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Nephrology Flashcards

1
Q

Glomerular disease causes what?

A

Nephrotic syndrome

Nephritic syndrome

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2
Q

AKI causes what?

A

HUS

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3
Q

How much blood is received through the kidneys?

A

Very high blood

25% CO / min

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4
Q

GFR in neonates compared to adults

A

20-30ml/min/1.73m2

So when dealing with neonates there is already compromised system

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5
Q

5 functions of the kidney

A 
Waste handling (urea, creatinine) 
Water handling 
Salt balance (Na, K, Ca, P)
Acid base control (bicarbonate)
Endocrine (red cells, BP, bone health)
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6
Q

What part of the glomerular filtration barrier is vulnerable to immune mediated injury?

A

The endothelial cell

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7
Q

Features of the endothelial cell of the glomerular filtration barrier

A

Fenestrated

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8
Q

Two proteins of the glomerular filtration membrane

A

Type IV collagen (COL4)

Laminin

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9
Q

How is the glomerular filtration membrane synthesised?

A

From

  • podocytes
  • endothelial cells
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10
Q

Functions of mesangial cells

A

Glomerular structural support
Embedded in GBM
Regulates blood flow of glomerular capilaries

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11
Q

Presentation of glomerulopathy

A

Haematuria

Proteinuria

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12
Q

Indications towards nephritic syndrome

A

Increasing haematuria

Intravascular overload

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13
Q

Indications towards nephrotic syndrome

A

Increasing proteinuria

Intravascular depletion

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14
Q

Pathology of acquired glomerulopathy

A

White component affected

  • epithelial cell (podocyte) - Minimal change disease, FSGS, lupus
  • Basement membrane - membranous glomerulopathy, MGPN, PIGN
  • Endothelial cell - HUS, MPGN, lupus, infection associated glomerulonephritis (PIGN)
  • mesangial cell - HSP, IgA nephropathy, lupus
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15
Q

Is acquired glomerulopathy common?

A

Yes

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16
Q

Is congenital glomerulopathy common?

A

No - it is rare

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17
Q

Layers involves in congenital glomerulopathy

A

Podocyte skeletal integrity
Basement membrane proteins
Endothelial / microvascular integrity

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18
Q

Presentation of nephrotic syndrome

A 
3 - 4 days
Nephrotic range proteinuria 
Frothy urine 
Blood in urine - not usually frank 
Hypoalbuminaemia 
Swollen face which is worse in the morning 
One eye closed in the morning 
Oedema
- Periorbital 
- legs (pitting)
- Ascites
- small pleural effusions 
Well but pale 
Weight up from baseline
BP can be raised  
Normal creatinine 
Protein creatinine ratio >250mg/mmol 
High levels of fat / lipids in the blood
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19
Q

Pathology of nephrotic syndrome

A

Interaction between lymphocytes (T and B cells) and podocytes
Loss of size and charge barrier of the GFB
Oncotic (Osmotic) vs hydrostatic
Protein (osmotic) = magnet to water

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20
Q

Can nephrotic syndromes have FH?

A

yes

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21
Q

How do you test for proteinuria?

A

Dipstix
- gives concentration ; > 3+ usually abnormal
Protein creatinine ratio
- > 250 = nephrotic
24 hour urine collection (gold standard)
- normal < 60mg/m2/24hrs
- nephrotic = >1g/m2/24 hours in children

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22
Q

Normal protein creatinine ratio

A

< 20mg/mmol

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23
Q

Nephrotic range for protein creatinine ratio

A

> 250 mg/mmol

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24
Q

What is the gold standard investigation for proteinuria?

A

24 hour urine collection

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25
Q

Treatment of nephrotic syndrome

A

Prednisolone for 8 weeks

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26
Q

S/Es of prednisolone

A 
Behaviour (irritable, moody, dont sleep)
High BP
Facial change
Growth (only if recurrent courses)
GI distress
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27
Q

Other considerations when treating nephrotic syndrome

A

Varicella status and pneumococcal vaccination as both act as immunosuppressants

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28
Q

What indicates minimal change disease/

A

Response to steroids

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29
Q

If steroid resistance / dependent when treating nephrotic syndrome, what does this indicate?

A

maybe not dealing with minimal change disease

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30
Q

Presentation of minimal change disease

A 
Resolving microscopic haematuria 
Proteinuria 
Oedema 
Weight gain 
Normal renal function 
Normal BP 
Atypical features
- suggestions of autoimmune disease
- abnormal renal function 
- steroid resistance 
Nephrotic syndromes
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31
Q

What age gets minimal change disease?

