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Paediatrics (Y4) > 6- Paediatric Nephrology (2/2) > Flashcards

6- Paediatric Nephrology (2/2) Flashcards

1
Q

Nephritic syndrome
Background

A
  • Nephritis refers to inflammation within the nephrons of the kidney
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2
Q

nephritis syndrome presentation

A

can vary in a combination of some or many of the following:
- AKI (sometimes GFR can drop drastically)
- On urine dipstick: blood +/- and/or protein+/-
o Sometimes visible haematuria
o Proteinuria <3.5g/24 hours (less than nephrotic)
- Mild to moderate oedema
- Hypertension

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3
Q

nephritic syndrome causes in children

A

Most common causes in children
- Post streptococcal GN
- IgA nephropathy

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4
Q

Post-streptococcal Glomerulonephritis (post-infective)

A

Background
- 1-2 weeks after group a B-haemolytic streptococci infection e.g. Strep pyogenes e.g. Tonsillitis
- Children aged 3-12

Pathophysiology: immune complexes made up of streptococcal antigens, antibodies and complement proteins get stuck in the glomeruli of the kidney and cause inflammation -> AKI

Investigations
- Positive throat swab
- Anti-streptolysin antibody titres in blood

Management
- 80% make a full recovery without treatment
- May require treatment with antihypertensives and diuretics if they develop hypertension and oedema

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5
Q

IgA nephropathy (Berger’s disease)

A

Background
- Related to Henoch-Schonlein Purpura -> IgA vasculitis
- Young adults and teenagers

Pathophysiology
- IgA deposits in nephrons of kidney cause inflammation (nephritis)

Investigations
- When renal biopsy is taken the histology will show IgA deposits and glomerular mesangial proliferation

Management
- Supportive treatment for renal failure
- Immunosuppressant medication
o Steroids
o Cyclophosphamide to slow progression

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6
Q

Polycystic kidney disease backgrounds

A

Two main types
1) Autosomal recessive (ARPKD)
- Presents in neonates
- Picked up on antenatal US

2) Autosomal dominant (ADPKD) – more common in adults

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7
Q

pathophysiology of PCKD

A
  • Mutation in polycystic kidney and hepatic disease (PKHD1) gene on chromosome 6
  • Gene codes for fibrocystin/polyductin protein complex (FPC) -> responsible for creation of tubules and maintenance of healthy epithelial tissue in kidney, liver and pancreas
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8
Q

Presentation of PCKD

A

Key features
* Cystic enlargement of the renal collecting ducts
* Oligohydramnios, pulmonary hypoplasia and Potter syndrome
* Congenital liver fibrosis

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9
Q

presentation of PCKD in antenatal periods

A

Oligohydramnios
- Lack of amniotic fluid due to reduced urine production by fetus
- Leads to Potter syndrome- dysmorphic features such as
–>Underdeveloped ear cartilage
–>Low set ears
–>Flat nasal bridge
–> Abnormalities of skeleton

Pulmonary hypoplasia -> respiratory failure shortly after birth

Polycystic kidneys
- Large cysts on kidneys can take up space in the abdomen which makes it hard for neonate to breath
- May require renal dialysis within first few days of life

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10
Q

Complications of PCKD

A
  • Liver failure due to liver fibrosis
  • Portal hypertension leading to oesophageal varices
  • Progressive renal failure
  • Hypertension due to renal failure
  • Chronic lung disease
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11
Q

management of PCKD

A

Management
- Renal dialysis

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12
Q

prognosis of PCKD

A

Prognosis
- Most patients develop end stage renal failure before reaching adulthood
- 1/3 die in neonatal period

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13
Q

haemolytic uraemic syndrome (HUS) background

A

Occurs when there is a thrombosis within small blood vessels throughout the body

Classic triad of

  • Haemolytic anaemia: anaemia caused by RBC destruction
  • AKI: failure of kidney to excrete waste products such as urea (released when RBC breakdown)
  • Thrombocytopenia: low platelets
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14
Q

