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Paediatrics > Renal > Flashcards

Renal Flashcards

1
Q

GFR is most accurately evaluated in a clinical setting via what parameter?
A) serum creatinine
B) inulin clearance
C) creatinine clearance
D) plasma clearance of radio-isotope EDTA/DTPA or iohexal

A

Plasma disappearance of radio isotope EDTA/DTPA or iohexal

  • DMSA scan does not provide info on GFR clearance.. looks at parenchymal function, shows scarring if areas don’t light up
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2
Q

What is the Schwartz equation ? (Estimates GFR)

A

eGFR = 36.5 x height (cm) x creat (umol/L)

Not accurate in ESKD

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3
Q

Renin release from the juxtaglomerular cells is stimulated by:

A

Sodium depletion
Sympathetic stimulation
Reduced vagal stimulation

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4
Q

How do you differentiate between acute GN and nephrotic syndrome (minimal change disease)

A

Onset of oedema - acute vs gradual (GN acute)

Haematuria in nephritic

Hypertension - most acute GN present with HTN (not nephrotic)

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5
Q

The epithelial Na channel in the collecting duct is regulated by which hormone ?

A

Aldosterone

Blocked by amiloride

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6
Q

What are the 4 clinical features of glomerulonephritis?

A

Haematuria
Reduced GFR
Hypertension
Oedema (Na & H2O retention)

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7
Q

Which types of GN have low complement levels ?

A

Post-infectious
MPGN aka mesangiocapillary
SLE

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8
Q

What are the clinical clues pointing you towards IgA nephropathy or Alports/Thin Basement Membrane ?

A

“Synpharyngitic”
Gross haematuria
Family history

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9
Q

What is the most common cause of GN?

A

Post infectious GN

  • age 2-12
  • group A strep causing immune complex deposition
  • 7-14 days post throat; later after skin
  • low c3
  • recurrence rare
  • supportive management
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10
Q

What should you suspect with a history of episodes of gross haematuria at the same time as URTI??

A

IgA nephropathy

  • IgA deposition in mesangium
  • persistent microscopic haematuria
  • normal complement
  • can be progressive
  • can not tell difference with HSP on biopsy (same disease?)
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11
Q

What is the most common vasculitis of childhood?

A 
HSP 
Younger children 
1/3 recurrence 
Renal involvement can occur 2 months after initial illness - weekly urine protein checks 
Early steroids not shown to reduce future renal involvement 
Treatment: 
Steroids, azathiprine
RPGN: cyclophosphamide
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12
Q

What should you suspect with: adolescent girl, Indian/Maori/Pacific Islander
Low WCC
Low C3/C4
Haematuria/proteinuria

A

Lupus nephritis

  • commonest presentation of SLE
  • renal biopsy to determine class and treatment
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13
Q

What should you suspect with boy, haematuria & proteinuria with family history ?
Haematuria with URTI, persistent microscopic haematuria
Sensorineural hearing loss

A

Alports
X linked mutation of type 4 collagen (basement membrane)
Dx Electron miscroscopy of biopsy
Can progress to ESKD
Treatment with ACEI aims to delay progression - the earlier the better

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14
Q

What should you suspect for
Microscopic haematuria
Macro haematuria with URTI
Family members with micro haematuria

A

Thin basement membrane disease (aka benign familial haematuria)
Autosomal dominant
Can actually progress therefore not totally benign

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15
Q

What are the causes of Rapidly progressive GN?

What is the defining feature on biopsy ?

A

HSP
ANCA disease
Goodpastures (anti GBM)

Presence of crescents (clumps of epithelial tissue within Bowman’s capsule)

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16
Q

How do you differentiate between the ANCA assoc small vessel vasculotides (Wegeners vs MPO)

A

Wegeners
C ANCA pos
Granulomas in resp tract & kidneys

Both progress to RPGN
Treatment strong immunosuppression
Plasmaphoresis (if pulmonary haemorrhage)

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17
Q

What should you suspect with pulmonary and kidney involvement - pulmonary haemorrhage & crescentic nephritis
Anti GBM on serology ?

A

Goodpastures (aka pulmonary renal syndrome)
Caused by autoimmune complex (anti GBM) deposition in GBM
Treatment steroids, plasmapharesis, cyclophosphamide
Doesn’t recur

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18
Q

Which types of GN have family history?

A

Alports (boys)
TBM
IgA

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19
Q

What are the defining clinical features of nephrotic syndrome?

A

Proteinuria
Hypoalbuminaemia (<25g/L)
Oedema
Hyperlipidemia

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20
Q

What are the causes of nephrotic syndrome ?