A

2 - 5 y / o

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32
Q

What presentation in minimal change disease would make you consider a renal biopsy?

A

Atypical features

  • suggestions of autoimmune disease
  • abnormal renal function
  • steroid resistance
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33
Q

Prognosis of Nephrotic syndrome

A

Remission 95% in 2 - 4 weeks
relapse 80%
- 50% frequent - 2 in 6 or 4 in a year
80% long term remission

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34
Q

If really frequent recurrences of nephrotic syndrome, what may be the problem?

A

Prednisolone toxicity

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35
Q

Acquired steroid resistant nephrotic syndrome condition and its pathology

A

Focal Segmental Glomeruloscerosis (FSG)

  • podocyte loss
  • progressive inflammation and sclerosis
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36
Q

What type of haematuria should always be investigated?

A

Macroscopic

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37
Q

When is microscopic haematuria investigated?

A

> trace on 2 occasions

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38
Q

Important causes of macroscopic haematuria

A 
Glomerulonephritis
Post infect GN
IGA / HSP 
UTI (dysuria)
Trauma 
Stones (pain)
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39
Q

Important causes of microscopic haematuria

A 
Glomerulonephritis 
Post infect GN
IGA / HSP 
UTI 
Trauma 
Stones / hypercalciuria
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40
Q

Symptoms of nephritic syndrome

A 
Haematuria 
Reduced GFR
oliguria 
fluid overload 
- raised JVP
- oedema
HTN
Worsening renal failure - rapidly progressive FN
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41
Q

What is nephritic syndrome an intrarenal cause of?

A

AKI

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42
Q

Causes of glomerulonephritis

A 
Post infectious GN
HSP / IgA nephropathy 
Membranoproliferative GN
Lupus nephritis 
ANCA positive vasculitis
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43
Q

Investigations of nephritic syndrome

A 
Renal USS 
Chase the most likely diagnosis
- ASOT 
- throat swabs 
- complement tests 
ANA, ANCA testing 
Biopsy 
- not needing when have a secure diagnosis
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44
Q

Age of onset of acute post infectious glomerulonephritis

A

2 - 5

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45
Q

Causes of acute post infectious glomerulonephritis

A

Usually group A strep
- beta haemolytic so completely haemolysis
Post throat infection 7-10 days
Post skin infection 2 - 4 weeks (impetigo common)

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46
Q

Investigations of acute post infectious glomerulonephritis

A

Bacterial culture
positive ASOT
Low C3 normalises

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47
Q

Prognosis of acute post infectious glomerulonephritis

A

Self limiting
good prognosis
can have haematuria for 1 - 2 years after but the function will improve

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48
Q

How does a e.g. Group A strep cause an AKI?

A

Nephrogenic antigens on the strep
Bind specific sites in the glomerulus
Also antibodies bind Ag forming circulating complexes with deposits in the kidney
Set up a humeral and cellular immune response
Activates alternative compliment pathway
—> AKI

49
Q

Treatment of acute post infectious glomerulonephritis

A

Antibiotics for infection
Support renal functions
Overload / HTN
- diuretics

50
Q

If post infectious glomerulonephritis is recurrent, what does this indicate?

A

It is not the right diagnosis

51
Q

What is the most common glomerulonephritis?

A

IgA nephropathy

52
Q

When does IgA nephropathy occur?

A

1 - 2 days after URTI

53
Q

Who gets IgA nephropathy?

A

Older children

Adults

54
Q

Genetics of IgA nephropathy

A

Genetic predisposition

- galactose deficient IgA

55
Q

Presentation of IgA nephropathy

A

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

56
Q

Diagnosis of IgA nephropathy

A

Clinical picture
Negative autoimmune workup
Normal complement
Confirmation biopsy

57
Q

Treatment of IgA nephropathy

A

Mild disease = ACEIs

Moderate to severe = immunosuppression (KDIGO)

58
Q

Prognosis of IgA nephropathy

A

25% ESRF by 10 years post diagnosis

Outcome better in children

59
Q

Age of onset of HSP IgA related vasculitis

A

5 - 15 years

60
Q

Presentation of HSP IgA related vasculitis

A 
Mandatory PALPABLE PURPURA
1 of
- abdominal pain 
- renal involvement 
- arthritis or arthralgia 
- biopsy (IgA deposition)
61
Q

What is the most common childhood vasculitis?

A

IgA vasculitis

62
Q

What vessels does IgA vasculitis affect?

A

Small vessels

63
Q

When does IgA vasculitis occur?