Pathophysiology of HUS

A
  • Triggered by bacterial toxin Shiga – e.coli 0157 or shigella
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15
Q

Risk factors HUS

A
  • Use of Abx and anti-motility medications such as loperamide to treat gastroenteritis increase risk of developing HUS
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16
Q

Risk factors HUS

A
  • Use of Abx and anti-motility medications such as loperamide to treat gastroenteritis increase risk of developing HUS
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17
Q

Presentation HUS

A

E. coli 0157 causes a brief gastroenteritis, often with bloody diarrhoea. The symptoms of haemolytic uraemic syndrome typically start around 5 days after the onset of the diarrhoea.

Signs and symptoms of HUS may include:

  • Reduced urine output
  • Haematuria or dark brown urine
  • Abdominal pain
  • Lethargy and irritability
  • Confusion
  • Oedema
  • Hypertension
  • Bruising
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18
Q

Management HUS

A

HUS is a medical emergency and has a 10% mortality. It needs to be managed by experienced paediatricians under the guidance of a renal specialist. The condition is self limiting and supportive management is the mainstay of treatment:
* Urgent referral to the paediatric renal unit for renal dialysis if required
* Antihypertensives if required
* Careful maintenance of fluid balance
* Blood transfusions if required

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19
Q

HUS prognosis

A

Prognosis
70 to 80% of patients make a full recovery.

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20
Q

UTI
Background

A
  • Infections anywhere in the urethra, bladder, ureters and kidneys
  • Pyelonephritis -> infection of the kidney (can lead to scarring and reduction in kidney function)
  • Cystitis -> inflammation of the bladder
21
Q

Risk factors UTI

A
22
Q

Presentation UTI

A

Fever may be the only symptom of a urinary tract infection, especially in young children. Always consider (and exclude) a urinary tract infection in a child with a temperature, unless there is a clear alternative source of infection.
Babies will present with very non-specific symptoms:

  • Fever
  • Lethargy
  • Irritability
  • Vomiting
  • Poor feeding
  • Urinary frequency

Signs and symptoms in older infants and children are more specific:

  • Fever
  • Abdominal pain, particularly suprapubic pain
  • Vomiting
  • Dysuria (painful urination)
  • Urinary frequency
  • Incontinence
23
Q

Investigations UTI

A

1) Urine dipstick (clean catch tricky in children)

  • Nitrites – bacteria in urine
    –>Better indication of infection than leukocytes
    –> If only nitrites- treat as UTI
  • Leukocytes – infection or inflammation
    –>If only leukocytes -> should not be treated as UTI unless clinical evidence
  • If both N and L are present -> patient should be treated for UTI

2) Urine microscopy if N or L present

-Mid-stream urine sample

24
Q

Atypical UTI features:

A

Seriously ill.
Septicaemia.
Failure to respond to suitable antibiotics within 48 hours.
Infection with non-E.coli organisms.
Poor urine flow.
Abdominal mass.
Raised creatinine.

25
Q

Definition of recurrent UTI:

A
  • 3 or more UTIs with lower UTI.
  • 2 or more UTIs with acute upper UTI (acute pyelonephritis).
  • 1 episode of acute upper UTI and 1 episode of acute lower UTI.
26
Q

management of UTI in children <3 months with fever

A

should start IV antibiotics and have full septic screen
o Blood cultures
o Bloods
o Lactate
o Lumbar puncture may be considered

27
Q

management of children >3 that are otherwise well

A

oral antibitoics
- cefalexin
- nitrofurantoin

children with features of sepsis or pyleonephritis : IV antibiotics

28
Q

ways of preventing UTI in children

A

Use the potty more often:

Time child’s potty sessions
- Young children hold their pee as they don’t want to take breaks from their play.
- After experiencing a UTI, may be afraid to pee as it might burn.
- Ask child to empty bladder every 2-3 hours.

