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Paediatrics > Nephrology part 1 > Flashcards

Nephrology part 1 Flashcards

1
Q

What are the functions of the kidneys?

A 
○ Waste handling 
- Urine
- Creatinine 
○ Water handling 
○ Salt balance 
- Sodium
- Potassium 
- Calcium 
- Phosphate 
○ Acid base control
- Bicarbonate
○ Endocrine
- Red cells- Erythropoietin 
- Blood pressure- renin aldosterone angiotensin system
- Bone health- PTH, activation of vitamin D
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2
Q

What are the two main presentations of nephrology?

A

○ Haematuria

○ Proteinuria

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3
Q

In glomerulonephropathy what does blood and protein dictate?

A
  • clinical presentation

- sugersted diagnosis

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4
Q

What are the two main signs of nephritic syndrome?

A
  • Increasing haematuria

- Intravascular overload

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5
Q

What are the two main signs of nephrotic syndrome?

A
  • Increasing proteinurea

- Intravscular depletion

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6
Q

How common are aquired glomerulopathy and congenital glomerulonephropathy?

A

Acquired- common

Congential- rare

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7
Q

Which componants are affected in acquired glomerulopathy?

A
  • Epitherlial cell (podocyte)
  • Basement membrane
  • Endothelial cell
  • Mesangial cell
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8
Q

What acquired glomerulopathies cause epithelial cells to be damaged?

A

□ Minimal change disease
□ FSGS (Focal segmental glomerulosclerosis)
□ Lupus
□ Congenital nephrotic syndrome

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9
Q

What acquired glomerulopathies cause the basement membrane to be damaged?

A
  • membranous glomerulopathy
  • MPGN (Membranoproliferative glomerulonephritis )
  • post infectious glomerulonephritis (PIGN)
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10
Q

What acquired glomerulopathies cause endothelial cells to be damaged?

A

□ Infection associated glomerulonephritis (PIGN)
□ Haemolytic Uraemic syndrome (HUS)
□ Membranoproliferative glomerulonephritis (MPGN)
□ Lupus
□ Thin basement membrane

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11
Q

What acquired glomerulopathies cause mesangial cells to be damaged?

A

□ HSP (Henoch-Schonlein purpura )
□ IgA nephropathy
□ Lupus

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12
Q

What are the layers involved in congenital glomerulonephropathy?

A
  • podocyte cytoskeletal integrity
  • Basement membrane proteins
  • Endothelial/ microvascular integrity
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13
Q

What is the definition of nephrotic syndrome?

A

Nephrotic range proteinuria results in hypalbuminaemia which results in oedema

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14
Q

How is proteinurea tested for?

A 
□ Dipstix
® Give concentration
® >/=3+ usually abnormal
® False positives
® False negative
□ Protein creatinine ration (practical)
® Early morning urine (best)
◊ Normal Pr:Cr ration <20mg/mmol
◊ Nephrotic range >25mg/mmol
□ 24 hour urine collection (gold standard)
® Normal <60mg/m^2/24 hours
® Nephrotic range >1g/m^2/24 hours
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15
Q

How is nephrotic syndrome diagnosed?

A
  • Oedema
  • Proteinuria
    □ Urine dipstix
    ® Protein 3+
    ® Blood 2+ blood (not frank)
    □ Protein creatinine ration- 1200mg/mmol creatinine
    □ Urine Na- 10
  • Bloods
    □ Albumin low 12mg/dl
    □ Normal creatinine- n the most common type
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16
Q

What are the typical features of minimal change disease?

A 
□ Age 1-10 but most commonly 2-5 years
□ Normal blood pressure
□ Resolving microscopic haematuria
□ Normal renal function
□ Steroid responsive
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17
Q

What are the atypical features of minimal change disease?

A

□ Suggestion of autoimmune disease
□ Abnormal renal function
□ Steroid resistance
□ Only if atypical consider biopsy

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18
Q

What is the treatment of typical minimal change disease?

A

Prednisolone for 8 weeks

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19
Q

What are the side effects from high dose corticosteroids in children?

A

□ Varicella status (infection)
□ Pneumococcal vaccination
□ Behaviour
□ Hypertension

20
Q

What is the pathogenesis of minimal change disease?

A
  • Interactions between lymphocytes (T and B cells) and podocytes
  • This is reversable with prednisolone
21
Q

What are the outcomes of minimal change disease?

A
  • 95% remission in 2-4 weeks
  • 80% relapse
    □ 50% frequent
  • 80% long term remission
22
Q

What are the second line immunosuppressions in minimal change disease?

A

Levamisole, Cyclosporin, Tacrolimus, mycophenolate mofetil, Rituximab

23
Q

Give an example of an aquired steroid resistant nephrotic syndrome?

