Renal Flashcards

1
Q

How may a child with a UTI present?

What is important about children with UTI’s?

A

Classic Sx:

  • Dysuria
  • Frequency (how many wet nappies?)
  • Flank pain
  • Recurrent UTIs
  • Offensive, cloudy urine
    • D&V, rigors, fever, enuresis

Infants:

  • Fever
  • Vomiting
  • Irritability, lethargy
  • Poor feeding/growth
  • Jaundice
  • Sepsis
  • Febrile seizures

Note: up to 50% have structural abnormalities of the urinary tract e.g. VUR

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2
Q

What investigations would you do in a child with suspected UTI?

A

Ix:

  • > Obs + Exam
  • > *Urine dip (nitrite stick test which v specific, leucocyte esterase test which is less specific/will be +ve in children without UTI and balanitis/vulvovaginitis also)
  • > Urine MC+S - Diagnose UTI (Bacteriuria)
  • > Imaging only indicated unless atypical or recurrent (USS + DMSA** (only in <3yo if atypical)
  • Clean catch preferably for urine collection, if not then urine collection pads, if not then catheter samples/suprapubic aspiration
  • *DMSA looks at renal scarring
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3
Q

How may you distinguish an upper and a lower UTI clinically?

A

Upper/pyelonephritis:

  • Bacteriruria + fever >38 degrees
  • Bacteriuria + loin pain/tenderness

Lower/cystitis:
- Anything else i.e. bacteriuria/dysuria but NO systemic symptoms

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4
Q
How would you manage a child with a UTI: 
i) Neonates and children under 3m?
ii) Children 3m+ ?
iii) Recurrent UTI's? 
How may you advise avoiding UTIs?
A

Note: always say that antibiotic choice is guided by local guidelines/resistance patterns [below is NICE guidance]

i) Under 3m:
- Low threshold for admission + full sepsis screen
- IV ABx - Cefotaxime/Gent, and Ampicillin and then switched to oral when cultures negative/clinical improvement
- Refer to paediatric specialist
- Urgent USS should be booked for within 4-6w

ii) 3m+
- Consider admission
- IV ABx 7-10d out of:
–> Co-amoxiclav
–> Ceftriaxone
–> Cefuroxime
–> Gentamicin
- OR Oral Abx for 7-10d, or 3d if 13+
–> Cephalexin
–> Co-amoxiclav
–> Trimethoprim
–> Ciprofloxacin
for 7-10 days if stable
- If <6m when they have their first UTI then urgent USS should be booked (4-6w)
- Safety net

Recurrent UTI

  • Scans: USS, MCUG (structure) and DMSA for scarring and reflux
  • Refer to specialist
  • Abx prophylaxis?

Medical measures to prevent UTI:

  • High fluid intake to produce increased output
  • Ensure complete bladder emptying
  • Good perineal hygiene
  • Regular voiding
  • Treating/preventing constipation
  • Probiotics (lactobacillus acidophilus)
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5
Q

When is a child normally potty trained/dry by night and day?

A

Potty training started around 2.5y but varies between children

  • > Dry by day - by 4yo
  • > Dry by day and night - by 5yo (most by 3-4y)
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6
Q

What is the difference between primary and secondary bedwetting?

What Ix would you do (if indicated)?

A

Primary:
-> Child has never been dry before

Secondary
-> Enuresis occurring after child has previously been dry for 6 months

Ix:
-> Abdominal exam, rule out DDx
-> Urine diary
-> Urine MC+S, Dipstick
Other:
-> Renal USS
-> MCUG
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7
Q

How would you manage primary enuresis (without or with daytime symptoms)?

A

With daytime Sx:
-> Referral to enuresis clinic, community paediatrician

Without daytime Sx:
- <5yo
= 1st line is conservative education:
–> encourage and easy access to toilet (bedside potty)
–> reduce fluids before bed, no caffeine
–> positive reward system
–> reassure parents that often resolves by 5y (as bladder capacity increases and learn to wake at the sensation of a full bladder) - if not can try other options
–> support of leaflets/site: ERIC)

  • > 5yo
    = 1st line is conservative + enuresis alarm (wakes child when wet)
    = 2nd line is desmopressin (1st line if >7yo OR requires short-term control e.g. a trip)
    = 3rd line = combination
    = Referral to enuresis clinic, community paediatrician if bedwetting hasn’t responded to 2 courses of treatment
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8
Q

What are some causes of secondary bedwetting?

