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FRACP > Renal > Flashcards

Renal Flashcards

1
Q

What stimulates the release of renin from the juxtaglomerular cells?

A

Renal artery hypotension
Reduced sodium delivery to distal tubule
Stimulation by the sympathetic nervous system

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2
Q

What effect does Angiotensin 2 have in the RAAS system?

A

Acts directly on the kidney
- Na and water retention

Acts on smooth muscle
- vasoconstriction

Acts on the adrenal glands to release Aldosterone
- Na and water retention at the collecting ducts

Acts on the pituitary to release ADH
- Na and water retention at collecting ducts

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3
Q

What is the classic triad of Haemolytic Uraemic Syndrome?

A

Acute Kidney Injury
Haemolytic Anaemia
Thrombocytopenia

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4
Q

What are the clinical and investigative features of HUS?

A

Prodrome of gastro with bloody diarrhoea
Haematuria, oliguria
Dehydration

Haemolytic anaemia
 - Coombes negative, schistocytes
AKI
Haematuria with RBC casts + dysmorphic cells
Low grade proteinuria
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5
Q

What are the clinical features of Membranoproliferative GN?

A

Peak incidence 5-15 yrs

Acute nephritic syndrome
- Haematuria, Hypertension, AKI

Varying proteinuria

May present with rapidly progressive GN

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6
Q

What are the diagnostic features of Membranoproliferative GN?

A

Low complement levels

  • Type 1 C3 + C4
  • Type 2 C3 only

Diagnosis by renal biopsy
- C3 (+/- C4) deposits on IF

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7
Q

Features differentiating PSGN vs Membranoproliferative GN

A

PSGN is more common
Nephrotic syndrome not present with PSGN
In PSGN C3 normalises within 6-8 weeks

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8
Q

Pathogenesis of SLE Nephritis?

A

Immune complex mediated

Autoantibodies bind to the glomeruli and cause direct damage

Alterations in the innate immunity cause amplification of inflammation

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9
Q

What are the clinical features of SLE Nephritis?

A

Adolescent females

Most common is Proliferative Nephritis

  • significant proteinuria
  • hypertension
  • active lupus serology
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10
Q

What are the extra renal manifestations of SLE?

A 
Anaemia
Malar rash
Synovitis/arthritis 
Photo sensitivity rash 
Serositis eg. Pleuritis, carditis
Neurological involvement eg. Seizures, psychosis
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11
Q

Diagnostic investigations of SLE Nephritis?

A

Renal biopsy

Low C3 and C4 levels (persistant)
ANA +ve
Autoantibodies - lupus anticoagulant,
anti-DsDNA, anti-Sm

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12
Q

What is the pathophysiology of anti-GBM disease?

A

Small vessel vasculitis

Antibodies directed against type 4 collagen in Alveoli, glomeruli

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13
Q

How does anti-GBM disease present?

A

Rare in children - peak incidence 20s and 60s

Rapidly progressive GN

  • Haematuria with casts + dysmorphic cells
  • Hypertension
  • Proteinuria (not nephrotic range)
  • AKI

Haemoptysis and Pulmonary haemorrhage

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14
Q

Diagnostic investigations for anti-GBM disease?

A 
Anti-GBM antibodies
Normal complement levels 
RENAL BIOPSY
 - LM - crescent formation in bowmans space 
 - IF - continuous IgG staining along BM
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15
Q

What are the clinical features of PSGN?

A

Preceding strep infection

  • 1-2 weeks post pharyngitis
  • 3-6 weeks post skin infection
ACUTE NEPHRITIC SYNDROME
Generalised peripheral oedema 
Macroscopic (microscopic) haematuria 
Hypertension
Oliguria
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16
Q

What investigations would indicate PSGN?

A

Haematuria with casts + dysmorphic cells
Proteinuria
LOW C3, LOW CH50
Evidence of strep infection - ASOT, anti-DNAse

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17
Q

What are the indications for a renal biopsy?

A

Persistently low C3 > 6 weeks
Persistant Proteinuria > 6 months
Atypical presentation
eg. Nephrotic syndrome, deteriorating RF

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18
Q

What would be the biopsy findings of PSGN?

Only needed in atypical cases

A

Diffuse proliferation of mesangium and endothelium

IF- C3 + IgG deposits along GBM

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19
Q

What are the basic management principles of PSGN?

A

Antibiotic therapy
Fluid restriction 400ml/m2/day
Consider furosemide
Manage severe hypertension

20
Q

Clinical features of IgA Nephropathy?

A 
Usually >5 years old
Episodic macroscopic Haematuria commonly 1-2 days post URTI
Persistant microscopic haematuria
Loin pain 
Mild hypertension may be present
21
Q

What are the diagnostic investigations for IgA Nephropathy?

A

Biopsy - mesangial proliferation with deposits of IgA on IF

Normal renal function
Normal C3 levels

22
Q

What are the differences between IgA Nephropathy and PSGN?

A

Haematuria develops 1-2 days post URTI (vs 1-2 weeks)
Resolves within 5 days
Normal C3 levels

23
Q

What are the clinical features of HSP?