A
  • Focal segmental glomerulosclerosis (FSGS)
    □ Podocyte loss
    □ Progressive inflammation and sclerosis
24
Q

Give examples of congenital steroid resistant nephrotic syndrome?

A
  • Infant presentations
  • NPHS1- nephrin
  • NPHS2- podocin
  • Podocyte loss
25
Q

What is the treatment of steroid resistant nephrotic syndrome?

A

Levamisole, Cyclosporin, Tacrolimus, mycophenolate mofetil, Rituximab

26
Q

When should you investigate macroscopic haematuria?

A
  • Always abnormal

- Investigate

27
Q

When should you investigate microscopic haematuria?

A
  • Investigate
    □ >trace on 2 occasions
  • Haemoglobinuria
    □ Stix positive + microscopy negative
28
Q

What are the common causes of macroscopic haematuria?

A 
□ Glomerulonephritis 
® Post infection GN 
® IGS/HSP
□ UTI (dysuria) 
□ Trauma 
□ Stones (pain)
29
Q

What are the common causes of microscopic haematuria?

A 
□ Glomerulonephritis 
® Post infection GN
® IGA/ HSP
□ UTI 
□ Trauma
□ Stones/ hypercalciuria
30
Q

What is nephritic syndrome?

A 
○ Clinical diagnosis
- Describes glomerulonephritis 
○ Haematuria and proteinuria 
○ Reduced GFR
- Oliguria 
- Fluid overload
□ Raised JVP
□ Oedema 
- Hypertension
- Worsening renal failure= rapidly progressing GN
○ Intrarenal cause of acute kidney injury (AKI)
31
Q

What are the causes of glomerulonephritis?

A 
○ Post infectious GN
○ HSP/ IgA nephropathy 
○ Membranoproliferative GN
○ Lupus nephritis 
○ ANCA positive vasculitis
32
Q

What causes post infectious glomerulonephritis?

A 
○ Age of onset
○ Cause
- Usually group A strep 
- Beta haemolytic 
- Site				                               □ Throat 7-10 days
□ Skin 2-4 weeks
33
Q

How is post infectious glomerulonephritis diagnosed?

A
  • Bacterial culture
  • Positive ASOT (anti streptolysin O titre)
  • Low C3 normalises
  • Remember
34
Q

What is the differential diagnosis of post infectious glomerulonephritis?

A

® IgA
® Lupus
® MPGN

35
Q

What is the treatment for post infectious glomerulonephritis?

A
  • Self limiting
  • Antibiotic: penicillin
  • Support renal functions
  • Overload/ hypertension
    □ Diuretics
36
Q

What is the outcome of post infectious glomerulonephritis?

A

Not recurrent?

37
Q

What is IgA nephropathy?

A

○ Most common glomerulonephritis
○ 1-2 days after URTI
○ Usually in older children and adults

38
Q

What is the clinical picture of IgA nephropathy?

A

> Recurrent macroscopic haematuria
+/- chronic microscopic haematuria
Varying degree of proteinuria

39
Q

How is IgA npehropathy diagnosed?

A
  • Clinical picture
    □ Negative autoimmune workup
    □ Normal compliment
  • Conformational biopsy
40
Q

What is the treatment of IgA nephropathy?

A
  • Mild disease
    □ Proteinuria with ACEi
  • Moderate to severe disease
    □ Immunosuppression (KDIGO)
41
Q

What is the outcome of IgA nephropathy?

A
  • Variable
  • 25% ESFR by 10 years post diagnosis
  • Outcome better in children?
42
Q

What is Henoch Scholein purpura?

A

○ IgA related vasculitis
○ Age of onset: 5-15 years
○ Non streptococcal post infectious GN

43
Q

How is Henoch Scholein purpura diagnosed?

A 
○ Clinical diagnosis
- Mandatory palpable purpura  
- One of 4
□ Abdominal pain
□ Renal involvement 
□ Arthritis or arthralgia 
□ Biopsy 
® IgA deposition
44
Q

What can trigger Henoch Scholein purpura?

A
  • Viral URTI in 70%

- Streptococcus, drugs

45
Q

When do symtoms start happening in Henoch Scholein purpura?

A

1-3 days post trigger

46
Q

How long do symptoms last in Henoch Scholein purpura?

A

> 4-6 weeks

> 1/3 relapse

47
Q

What is the treatment of Henoch Scholein purpura?

A 
- Symptomatic
□ Joints. Gut
- Glucocorticoid therapy 
□ Not helpful in mild nephritis 
□ May help with GI involvement 
- Immunosuppression 
□ Trial in moderate to severe renal disease 
- Long term
□ Hypertension and proteinuria screening

Paediatrics (13 decks)

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