A

Causes include:

  • UTI, recurrent UTI
  • Constipation

Secondary care Mx:

  • Diabetes
  • Psychological problems, developmental delay/LD
  • Neurological/physical problems
  • Family issues
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9
Q

What is Wilm’s tumour? Who does it tend to affect?

A

AKA Nephroblastoma (undifferentiated mesodermal tumour of intermediate cell mass - primitive renal tubules and mesenchymal cells)

  • > Most common intra-abdominal tumour of childhood (2nd most common cancer in children after ALL)
  • > 80% are <5y, often 3yo children
  • > 95% unilateral
  • > 1-2% have FHx
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10
Q

What are some associations with Wilm’s tumour?

A
  • Beckwith-Wiedmann syndrome (specific parts of the body overgrow, presenting at birth e..g islet cell hyperplasia)
  • WAGR syndrome (Wilms, Aniridia, GU malformations, mental retardation)
  • Hemihypertrophy
  • 33% with a loss of function mutation on WT1 gene on X11
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11
Q

How may a child with Wilm’s tumour present?

A

Sx:

  • Asymptomatic abdominal mass (painless, smooth, firm)
  • Painless haematuria
  • Less commonly: abode pain, anaemia due to haemorrhage into the mass, distension
  • RF e.g. FHx, Congenital syndromes
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12
Q

How would you Ix and stage Wilm’s tumours? How would you Mx it? What is its prognosis? What should you avoid?

A

Ix:

  • > USS
  • > CT/MRI for spread
  • > Avoid biopsy as may worsen condition
  • > Bloods - FBC, Cr/Urea, LFTs

Staging if 1-5:
1 = limited to kidney, completely excisable
2 = not limited to kidney, completely excisable
3 = not limited to kidney, not completely excisable
4 = spread beyond abdomen, haematogenous metastasis (LN and other organs)
5 = bilateral (each tumour graded separately

Mx:

  • Nephrectomy + chemotherapy (+radiotherapy before surgery if advanced disease)
  • 80% cure rate
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13
Q

What is phimosis? Is it always physiological and why is it important?

A

Inability to retract foreskin

Physiological at birth:
-> By 1y, 50% have non-retractable foreskin
-> By 4y only 10% do
-> by 17y, only 1% do
If persistent to puberty, it can increase the risk of infection + cause issues with urination and intercourse

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14
Q

How is phimosis managed?

note: what is Balanitis Xerotica Obliterans (BXO)

A

Mx:

<2y = reassure and review in 6m and promote personal hygeine (clean the external surface normally, don’t need to physically/forcibly retract foreskin until separates itself)

> 2y = circumcision or topical steroid cream depending on severity

BXO = pathological phimosis where there is scarring of the foreskin (rare before 5y)
-> haematuria, painful erections, recurrent UTI, weak stream, redness, tenderness

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15
Q

What is Paraphimosis and how is it managed?

A

Paraphimosis - where the foreskin is trapped in the retracted position, proximal to the swollen glans = EMERGENCY [restricted blood to head of the penis –> turns purple]

Mx:

  • Analgesia (local/nerve block) + attempt to reduce foreskin with gentle compression and saline soaked swab
  • Emergency referral to urologist + surgery if required (ischaemia, necrosis, prev interventions failed)
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16
Q

What is hypospadias (+epispadias) and how does it present? What is the management for it?

A

Hypospadias = wrongly positioned meatus (ventral in hypospadias, dorsal in epispadias)

Features:

  • Ventral foramen
  • Hooded foreskin
  • Chordee (ventral curvature)

Mx:

  • No intervention required but can do surgery (after 3m) –> aim for urinating in a straight line when standing and straight erections
  • HOWEVER, advise NO circumcision as the skin is required for the repair
17
Q

What is balanoposthitis and how is it managed?

A

balanoposthitis = inflamed/purulent discharge from the foreskin

  • single episodes common
  • managed by warm baths, broad spectrum Abx (if recurrent, then circumcision)
18
Q

What is testicular torsion and who does it tend to affect (RFs)? What is another form of torsion?

A

Torsion

  • Urological emergency where there is twisting of the testicle on the spermatic cord (processus vaginalis) causing ischaemia of the testes
  • Post-pubertal age most commonly affected i.e. 16y but ranges from 11-30y
  • RF = undescended testes, ‘clapper bell’ testes (on the side)
  • MUST be excluded in any boy with acute abdomen

NOTE: Torsion of the appendix testes (Hyatid of Morgani) is more common but the pain evolves over MULTIPLE days.
-> Often surgery is needed as can’t distinguish between true torsion but if a BLUE dot is seen over the superior pole of the testes then no surgery may be required/just analgesia

19
Q

How would someone with TT present?