A

1 - 3 days post trigger

64
Q

Triggers of IgA vasculitis

A

Viral UTI in 70%
Streptococcus
Drugs

65
Q

Duration of symptoms of IgA vasculitis

A

4 - 6 weeks
1 / 3rd relapse
- skin and kidney relapse

66
Q

Pathology of IgA vasculitis

A

Nephritis - mesangial cell injury

67
Q

Treatment of IgA vasculitis

A 
Symptomatic - joints, gut
Glucocorticoid therapy (not for renal disease, helps GI disease)
Immunosuppression
68
Q

Long term prognosis of IgA vasculitis and any screenings that are carried out

A

Very good

Hypertension and proteinuria screening

69
Q

Definition of AKI

A

Abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes

70
Q

Causes of AKI

A

Perfusion problem
- drugs
- renal artery stenosis
Intrinsic
- Glomerular disease (HUS, glomerulonephritis)
- Tubular injury (acute tubular necrosis as a consequence of Hypoperfusion or drugs)
- interstitial nephritis (NSAIDs, autoimmune)
Post renal
- obstructive

71
Q

Presentation of AKI

A

HUS
Anuria / oliguria (<0.5ml/kg/hr) for 8 hours
HTN with fluid overload
Rapid rise in plasma creatinine >1.5x age

72
Q

AKI warning score

A

AKI 1; measured creatinine >1.5-2x reference creatinine/ULRI
AKI 2; measured creatinine 2-3x reference creatinine/ULRI
AKI 3; serum creatinine >3x reference creatinine/ULRI

73
Q

Management of AKI (the 3Ms)

A 
Monitor 
- urine output
- PEWS 
- BP
- weight 
Maintain 
- good hydration 
Minimise
- further injury 
- particular with drugs
74
Q

What does PEWS stand for?

A

Paediatric Early warning score

75
Q

Long term consequences of AKI

A

BP
Proteinuria (has to be monitored)
Evolution to CKD

76
Q

When does HUS usually occur?

A

Post diarrhoea
- Entero-haemorrhagic E Coli
Either verotixin producing E coli or Shiga toxin

77
Q

Causes of HUS

A

Post diarrhoea
pneumococcal infection
drugs e.g. chemotherapeutic drugs
Congenital or acquired autoimmune processes

78
Q

How do toxins from bacteria cause HUS?

A

Toxins cross enterocytes and bind to white cells on the endothelium, causing endothelial damage calling an hypethrombic state causing haemolysis

79
Q

Triad of HUS

A
  1. microangiopathic haemolytic anaemia
  2. thrombocytopenia
  3. acute renal failure / AKI
80
Q

Presentation of HUS

A 
E coli 0157;H7 serotype 
Bloody diarrhoea
Neurological involvement 
- reduced consciousness
- seizures 
renal failure
81
Q

Where do you get E Coli 0157;H7?

A

Cattle

Sheep

82
Q

Period of risk of HUS after diarrhoea, and how many get HUS?

A

Up to 14 days after onset of diarrhoea

15 % develop HUS

83
Q

Management of HUS (3 Ms)

A 
Monitor (the 5 kidney functions)
- fluid balance
- electrolytes
- acidosis 
- HTN
- aware of other organs
Maintain 
- IV normal saline and fluid 
- RRT 
minimise 
- no antibiotics
84
Q

What does CAKUT stand for?

A

Congenital anomalies of the kidney and urinary tract

85
Q

Presentation of CAKUT

A

Reflux nephropathy
Dysplasia
Obstructive uropathy

86
Q

Hereditary chronic kidney diseases

A

Cystic kidney disease

Cystinosis

87
Q

What can CAKUT be associated to?

A

Turner
Trisomy 21
Bracio-oto-renal
Prune belly syndrome

88
Q

Presentation of CKD

A

Variable depending on which function is altered

  • bladder dysfunction
  • salt wasting (low P, K high)
  • renal tubular acidosis
  • waste handling
  • water handling
  • endocrine
89
Q

What is needed to diagnose a UTI

A

Clinical signs PLUS

Bacterial culture midstream urine

90
Q

Most common presenting symptoms of neonates with a UTI

A 
Fever
vomiting 
lethargy 
Irritability 
Poor feeding 
Failure to thrive
91
Q

Most common presenting symptoms of pre verbal children with a UTI

A

Fever
abdo / loin pain / tenderness
vomiting
poor feeding

92
Q

Most common presenting symptoms of verbal children with a UTI

A 
Frequency 
Dysuria 
Dysfunctional voiding 
Changes to continence 
Abdominal / loin  pain / tenderness
93
Q

Septic shock secondary to UTI is more common in who?

