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Paediatrics > Paediatric nephrology > Flashcards

Paediatric nephrology Flashcards

1
Q

Functions of the kidneys

A
  • Waste handling
  • Water handling
  • Salt balance
  • Acid base control
  • Endocrine → red cells, blood pressure, bone health
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2
Q

Glomerular filtration barrier

A
  • Endothelial cells → fenestrated
  • Glomerular basement membrane → 2 proteins
  • Podocyte → podocin, nephron
  • Mesangial cells → support
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3
Q

Nephritic vs nephrotic syndrome

A
  • Nephritic
    • Increasing haematuria
    • Intravascular overload
  • Nephrotic overload
    • Increased proteinuria
    • Intravascular depletion
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4
Q

Acquired glomerulonephropathy

A
  • Minimal change syndrome → podocyte
  • Post-infectious glomerulonephritis → Basement membrane and endothelial cell
  • Haemolytic-uraemic syndrome → endothelial cell
  • IgA nephropathy/ HSP → mesangial cel
  • Systemic lupus erythematosis
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5
Q

Congenital glomerulonephropathy

A
  • Congenital nephrotic syndrome → podocyte cytoskeletal integrity
  • Alport syndrome → basement membrane
  • Thin basement membrane disease → basement membrane
  • Membrano-proliferative glomerulonephritis → complement regulatory proteins
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6
Q

Proteinuria: how much is too much

A
  • Dipstix → > 3+ abnormal
  • Protein creatinine ratio → >250mg/mol
  • 24 urine collection (gold standard) → 1g/m2/24 hours
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7
Q

Pathophysiology of nephrotic syndrome

A
  1. Proteinuria
  2. Hypoalbuminaemia
  3. Peripheral oedema
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8
Q

Clinical features of nephrotic syndrome

A
  • Typical
    • Age 1-10
    • Normal blood pressure
    • No frank haematuria
    • Normal renal function
  • Atypical
    • Suggested autoimmune disease
    • Abnormal renal function
    • Steroid resistance
  • Only then consider renal biopsy
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9
Q

Management of nephrotic syndrome

A
  • PREDNOS → prednisolone in nephrotic syndrome
  • 8 weeks
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10
Q

Side effects of high dose glucocorticoids

A
  • Cushings syndrome
    • Personality changes
    • Hypertension
    • Increased susceptibility to infection
    • GI distress/ increased gastric acid
    • Growth retardation
  • Emotional lability
  • Behavioural changes
  • Sleep disturbances
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11
Q

Steroid resistant nephrotic syndrome

A
  • Acquired → focal segmental glomerulosclerosis (FSGS)
  • Congenital
    • NPHS1 → nephron
    • NPHS2 → podocin
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12
Q

Haematuria

A
  • Macroscopic/ frank
  • Micoscopic
    • Investigate
    • Haemoglobinuria
      • associated proteinuria = glomerular disease
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13
Q

Causes of haematuria

A
  • Lower urinary tract
    • Urethritis
    • Trauma
    • UTI
    • Malignancies →
  • Upper urinary tract
    • Cysts
    • Tumours → Wilm’s nephroblastoma
    • Glomerulonephritis
    • Systemic → clotting disorder
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14
Q

Nephritic syndrome

A
  • Clinical diagnosis
  • Haematuria and proteinuria
  • Reduced GFR
    • Oliguria
    • Fluid overload → oedema and raised JVP
  • Hypertension
  • Worsening renal failure → rapidly progressive glomerulonephritis
  • Intrarenal cause of Acute Kidney Injury (AKI)
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15
Q

Acute post-infectious glomerulonephropathy

A
  • Between aged 3-5
  • Usually group A strept
  • Causes beta haemolytic
  • Site
    • Throat → 7-10 days
    • Skin → 2-4 weeks
  • Self-limiting
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16
Q

Pathogenesis of PIGN

A
  • Nephrotgenic antigens on strep
  • Binds to specific sites in glomerulus/ formation of antibody-antigen complex deposit in kidneys
  • Activation of immune response/ alternative complement pathway
  • Acute kidney injury
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17
Q

Diagnosis of PIGN

A
  • Diagnosis
    • Bacterial culture
    • Positive ASOT (anti streptolysin O titer)
    • Low C3
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18
Q