A

Sx:

  • SUDDEN onset pain; localised to testis or in abdomen
  • N+ V
  • Redness
  • Oedema
20
Q

How would you Ix and Mx suspected TT? What is its prognosis?

A

Ix:

  • Clinical Dx
  • -> [lifting testes increases pain whereas in epididymitis it reduces pain - Prehn’s sign]
  • Doppler USS (but this shouldn’t delay surgery)

Mx:
- Urgent urological/paeds surgery referral + NBM
- Exploratory surgery with bilateral orchidiopexy vs orchidectomy, and fixation of contralateral testes**
- Supportive care (analgesia/sedation/antiemetics)
note:
- If caught within <6h then >90% saved whereas if <24h then <10% saved

*Process: Raphe incision -> untort testes -> watch reperfusion in warm saline -> decide if orchidectomy needed

21
Q

How can renal disease (AKI) be categorised?

A

AKI Stage 1:
= Increase ≥26 µmol/L serum Cr; or by 1.5-1.9x the reference sCr
= Urine output <0.5mL/kg/hr, 6-12hr

AKI Stage 2:
= Increase 2.0-2.9x the reference sCr
= UO <0.5mL/kg/hr, ≥12hr

AKI Stage 3:
= Increase ≥354 µmol/L; or by ≥3x the reference sCr
= UO <0.3mL/kg/hr, ≥24hr
or Anuric for ≥12hr

22
Q

What is orthostatic proteinuria? How would you assess it?

A

Common transient cause of proteinuria

- measure urine PCR (protein:Cr ratio) in a series of early morning specimens

23
Q

What is nephrotic syndrome? What is the most common cause of it in children?
How would a child present?

A

Triad of: low albumin, peripheral oedema and proteinuria
–> Most commonly = Minimal Change Disease in kids (90%; children aged 2-4y)

Sx:

  • 1st sign is peri-orbital oedema (often misdiagnosed as allergy)
  • 2nd is other delayed features of oedema i.e. leg swelling, features of underlying diagnosis
24
Q

How would you Ix and manage suspected nephrotic syndrome?

A

Ix:

  • Urine dip
  • Urine MC+S
  • Bloods - FBC, ESR/CRP, Cr, Albumin, Complement [C3,C4]
  • Anti-streptolysin O or anti-DNase B titres (recent strep throat infection)
  • HBV, HCV, malaria screen
  • [renal biopsy but normally in kids, only if unresponsive to steroids]

Mx:
1st line:
–> Oral 60mg/m2 prednisolone for 4-6w, reducing the dose from 4w
–> Fluid restricted and low salt diet
–> If advanced, may require albumin and furosemide

2nd line:

  • -> specialised renal biopsy
  • -> unresponsive to steroids/atypical - CNIs and methylprednisolone

[Renal histology shows steroid sensitive nephrotic syndrome (normal on light microscopy) but electron microscopy shows fusion of podocytes (MCD)]

Complications:

  • > Thrombosis (loss of AT-III in urine)
  • > Infection (loss of Ig in urine)
  • > Hypercholesteraemia (due to urinary albumin loss)
25
Q

What are the most common causes of [acute] renal failure in children?

A

ARF causes:

  • > HUS (low RBC, platelets and AKI) - require admission, may find schistocytes on blood film, -> Haemorrhagic E.coli O157 [shiga toxin] causes infectious diarrhoea
  • > Acute tubular necrosis, usually due to organ failure in ITU/after cardiac surgery, sepsis
26
Q

How would a child with ARF/CRF present? How would you specifically treat pre, intrinsic and post-renal ARF?

A

Sx:

  • Oligouria/Anuria
  • Oedema (feet, legs, abdomen, weight gain)
  • Brown urine
  • Fatigue, lethargy, N+V

Pre-renal failure (i.e. hypovolaemia)

  • -> Urgent fluid replacement is key in these patients
  • -> Adrenaline if severely hypotensive
  • -> Furosemide if overloaded

Intrinsic renal failure:

  • -> Monitor water and electrolyte balance
  • -> High calorie, normal protein diet
  • -> Furosemide if overloaded, IV fluids if pre-existing pre-renal failure
  • -> Consider RRT

Post-renal failure:

  • -> Refer immediately to urology if any of: pyonephrosis, obstructed solitary kidney, bilateral upper urinary tract obstruction + complications of AKI due to obstruction
  • -> Assessment is needed of site of obstruction
  • -> Relief can be given by nephrostomy or bladder catheterisation
  • -> Furosemide if overloaded
  • -> Consider RRT
27
Q

How would you Ix and Mx ARF? What are 7 indications for dialysis?