94
Q

How can a urine specimen be obtained in children?

A 
Normal social cleanliness - water
Clean catch urine or mid stream urine 
Collection pads or urine bags (easily contaminated)
Sick infants
- catheter samples
- suprapubic aspiration (USS)
95
Q

Suggestive tests of UTI

A 
Dipstix
- leucocyte esterase activity, nitries 
Microscopy
- pyuria > 10 WBC per cubic mm
- bacteria 
Culture > 10 5 colony forming units
- E coli
96
Q

Why worry about UTIs?

A

UTI, VUR and vulnerable kidneys can lead to scarring

97
Q

Treatment of UTI

A

lower tract
- 3 days oral Ax
upper tract / pyelonephritis
- antibiotics 7 - 10 days (oral if systemically well)

98
Q

Prevention of UTI

A

Hygiene
Constipation
Voiding dysfunction

99
Q

Indications to use imaging to investigate the renal tract

A 
Upper tract symptoms
 - temp > 38C
- vomiting 
- systemically unwell etc 
Younger
- younger you are = higher risk of renal dysplasia
100
Q

Renal imaging used

A

USS - first line
DMSA
Micturating cytourethrogram
MAG 3 scan

101
Q

Factors affecting the progression of CKD

A 
late referral 
HTN
Proteinuria
High intake of protein, phosphate and salt 
Bone health 
- PTH 
- P
- Vitamin D 
Acidosis
Recurrent UTIs
102
Q

What is used to investigate BP?

A

Doppler (gold standard < 5s)
Sphigmanomter
oscillometry

103
Q

Factors affecting BP

A

Sex
age
height

104
Q

Management of CKD

A 
Nutrition / protein intake 
- low K diet
- avoid hypercalcaemia
- reduce P in diet 
Give / restrict fluids 
Bicard if needed for acid base control 
Support for anaemia 
ACEIS
Bone health 
Bladder dysfunction
105
Q

Treatment for metabolic bone disease

A

Low phosphate diet
Phosphate binders
Active Vit D
If ongoing poor growth - growth hormone

106
Q

Why is metabolic bone disease involved with the kidneys?

A

The kidneys pee out phosphate
High phosphate - increases PTH
High PTH is associated with CVS in adults and IHD

107
Q

Types of cystic renal disease

A 
Simple
Developmental 
- dysplasia 
- multicystic dysplastic 
Genetic
- autosomal recessive (ARPKD)
- autosomal dominant (ADPKD)
- syndromic 
Acquired 
- cancer
108
Q

Pathology of multicystic dysplastic kidney (MCDK)

A

Non functioning kidney
ureteric atresia
Hypertrophy of normal collateral kidney - usually unilateral (75%)

109
Q

Pathology of ARPKD and potters sequences

A

Antenatally large bright kidneys

110
Q

Presentation of ARPKD and potters sequence

A 
Oligohydramnios
Severe respiratory distress
- pulmonary hyperplasia 
- nephromegaly mass effect
Potters sequence
- decreased amniotic fluid
- pulmonary hyperplasia 
- foetal compression of faces, contracture 
- bilateral renal agenesis (absent uteteric bud) 
- AR polycystic kidney disease 
Loss of function
111
Q

What is Renal cysts and diabetes (RCAD)?

A 
autosomal dominant glomerulocystic kidney disease
early onset DM (MODY)
US = cortical cysts 
Genetic heterogenecity 
= HNF1B mutations
112
Q

What is Alport syndrome?

A

Glomerular basement membrane disease

113
Q

Pathology of Alport syndrome

A

Collagen 4 abnormalities

X linked dominant inheritance

114
Q

Presentation of Alport syndrome

A 
Haematuria - micro and macroscopic 
Proteinuria 
HTN
deafness - high tone and senori neural loss 
Renal failure in early adult life (20-30 yrs) 
eye changes 
- lenticonous 
- macular changes in retina
115
Q

Investigation for renal scarring in a child with VUR

A

Radionucleotide scan using dimercaptosuccinic acid (DMSA)

116
Q

What does VUR look like on a micturating cystourethrogram?

A

Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity

117
Q

Features of an atypical UTI in children

A 
Seriously ill
Poor urine flow
Abdominal or bladder mass
Raised creatinine
Septicaemia
Failure to respond to treatment with suitable antibiotics within 48 hours
Infection with non E coli organisms
118
Q

Investigation to diagnose VUR

A

Micturating cystourethrogram

Paeds (28 decks)

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