Treatment of PIGN

A
  • Antibiotics
  • Support renal function → electrolyte/ acid-base balance
  • Overload/ hypertension → diuretics
  • Outcome → not often recurrent
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19
Q

IgA nephropathy

A
  • Most common glomerulonephritis
  • 1-2 days after URTI
  • Older children and adults
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20
Q

Differential of Acute post-infectious glomerulonephritis

A
  • IgA nephropathy (Berger’s disease)
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21
Q

Clinical features of IgA nephropathy

A
  • Recurrent macroscopic haematuria
  • +/- chronic microscopic haematuria
  • Varied proteinuria
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22
Q

Pathogenesis of IgA nephropathy

A
  • Increased circulating levels of Gd-IgA1
  • Production of antibodies in response (IgA or IgG)
  • Immune complexes form in kidneys and circulation
  • Invasion of immune complexes to mesangium
  • Local inflammation and injury
  • Glomerunephritis
23
Q

Diagnosis of IgA nephropathy

A
  • Negative autoimmune workup
  • Normal compliment
  • Definitive diagnosis → renal biopsy
    *
24
Q

Treatment of IgA nephropathy

A
  • Mild → ACEI for proteinuria
  • Moderate/ severe → immunosuppression (KDIGO guidelines)
  • Outcomes → better in children
25
Q

Henoch Scholein Purpura related to IgA vasculitis

A
  • Age 5-15
  • Palpable purpura
  • 1 of following
    • Abdo pain
    • Renal involvement
    • Arthritis/ arthralgia
    • Biopsy → IgA deposits
26
Q

IgA vasculitis

A
  • Most common vasculitis of children
  • Affects small vessels
  • Associated with IgA nephropathy
  • 1-2 days post-trigger
    • Viral URTI
    • Streptococcus
    • Drugs
  • 4-6 week duration
  • Mesangial cell injury → nephritis
27
Q

Treatment of IgA vasculitis

A
  • Symptomatic → joints and gut
  • Glucocorticoid therapy → only severe and GI related disease
  • Immunosuppression → moderate and severe
  • Long-term → hypertension and proteinuria screening
28
Q

Definition of Acute Kidney Injury (AKI)

A
  • Acute loss of kidney function leading to:
    • Retention of urea and other waste products
    • Dysregulated extracellular volume
    • Electrolyte imbalance
  • Anuria/oliguria (<0.5ml/kg/hr for 8 hours)
  • Hypertension of fluid overload
  • Raised creatinine >1.5 age specific reference
29
Q

AKI warning stages

A
  • AKI 1 → 1.5-2x reference creatinine
  • AKI 2 → 2-3x reference creatinine
  • AKI 3 → >3x reference creatinine
30
Q

Clinical features of AKI

A
  • Raised urea and creatinine
  • Fluid overload
  • Hyperkalaemia
  • Hyperphosphataemia
  • Hyponatraemia
  • Hypocalcaema
  • Metabolic acidosis / bicarb loss
  • Hypertension
31
Q

Management of AKI

A
  • Prevention
  • 3 Ms
    • Monitor → Paediatric early warning scores, urine output, weight
    • Maintain → hydration, electrolytes, acid-base balance
    • Minimise → drugs
32
Q

Causes of AKI

A
  • Pre-renal
    • Perfusion problems
  • Renal
    • Glomerular disease
    • Tubular injury
    • Interstital nephritis
  • Post-renal
    • Obstructive uropathy
33
Q

Haemolytic-uraemic syndrome (HUS)

A
  • Packed cell volume >30%
  • Haemoglobin level <10g/dl + fragmented erythrocytes on blood film
  • Thrombocytopenia
  • AKI
    • High serum creatinine
    • GFR < 80ml/min/1.73m2
    • Proteinuria
34
Q

Cause of HUS

A
  • Post-diarrhoea
  • Entero-haemorrhagic E.coli (EHEC)
    • Verotoxin producing
    • Shiga toxin producing (STEC)
  • Pneumococcal infection
  • Drugs
  • Atypical HUS
35
Q

Presentation of HUS

A
  • Infection by E.coli 0157:H7
  • Up to 14 days post diarrhoea
  • Abdominal pain
  • Fever
  • Vomiting
  • Bloody diarrhoea
  • Resolution/ HUS (15%)
36
Q