A

Idiopathic (MCD 70%, FSGS, MPGN)
Hep B
Systemic inflammatory diseases (lupus, HSP)
Part of a syndrome (Denys drash, nail patella, Frasier, Pierson)

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21
Q

How do you define remission of nephrotic syndrome?

A

0/ trace albumin on Albustix for 3 consecutive days

Frequent relapsing = > 2 relapses in 6 months
Steroid dependent = 2 consecutive relapses within 2 weeks of stopping steroids
Steroid resistant = no remission after 4 weeks of steroids

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22
Q

What is the recommended treatment of steroid dependent nephrotic syndrome?

A

Cyclophosphamide
MMF
Cyclosporine

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23
Q

What are the complications of nephrotic syndrome?

A

Infection (due to low IgG, low complement, impaired lymphocyte function, immunosuppressive drugs)
Cellulitis
Bacterial peritonitis
thrombosis

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24
Q

How do you differentiate between CKD and AKI?

A

Chronic - short/stunted growth, relatively normal potassium, high phosphate, anaemia

AKI- hyperkalaemia

Both might have metabolic acidosis

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25
Q

What are the causes of tubular disease (acute and chronic)

A

Acute - tubulointerstitial nephritis

Chronic - nephronophthisis

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26
Q

How do you calculate the fractional excretion of sodium?

A

FENa = Urine Na x Plasma Cr
——————————-
Urine Cr x Plasma Na X 100%

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27
Q

How does FENa help distinguish between causes of renal failure?

A

Low FEN = prerenal AKI

High FEN = renal cause AKI (inappropriately losing Na)

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28
Q

What is the triad defining HUS?

A

Acute renal failure
Thrombocytopenia
Microangiopathic haemolytic anaemia

  • raised LDH, bilirubin
  • low haptoglobin
  • blood film shows fragmented cells

Most common cause of AKI in western world

29
Q

What are the causes of HUS?

A

Typical - shigatoxin E. coli

Atypical - pneumococcal pneumonia/meningitis

30
Q

What type of RTA is most likely to present with hyperkalaemia?

A

Type IV “hyperkalaemic RTA”
Aldosterone deficiency
Causes include hypoaldosteronism, Addison’s disease, CAH

31
Q

Name 3 inherited causes of Fanconi syndrome

A

Dent’s disease
Wilson’s disease
Galactosemia

32
Q

What is the principle mechanism which ensures excretion of excess sodium when the dietary intake of salt is high?

A

Atrial natriuretic factor
= polypeptide hormone secreted by cardiac atria in response to atrial dilatation
- regulates blood pressure and blood volume
- inhibits renin secretion & aldosterone synthesis
- causing increased GFR and sodium excretion
- inhibits angiotensin II and noradrenaline induced vasoconstriction
- decreases desire for salt - inhibits release of ADH
- net effect = decrease in blood volume/pressure

33
Q

In Alports sydnrome, what is the risk of developing ESKD for x linked homozygotes?

A

85%

34
Q

Which structure derives from the ureteric bud ?

A

Collecting duct

35
Q

What effect do thiazides have on calcium ?

A

Low calcium in urine

36
Q

What is the diagnosis ? Immunofluorescence positive for IgG, IgA, IgM, C3, C1q

A

SLE

37
Q

What is the mechanism of action of loop diuretics ?

A

Inhibits Na K Cl2 cotransporter

Causes hypo Na, K, Mg
Gout

38
Q

what is the mechanism of action of thiazides ?

A

Distal convoluted tubule

Inhibits Na Cl cotransporter (NCCT)

39
Q

What is the mechanism of Amiloride?

A

K sparing diuretic
Blocks ENaC
Late distal tubule collecting duct
Inhibits Na reabsorption and K excretion

40
Q

What is the mechanism of action of spironolactone?

A

Inhibits aldosterone
K sparing diuretic
Inhibits K secretion

41
Q

What is the diagnosis ?
Gross haematuria and HTN post skin infection
IgG and C3 on IF
Subepithelial jumps on EM

A

Post strep GN

42
Q 
What is the diagnosis ? 
Recurrent gross haematuria 
Assoc with URTI 
Fam hx 
IgA mesangial deposits on IF 
Normal C3
A

IgA nephropathy

43
Q

What is the inheritance and genetics of Alports syndrome ?

