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renal > haematuria/nephritic syndrome > Flashcards

haematuria/nephritic syndrome Flashcards

1
Q

mnemonic to remember causes of haematuria

A

Stone
Haematological / hereditary
Infectious/iatrogenic/idiopathic/immune
Renal
Tumour/trauma

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2
Q

factitious haematuria - some causes

A

urate crystals in infants, foods/dyes, haemoglobinuria from haemolytic anaemia, myoglobinuria from rhabdo, drug metabolites

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3
Q

extraglom vs glomerular haematuria

A

extraglom: red/pink, can have clots, usually no protein, rbc morph normal, no casts

glomerular: cola, no clots, can have protein, rbc dysmorphic, can have casts

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4
Q

types of RPGN

A

type I = anti-GBM (goodpastures); linear on IF
type II = immune complexes e.g. IgA, SLE, PSGN, HSP; granular on IF
type III = ANCA, pauci-immune; nothing on IF

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5
Q

cANCA vs pANCA vasculitides

A

CAW: cANCA = Wegner’s
PAMC: pANCA = microscopic polyangitis, Churg-Strauss

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6
Q

RPGN also known as what?

A

crescentic GN - crescent shape proliferation of cells into Bowman’s capsule

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7
Q

causes of haematuria with low C3 vs low C3 AND C4

A

Low C3 = typically due to activation of the alternate C’ pathway
- APSGN
C3 glomerulopathies including DDD (subtype of MGPN)

Low C3 + C4 = indicates activation of classic pathway due to complex formation
- Lupus nephritis
- MPGN I
- Shunt nephritis + associated with bacterial endocarditis

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8
Q

What would the follows IF stains suggest?
i. IgG and C3 on external side of GBM
ii. IgG and C3 found along GBM + mesangium
iii. IgG1, IgG3, IgA, IgM, C3, C4, C1q

A

i. IgG and C3 on external side of GBM = APSGN (‘starry sky’)
ii. IgG and C3 found along GBM + mesangium = MPGN type I + II
iii. IgG1, IgG3, IgA, IgM, C3, C4, C1q = ‘full house’ ie. SLE

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9
Q

what are these pathognomonic features of?

i. Crescentic
ii. Tram tracking
iii. Wire loops
iv. Starry sky
v. Subepithelial humps

A

i. Crescentic = RPGN – ANCA associated, anti-GBM, post strep
ii. Tram tracking = MPGN
iii. Wire loops = lupus class III/ IV
iv. Starry sky = APSGN (granular pattern) on immunofluorescence
v. Subepithelial humps = APSGN on EM

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10
Q

name some synpharyngitic causes of haematuria besides PSGN

A

• Alports
• Thin basement membrane
• IgA
• HSP nephritis

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11
Q

pathogenesis in goodpasture’s

A

anti-GBM Abs against alpha3 chain of collagen IV of BM
esp HLA DR15
environmental stress will expose the alpha 3 further
lung Sx first, then kidneys

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12
Q

PSGN vs IgA nephropathy - timeline after infection

A

IgA = 1-2 DAYS (by definition <5/7 days)
VS. postinfectious GN = 10-14 days post pharyngitis, or 3-6 weeks post skin infection

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13
Q

5 key presentation types of IgA nephropathy

A
  1. haematuria
  2. nephritic
  3. RPGN
  4. nephrotic (rare <10%)
  5. mixed nephrotic/nephritic
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14
Q

HTN treatment in IgA nephropathy vs PSGN

A

IgA = ACE/ARB
PSGN = frusemide

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15
Q

IgA biopsy findings similar to what disease?

A

HSP, but IgA isolated to renal disease

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16
Q

ESKD likelihood with IgA nephropathy?

A

20-30% of children will develop ESKD in 15-20 years after disease onset

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17
Q

genetics of alport’s syndrome

A

mutation in COL4A3/4/5 causing collagen IV abnormality
- COL4A3 and 4 autosomal (AR - early onset/AD - late onset)
- most COL4A5 which is X-linked

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18
Q

clinical manifestations of alport’s

A

ALPORT:
anterior lenticonus
persistent haematuria
ototoxicity and SNHL
renal - FSGS, basket weave
Treatment - ACEI, renal transplant

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19
Q

pathognomonic features of Alport’s

A

anterior lenticonus
basket weave BM pattern on EM
*IF will be non-diagnostic…nothing will light up

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20
Q

thin basement membrane disease associated with what condition and why?

A

alport’s
also a/w COL4A3 and COL4A4 mutations
in fact, homozygous mutations will result in AR Alport’s
also a/w haematuria and BM thinning

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21
Q

TBMD - gross haematuria present when?

A

associated with resp illness

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22
Q

when is TMBD termed benign familial haematuria?

A

isolated haematuria in multiple family members, not associated with other signs of renal disease (proteinuria, renal impairment)

23
Q

age range of PSGN

A

2-13, uncommon <3yo

24
Q

when does ASOT and anti-DNase B rise post strep infection?