HUS triad

A
  • Microangiopathic haemolytic anaemia
  • Thrombocytopenia
  • AKI
37
Q

Management of haemolytic uraemia syndrome

A
  • 3 Ms
    • Monitor → fluid balance, electrolytes, acidosis, waste, hormones, other organ function
  • Maintain → IV saline + fluids, renal replacement therapy
  • Minimise → no antibiotics/ NSAIDs
38
Q

Complications of AKI

A
  • Evolution to CKD
  • Monitor blood pressure and proteinuria
39
Q

Causes of chronic kidney disease in paediatrics

A
  • Congenital anomalies of the kidneys and urinary tract (CAKUT)
    • 55% of paediatric CKD
    • Reflux nephropathy
    • Dysplasia
    • Obstructive uropathy → e.g. posterior urethral valves
  • Hereditary conditions
    • 17%
    • Cystic kidney disease
    • Cystinosis
  • Glomerulonephritis → 10%
40
Q

Presentation of CKD

A
  • Symptoms variable depending on which function affected
    • Waste handling
    • Water handling
    • Salt balance
    • Acid-base control
    • Endocrine → red cells/ blood pressure/ bone health
      *
41
Q

Obtaining urine specimen in children

A
  • Requires normal social cleanliness
  • Clean catch urine or midstream urine
  • Collection pads, urine bags → not accurate
  • Sick infants → catheter or suprapubic aspiration
  • Acutely unwell → don’t delay treatment
42
Q

Diagnosis of UTI

A
  • Urine dipstix
    • Leucocyte esterase activity
    • Nitrites
    • Unreliable <2 years old
  • Microscopy
    • pyuria
    • Bacturia
  • Culture → > (10)5 colony → gram negative bacteria e.coli
43
Q

Why are UTI’s relevant in paediatrics

A
  • Vesico-ureteric reflux disease → kidney injury
  • Graded 1-5
  • Higher grade associated with renal dysplasia
  • Combination of UTI, vesico-ureteric reflux and vulnerable kidney → permanent scarring
44
Q

What to look out for

A
  • Screening for children at risk of progressive scarring → reflux nephropathy
  • Capture those with renal dysplasia
  • Urological abnormalities
  • Unstable bladder → voiding dysfunction
    *
45
Q

Investigations VUR

A
  • Ultrasound → structural
  • DMSA (isotope scan) → scarring and function
  • Micturating cysto-urethrogram (MAG 3 scan) → dynamic
46
Q

Treatment of UTI

A
  • Lower tract → 3 days oral antibiotics
  • Upper tract/ pyelonephritis
    • Antibiotics for 7-10 days
    • Oral if systemically well
  • Prevention → fluids, hygiene, constipatio
  • Manage voiding dysfunction
47
Q

Risk factors of developing CKD

A
  • Late referrale
  • Hypertension
  • Proteinuria
  • Diet high in protein, phosphate and salt
  • Poor bone heaoth
    • PTH
    • Phosphate
    • Vitamin D
  • Acidosis
  • Recurrent UTIs
48
Q

Role fo blood pressure control

A
  • Gold standard to monitor hypertension → risk factor to CKD
  • Sphygmomanometer
  • Oscillometry
  • Prevent white coat effect → 24 hours ambulatory BP
49
Q

Factors affecting BP

A
  • Sex, age, height
50
Q

Criteria for hypertension

A
  • 3 separate ocassiona
  • Hypertension → >95 percentile
  • Borderline → >90 but <95th percentile
51
Q

Management of CKD

A
  • Depends of kidney function affected
  • Waste handling → reduce protein intake
  • Water handling → fluid restriction
  • Salt balance → reduce salt
  • Acid-base control
  • Endocrine
  • Bladder dysfunction
51
Q

Management of CKD

A
  • Depends of kidney function affected
  • Waste handling → reduce protein intake
  • Water handling → fluid restriction
  • Salt balance → reduce salt
  • Acid-base control
  • Endocrine
  • Bladder dysfunction
52
Q

Metabolic bone disease in CKD

A
  • Kidneys function to excrete phosphate (high phosphate → increase in PTH)
  • Kidneys activate vitamin D3
  • Treatment
    • Low phosphate diet
    • Phosphate binders
    • Active vitamin D
    • Growth hormone → if poor growth
53
Q

Cardiovascular risk in CKD

A
  • Accelerated atherosclerosis
  • Traditional risk factors + anaemia/ metabolic bone disease (PTH)

Paediatrics (10 decks)

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