A

X linked
COL4A5 mutation
Type 4 collagen

44
Q 
What is the diagnosis ? 
Recurrent gross haematuria on bg asymptomatic microscopic 
Anterior lenticonus 
EM splitting and laminated GBM 
Normal C3
A

Alports

45
Q 
What is the diagnosis ? 
Teenage girl 
Nephritic syndrome 
Full house on IF 
Low C3
A

Lupus nephritis

46
Q

What is the inheritance and genetics of Thin Basement membrane disease ?

A

Autosomal dominant
COL4A mutation
Fam hx microscopic haematuria

47
Q

What is the diagnosis ?

Pulmonary haemorrhage and anti GBM antibodies

A

Goodpastures

48
Q

What is the diagnosis ?
Granuloma in resp tract
cANCA pos

A

GPA

Aka wegeners

49
Q

Minimal change disease is steroid responsive true or false

A

True
98%

If not - more likely FSGS

50
Q

What is the mechanism behind hypercoagulability as complication of nephrotic syndrome ?

A

Reduced antithrombin III

And protein C and S

51
Q

What are the encapsulated organisms?

A 
Strep 
Neisseria 
Klebsiella 
Haemophilus 
Salmonella 
Cryptococcus 
Pseudomonas 
E. coli some strains
52
Q

What is the mechanism of action of levimasole?

A

Anti helmithic
Immunodulator
Used for frequent relapsed nephrotic syndrome

53
Q

What is the mechanism of action of cyclosporine ?

A

Calcineurin inhibitor

Used for steroid dependent nephrotic syndrome

54
Q

What stimulates aldosterone secretion and what does it do?

A 
Angiotensin II (hyper K)
Stimulates aldosterone release from adrenal medulla 
Causes de novo synthesis of Na K ATPase to increase Na retention and K excretion

NB spironolactone inhibits aldosterone

55
Q

What are the effects of angiotensin II?

A

Stimulates aldosterone secretion from adrenal medulla
ADH secretion from posterior pituitary
Renal arteriolar vasoconstriction
Sympathetic activity

All results in Na, H2O retention
Increased perfusion of JG apparatus
Increased circulating blood volume

56
Q 
What is the diagnosis ? 
Proximal RTA (impaired bicarb reabsorption) 
HypoPO4 
Hypoglycaemia 
Hypoproteinaemia
A

Fanconi’s syndrome

Great with sodium bicarbonate
Postassium citrate

57
Q

What type of RTA

  • hypoK, hypercalcinuria - stones
A

Type 1
Distal tubular
Inhibition of H excretion

58
Q

What type of RTA?

HyperK

A

Type 4

Aka hypoaldoseronism

59
Q

How do you differentiate between Bartters and Gitelman’s?

A 
Barrters acts like a loop diuretic 
Causes hypoK, hypercalinuria - stones 
Gitelmans acts like a thiazides 
Causes hypoK and more pronounced hypoMg
Presents later in life, more mild

Batters bad
Gitelmans good

60
Q

At what stage of CKD do you get bone disease and anaemia ?

A

Stage 3 (GFR 30-60)
Bone disease
Low Ca due to low Vit D causes increased PTH - osteoclast activity
Also increase PO4

Stage 4 - GFR 15-29
Anaemia
Due to low production EPO
Acidosis

61
Q

What is the mechanism of action of tacrolimus?

A

Calcineurin inhibitor

62
Q

What is the mechanism of action of sirolimus?

A

mTOR inhibitor
Inhibits repose to Il2
(Cell proliferation)

63
Q

What is the mechanism of action of basilizumab?

A

Anti IL 2

64
Q

What is the mechanism of action of mycophenylate?

A

Inhibits purine synthesis

Suppresses B and T cell proliferation

65
Q

What is the mechanism of action of azarhioprine?

A

Purine analogue causing cell cycle arrest

66
Q

What renal imaging is used to exclude PUJ?

A

MAG3 - tracer should clear, if not - obstructed

67
Q

What is the best renal imagine for scarring ?

A

DMSA

68
Q

How do you differentiate between juvenile nephronopthisis and ARPKD?

A

JN - small echogenic kidneys on US
Normotensive (chronic hypovolaemia)
ARPKD - large echogenic kidneys, microcysts enlarge over time; always assoc with hepatic fibrosis (massive intrahepatic bilary duct dilatation on US)

69
Q

How do you differentiate between central and nephrogenic DI?

A

Both have low urine urine lamp on water deprivation test
- dDAVP stimulation
Urine osmo will increase for central (deficiency of ADH but ability to concentrate urine is intact)
Urine osmo unchanged for nephrogenic (inability to concentrate urine despite adequate amounts ADH)

Paediatrics (17 decks)

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