Empty bladder completely
- Some children don’t empty bladder completely when peeing.
- Just pee enough to make sensation go away because they are in a hurry to go back to play.
- Ask child to ‘double pee’ each time; or try again before wiping.

Proper wiping
- Wipe from front to back.

Stay hydrated
- Drink frequently so urine is a very light colour; almost like water!

Avoid constipation

Choice of clothing
- Cotton underpants are recommended.
- Avoid nylon, synthetic, tight-fitting underwear.

No bubble baths
- Frothy soapy water can lead to skin irritation.

29
Q

recurrent UTI investigations

A

Should be investigated for underlying cause and renal damage
Investigation cause:
1) US scans
* All children under 6 months with their first UTI should have an abdominal ultrasound within 6 weeks, or during the illness if there are recurrent UTIs or atypical bacteria
* Children with recurrent UTIs should have an abdominal ultrasound within 6 weeks
* Children with atypical UTIs should have an abdominal ultrasound during the illness

2) Micturating cystourethrogram (MCUG)
* Used to investigate atypical or recurrent UTIs in children <6 months or when family history of VER or poor urinary flow on US
* Involves: catheterising child, injecting contrast into bladder and taking X-rays to determine whether contrast is refluxing into ureters
o Children given prophylactic antibiotics for 3 days before

Investigating renal damage: DMSA (Dimercaptosuccinic acid) scan
- Used 4-6 months after illness
- Involves injecting radioactive material (DMSA) and using a gamma camera to assess how well material is taken up by the kidneys
- If patches of kidney doesn’t take up material -> indicates scarring due to previous infection

30
Q

recurrent UTI investigations

A

Should be investigated for underlying cause and renal damage
Investigation cause:
1) US scans
* All children under 6 months with their first UTI should have an abdominal ultrasound within 6 weeks, or during the illness if there are recurrent UTIs or atypical bacteria
* Children with recurrent UTIs should have an abdominal ultrasound within 6 weeks
* Children with atypical UTIs should have an abdominal ultrasound during the illness

**
2) Micturating cystourethrogram (MCUG)**
* Used to investigate atypical or recurrent UTIs in children <6 months or when family history of VER or poor urinary flow on US
* Involves: catheterising child, injecting contrast into bladder and taking X-rays to determine whether contrast is refluxing into ureters
o Children given prophylactic antibiotics for 3 days before

**
Investigating renal damage: DMSA (Dimercaptosuccinic acid) scan**
- Used 4-6 months after illness
- Involves injecting radioactive material (DMSA) and using a gamma camera to assess how well material is taken up by the kidneys
- If patches of kidney doesn’t take up material -> indicates scarring due to previous infection

31
Q

Vesico-Ureteric Reflux (VUR)
Background

A

Vesico-ureteric reflux (VUR) is where urine has a tendency to flow from the bladder back into the ureters.
- This predisposes patients to developing upper urinary tract infections and subsequent renal scarring.

32
Q

investigations for VUR

A

Micturating cystourethrogram (MCUG).

33
Q

Management of VUR

A

Depends on severity
* Avoid constipation
* Avoid an excessively full bladder
* Prophylactic antibiotics
* Surgical input from paediatric urology

34
Q

posterior urethral valve

A
  • Where there is tissue at proximal end of urethra (closest to the bladder) that causes obstruction of urine output
  • Occurs in newborn boys

are obstructive membranes that develop in the urethra (tube that drains urine from the bladder), close to the bladder. The valve can obstruct or block the outflow of urine through the urethra.

