complex deposits in the mesangium of the glomerulus (type III hypersensitivity). It is closely related to IgA vasculitis (Henoch–Schönlein purpura), which can be thought of as the systemic form of IgA nephropathy. Its pathogenesis is not fully understood.

Most patients with IgA nephropathy present with recurrent haematuria following an upper respiratory tract infection (URTI) or gastroenteritis. Less than 10% of patients may present with rapidly progressive glomerulonephritis (RPG).

25
Q

risk factorys for IgA nephropathy

A

Risk Factors

1) Recent URTI or gastroenteritis

  • Thought to be due to mucosal immune system dysfunction, as IgA plays a key role in the immune function of mucous membranes

2) IgA vasculitis

  • May cause kidney disease

3) Chronic liver disease

  • Thought to be due to impaired hepatic IgA clearance
26
Q

presentation of IgA nephropathy

A

Patients classically present with recurrent episodes of macroscopic (usually painless) haematuria following a URTI or gastroenteritis. Other features include:

  • Asymptomatic microscopic haematuria
  • Proteinuria – uncommon and usually very small amounts, not enough to cause nephrotic syndrome
  • Features of nephritic syndrome – rare
27
Q

IgA vasculitis vs IgA nephropathy

A

Ig A vasculitis (Henochs-Schonlein pupura) may cause kidney disease

IgA vasculitis has characteristic symptoms of a purpuric rash, abdominal pain, and joint pain, whereas IgA nephropathy does not
Although both have similar histopathological findings, evidence of IgA-containing immune complex deposition outside of the kidneys suggests IgA vasculitis

28
Q

management of IgA nephropathy

A
  • ACEi or ARB
  • if proteinuria >3.5g/day - treat as minimal change with corticoisteroids
29
Q

post-streptococcal glomuerlonephritis

A

type III hypersensitivity reaction characterised by the deposition of immune complexes consisting of complement C3 (C3) and immunoglobulin G (IgG) in the glomeruli leading to glomerulonephritis.

PSGN generally presents with an acute nephritic syndrome 1-2 weeks following infection with group A Streptococcus species (GAS), particularly Streptococcus pyogenes. It is usually self-limiting within 2-4 weeks.

30
Q

presentation of post-streptococcal glomerulonephritis

A

Patients may present with an acute nephritic syndrome 1-2 weeks following infection with GAS:

  • Proteinuria
  • If severe enough, this can lead to oedema which can lead to complications of fluid overload such as pulmonary oedema
  • Haematuria
  • Hypertension
  • Oliguria
31
Q

management of post-streptococcal glomerulonephritis

A
  • Antibiotics – if there is evidence of a GAS infection
  • ACE inhibitors – may be required to control blood pressure
  • Haemodialysis may be needed in some cases
32
Q

complications of post-streptoccocal

A
  • Fluid overload and its consequences (e.g. pulmonary oedema)
  • Hypertensive encephalopathy – if severe hypertension develops
  • Acute kidney injury (AKI)
  • Chronic kidney disease (CKD)
33
Q

goodpastures syndrome (anti-glomerular basement membrane disease)

A

is a type of rapidly progressive glomerulonephritis (RPG) characterised by the presence of autoantibodies against the alpha-3 chain of type IV collagen which is mostly found in the basement membranes of the glomerulus and alveoli.

34
Q

Goodpastures RF

A

HLA-DRB1*1501 or HLA-DR4
Smoking

35
Q

goodpastures presentation

A

Due to the presence of anti-GBM antibodies against type IV collagen found in the lungs and glomeruli, patients may present with:

**Pulmonary haemorrhage **– haemoptysis

Nephritic syndrome and RPG:
* Haematuria
* Proteinuria
* Oliguria
* Hypertension

Other features:
* Anaemia secondary to pulmonary haemorrhage
* Constitutional symptoms (e.g. fever, fatigue, malaise, weight loss)

36
Q

investigations for goodpastures

A

Investigations

Urea and electrolytes (U&Es):
Abnormal

Anti-GBM titres:
Positive, but may sometimes be negative

Renal biopsy:
* May show crescenteric glomerulonephritis, suggesting RPG
* May show IgG deposits along the basement membrane

37
Q

management of goodpastures

A
  • Removal of circulating anti-GBM antibodies: plasmapheresis
  • Stop further production of anti-GBM antibodies: immunosuppressants (e.g. corticosteroids with cyclophosphamide)
  • Managing end-stage kidney disease if appropriate with haemodialysis or renal transplantation
38
Q

complications of goodpastures

A

Pulmonary haemorrhage

  • Potentially fatal and more common in patients who smoke
  • Patients should be offered help with smoking cessation if appropriate

Chronic kidney disease (CKD)

  • Damage due to inflammation can leave residual renal damage and hence, CKD

Medicine (Year 5) (34 decks)

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