A

Purpuric rash- buttocks + extensors
Arthritis
Abdominal pain - intussusception rarely
Scrotal pain/tenderness

Haematuria +/- Proteinuria
Hypertension
AKI

24
Q

What is the management of HSP?

A

Mostly supportive
NSAIDs for arthritis (avoid if renal disease present)
Corticosteroids for severe abdominal pain/renal disease

Close follow up - BP and urinalysis
Relapses are common

25
Q

What is the genetic background of Alports syndrome?

A

Genetic mutations cause dysfunctional coding for Type 4 Collagen

X-Linked transmission most common - COL45 gene mutation

Can be AD/AR

26
Q

What are the clinical features of Alports Syndrome?

A

Persistant microscopic haematuria
Progressive Proteinuria

BILATERAL SENSORINEURAL HEARING LOSS
- never congenital, develops late childhood

ANTERIOR LENTICONUS (‘oil drop’ on red reflex)

Family hx of deafness and renal failure

27
Q

What would be seen on a renal biopsy of Alports Syndrome?

A

Diffuse BM thinning + splitting
‘Basket weave’ appearance of BM

IF - Absence of BM staining for alpha-5 collagen (males only)

28
Q

What are the clinical features of Nephritic Syndrome?

A

Haematuria
Proteinuria
Peripheral oedema
Hypertension

29
Q

Hereditary causes of Nephritic syndrome?

A

Alports syndrome

Thin BM disease

30
Q

What are the causes of Rapidly Progressive GN?

A

Anti-GBM disease
HUS
SLE Nephritis
Granulomatosis with Polyangiitis

31
Q

What are the causes of low C3 levels?

A

Immune complex mediated disease!
Post-Strep GN
Membranoproliferative GN
SLE Nephritis (low C3 + C4)

32
Q

What are the cardinal features of Nephrotic Syndrome?

A

Generalised Oedema
Proteinuria >4g/24hrs or PCR>2
Hypoalbuminaemia

33
Q

What is the basic pathogenesis of Nephrotic syndrome?

A

Primarily podocyte damage leading to increased permeability of capillary walls

Both immune and non-immune insults cause: effacement of podocytes
Reduced number of functional podocytes and altered integrity of slit diaphragm

34
Q

What are the primary causes of Nephrotic syndrome?

A

Minimal Change Disease
Membranous Nephropathy
Focal Segmental Glomerulosclerosis
Congenital Nephrotic syndrome

Secondary causes are vasculitis (SLE, HSP) and medications (pamidronate, NSAIDs)

35
Q

What are the presenting features of nephrotic syndrome?

A 
More commonly males
Microscopic haematuria 
Proteinuria ++
AKI (2ndry to hypovolaemia)
Oedema ++
36
Q

What are the complications of Nephrotic Syndrome?

A
  1. Increased susceptibility to infection
    - urinary loss of Ig + complement
    - esp encapsulated bacteria (S Pneumonia)
  2. Thrombosis
  3. Hypovolaemia
37
Q

What are the basic management principles of Nephrotic Syndrome?

A

Steroid Therapy
Antibiotics
Rx severe hypovolaemia - 20% albumin
Rx of oedema - fluid restriction, salt restriction
Can consider diuretics if no hypovolaemia

38
Q

What are the volume differences between Nephrotic + Nephritic syndromes?

A

Nephrotic - low/normal BP, hypovolaemic

Nephritic - hypertension, hypervolaemic

39
Q

What are the clinical features of minimal change disease?

A

Mild periorbital oedema
Proteinuria
Occasionally microscopic haematuria
- no casts or dysmorphic cells

40
Q

What are the investigations for MCD?

A 
Urine PCR > 300 or significant Proteinuria
May be AKI
Albumin < 25
Normal complement levels
Increased cholesterol

Renal biopsy not usually needed

41
Q

Findings on renal biopsy for MCD?

A

Normal glomeruli
Podocyte Effacement on Electron Microscopy
No staining on IF

42
Q

What is the management of MCD?

A 
STEROIDS - Pred for 4 weeks 
 - May relapse after steroid withdrawal
Vaccinations - full pneumococcal + flu
Antibiotics - initial illness + relapses
Manage oedema - Albumin vs. fluid restriction
43
Q

What are the indications for renal biopsy in suspected MCD?

A 
<1yr or >16 yrs
Steroid resistance
Low C3 levels 
Persisting impaired renal function 
Persistant microscopic haematuria 
Hypertension
44
Q

What are the findings seen on renal biopsy for FSGS?

A

Focal segmental sclerosis
Mesangial cell proliferation + scarring
IF- IgM + C3 staining in areas of sclerosis

45
Q

What features in a child with Nephrotic syndrome suggest possible FSGS?

A

Steroid resistance
Adolescents

Signs of peristant AKI or hypertension

46
Q

What is the management of FSGS?

A

Trial treatment with steroids (only 20% are responsive)

Cyclophosphamide

47
Q

Membranous Nephropathy is commonly due to an underlying condition, what conditions cause this?

A

SLE
Chronic infections eg. Hep B/C
Congenital syphilis

FRACP (4 decks)

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