A

ASOT - 3-4 weeks post
anti-DNase B - 6-8 weeks post

25
Q

PSGN - Abx or not?

A

doesn’t stop it - but if strep still present, can consider treating to reduce severity

26
Q

how long does haematuria last after PSGN resolves?

A

Persistent microscopic haematuria can persist for 1-2 years

27
Q

criteria for SLE diagnosis

A

DOPAMINE RASH (4/11):
discoid rash
oral ulcers (painless)
photosensitivity
arthritis
malar rash
immune markers
neurological
ESR

Renal
ANA
serositis
haematological

28
Q

how many childhood SLE will develop renal disease?

A

most common manifestation - up to 80%

29
Q

what is the strongest single genetic factor for SLE

A

Deficiency of C1q is rare but the strongest single genetic factor

30
Q

what is the most common type of lupus nephritis?

A

Class III and IV = mesangial and endocapillary lesions (‘wire loop lesions’)

31
Q

how may lupus nephritis manifest clinically?

A

nephrotic (class V) or nephritic (I-II mild, some III and all IV need treatment)

32
Q

C3 and C4 activity with SLE flare

A

low C3 during flare, low C4 pre-flare

33
Q

% of HSP patients who will develop nephritis

A

50%

34
Q

when does nephritis manifest with HSP?

A

usually after rash

35
Q

what monitoring of BP and urinalysis must there be with HSP?

A

at diagnosis, then
weekly for first month
fortnightly until end of month 3
then once at 6mo and 12mo

36
Q

classic symptoms of HSP

A

Palpable purpura without thrombocytopenia and coagulopathy
Arthritis/arthralgia
Abdominal pain
Kidney disease

37
Q

pulmonary renal syndrome - examples

A

ANCA associated vasculitis - Wegner’s
ANCA not associated vasculitis - HSP
Goodpasture’s
SLE

38
Q

examples of upper tract non-renal tissue causes of haematuria

A

obstruction: renal vein thrombosis, nephrocalcinosis
idiopathic hypercalcuria
haem: sickle cell
iatrogenic: haemorrhagic cystitis e.g. cyclophos, ifos

39
Q

pathogenesis of sickle cell nephropathy

A

esp in renal medulla - hypoxic, acidotic and hypertonic area
increased sickling causes stasis, RBC adhesion, tubular damage and scarring

40
Q

how to treat hypercalcuria?

A
  1. Oral thiazide diuretics – stimulating calcium reabsorption in the proximal and distal tubules
  2. Potassium citrate – helpful in patients with low urinary citrate excretion and symptomatic dysuria
  3. Sodium restriction - Urinary calcium excretion parallels sodium excretion

not usually reduced Ca intake

41
Q

why are patients with IE/infected cardiac shunts at risk of renal disease?

A
  • septic emboli
  • drug-induced AI nephritis
  • AKI from nephrotoxics e.g. aminoglycosides
  • immune complex mediated GN
42
Q

most common organism associated with IE nephritis

A

staph aureus in 55%

43
Q

triad of HUS features

A

i. Microangiopathic haemolytic anaemia (DAT –ve)
ii. Thrombocytopenia
iii. AKI

44
Q

DDx for HUS

A

1) DIC - abnormal coags, prolonged PTT
2) TTP - abnormally low ADAMTS13
3) systemic vasculitis

45
Q

most common cause of infection induced HUS? worst cause of infection HUS?

A
  1. Shiga-toxin producing Escherichia coli (STEC) = most common in Western world
  2. Shigella dysenteriae type 1 = most common in Asia and South Africa

Worst prognosis = Neuraminidase producing Streptococcus pneumoniae

46
Q

STEC HUS - which is the most common serotype?

A

O156:H7

47
Q

Abx in infective HUS - yay or nay

A

nay - dead bacteria release more toxin!

48
Q

pathogenesis of TTP

A

deficiency of ADAMTS13, protease that cleaves VWF (sticky tape for platelets)

49
Q

what drugs are associated with causing HUS?

A

calcineurin inhibitors e.g. cyclosporin, tacro
cytotoxics e.g. cisplastin

50
Q

pathogenesis of all HUS

A
  • Microvascular injury with endothelial damage > localised thrombosis
    — in kidneys: AKI
  • Progressive platelet aggregation > consumptive thrombocytopenia
  • mechanical damage to RBC bumping into clots > microangiopathic anaemia > schistocytes, helmet cells
51
Q

aetiology of atypical, hereditary HUS

A

1) complement mediated
2) non-complement mutations A) coagulation pathway B) cobalamin

52
Q

most common complement-mediated HUS genetic mutations

A

factor H = 11-30%
CD46 = factor I = C3 = 3-17%

53
Q

treatment options for hereditary HUS

A
  • plasmapheresis
  • eclizumab (C5 inhibitor)

renal (6 decks)

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