35
Q

pathophysiology of posteiror urethral valve

A

1) Hydronephrosis
- Obstruction can increased back pressure into the bladder, ureters and up to the kidneys causing hydronephrosis

2) UTI
- Restriction in outflow prevents bladder from fully emptying

36
Q

Presentation of posterior urethral valve

A

It can vary in severity. Mild cases may be asymptomatic or present with:
* Difficulty urinating
* Weak urinary stream
* Chronic urinary retention
* Palpable bladder
* Recurrent urinary tract infections
* Impaired kidney function

37
Q

posterior urethral valve: fetal and neonatal problems

A

Fetal and neonatal problems
- Severe cases can cause obstruction to urine outflow in the developing fetus resulting in bilateral hydronephrosis and oligohydramnios (low amniotic fluid volume).
- The oligohydramnios leads to underdeveloped fetal lungs (pulmonary hypoplasia) with respiratory failure shortly after birth.

38
Q

Investigations for posterior urethral valve

A
  • May be picked up on antenatal scans – oligohydramnios and hydronephrosis
  • Abdominal US – enlarged thickened bladder and bilateral hydronephrosis
  • MCUG
  • Cystoscopy
39
Q

Management of posterior urethral valve

A

Mild- observe and monitor
- If required a temporary catheter can be inserted to bypass valve whilst awaiting definitive management

Definitive management (sounds a bit like uretrocele surgery you saw
- Ablation of extra urethral tissue during cytoscopy

40
Q

acute kidney injury

A

a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days.
Associated with increased mortality and morbidity

41
Q

RF for AKI

A

Risk factors
* Diabetes
* CKD
* Any major medical co-morbidity
* Sepsis
* Medications - NSAIDs, Antibiotics

42
Q

investigations for AKI

A
  • Urine dipstick- protein and blood
  • To look for …… perform:
    o Vasculitis: c-ANCA (PR3) and p-ANCA (MPO)
    o Lupus nephritis: anti-GBM, ANA, C3, C4
    o Myeloma: serum immunoglobulins and electrophoresis to look for myeloma
  • Daily FBC, UandEs, LFTs, bone profile, CRP, serum bicarbonate, CK
  • Urine PCR, MC+S, USS KUB
  • If suspected post-streptococcal GN- anti-streptolysin O titres
  • In case of associated thrombocytopenia consider HUS/TTP/Disseminated Intravascular Coagulopathy, request haemolysis screen - blood film, LDH, bilirubin, reticulocytes, haptoglobin, and call Renal SpR urgently.
  • Check cryoglobulins if unexplained rash, peripheral neuropathy, hypocomplementemia, known hepatitis C, history of lymphoproliferative disorder, or +ve RhF.
43
Q

Management AKI

A
  • Discontinue nephrotoxic agents e.g. NSAID, ACEi
  • Ensure volume status and perfusion pressure
    o If dehydrated- IV fluids
    o If overloaded- diuretics
    o Aim for euvolemia
  • Be aware of third space losses
  • Urine output and daily bloods
  • Avoid hyperglycaemia
  • Treat underlying causes
  • Refer to specialist
  • Consider ICU admission
44
Q

causes of AKI split into

A

prerenal
intirnsic
postrenal

45
Q

prerenal causes of AKI

A

o Hypovolemia e.g. shock
o Decreased CO
o Decreased effective circulating volume (CCF, liver failure)
o Impaired autoregulation (NSAIDs, ACEi, ARB, cyclosporin)

46
Q

intrinsic causes of AKI

A

Glomerular
- Acute glomerulonephritis
- Tubules and interstitium
o Ischaemia
o Sepsis/infection
o Nephrotoxins
–>Exogenous
* Iodinated contrast, aminoglycosides, cisplatin, amphotericin B
–>Endogenous
* Haemolysis
* Rhabdomyolysis
* Myeloma
* Intratubular crystals
**- Vascular **
o Vasculitis
o Malignant hypertension
o TTP-HUS

47
Q

postrenal causes of AKI

A

Bladder outlet obstruction

48
Q

staging of AKI

A
49
Q

fluid prescribing question

A

Paediatrics (Y4) (42 decks)

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