A

Ix:

  • > Urine dip for protein
  • > Renal USS for obstruction identification
  • AKI can show large, bright kidneys with loss of cortical and medullary differentiation
  • CKD may show small kidneys
Mx:
- Diuretics PRN to treat fluid overload/oedema whilst awaiting dialysis
- Fluid restriction
- Dialysis:
Indicated when one of the following:
-> Failure of conservative Tx
-> Multisystem failure
-> Refractory hyperkalaemia, or low/high Na
-> Pul. oedema/refractory fluid overload
-> Metabolic acidosis
-> Uraemic sx (encephalopathy, nausea, pruritus)
-> CKD stage 5 (GFR<15)
'FRUMMPE'

Good prognosis in childhood unless serious condition/masked by other things e.g. infection post cardiac surgery

28
Q

What are some causes of acute glomerulonephritis?

What are some immune mediated disorders?

A

Many causes (see diagram by A.Ludley) but may present as nephrotic (protein losing) or nephritic (haematuria) syndrome:

  • > Minimal change disease
  • > IgA nephropathy (adults but includes HSP in children)
  • > Vasculitis (SLE, ANCA+)
  • > Goodpasture’s
  • > Post-infectious (post-strep in children)

Immune-mediated:

  • > Minimal change
  • > Diffuse (all glomeruli)
  • > Focal (some glomeruli)
  • > Segmental (only parts of affected glomerulus)
29
Q

What is focal segmental glomerulonephritis?

A

Segmental scarring and foot process fusion

  • Nephrotic syndrome
  • Common in older children, may be secondary to obesity or HIV
  • HTN and impaired renal function is seen
  • 50% respond to steroids
30
Q

What is membranous nephropathy?

A

Widespread thickening of basement membrane of the glomeruli due to granular deposits of Ig and complement

  • More common in adults
  • Linked to SLE, drugs, idiopathic also
31
Q

What are some signs of glomerulonephritis? {think nephrotic, nephritic syndrome signs}

A

Sx:

  • > Nephrotic syndrome - hypoalbuminaemia, swelling/oedema, proteinuria
  • > Nephritic syndrome - HTN, haematuria, proteinuria (mild-moderate)
  • > Reduced urine output
  • > Fluid overload
  • > Hypertension and seizures
32
Q

What investigations would you do in someone with suspected glomerulonephritis?

A

Ix:

  • Urine dip
  • Urine MC+S
  • Bloods - FBC, ESR, Cr, Albumin, U&Es, Complement levels
  • Antistreptolysin O/antiDNase B titres
  • HBV, HCV, malaria screen
33
Q

How would you manage glomerulonephritis?

A

Mx depends on type, severity and complications:

Mild

  • Tx cause and supportive treatment
  • May require Abx if post-streptococcal GN i.e. phenoxymethylpenicillin

Moderate:

  • ACEi/ARBs
  • May require Abx if post-streptococcal GN i.e. phenoxymethylpenicillin
  • Furosemide

Severe:

  • Corticosteroids
  • Immunosuppresants e.g, Rituximab
  • Prophylactic trimethoprim for early phases of Tx due to immunosuppression
34
Q

Who does Henoch-Schonlein Purpura affect? What is it?

A

HSP = an IgA small vessel vasculitis; the most common vasculitis of childhood

  • affects mainly boys aged 3-10y
  • often preceded by an URTI (2-3 days before; if 1-12w before then think post-infectious glomerulonephritis)
  • peaks in winter
  • caused by IgA and IgG complexes depositing in the organs and activating complement
35
Q

How would a child with HSP present?

A

Sx:

  • > Purpuric rash on the extensor surfaces of legs, arms, buttocks and ankles (maculopapular, spares trunk)
  • > Arthralgia and periarticular oedema: large joints with swelling of knees and ankles
  • > Abdominal pain: colicky nature, haematemesis, melaena, intussusception
  • > Glomerulonephritis (by 3m, most have this): microscopic/macroscopic haematuria, nephrotic syndrome is rare
36
Q

What investigations would you consider for a child with suspected HSP?

A

Ix:

  • Urine dip
  • Bloods = FBC, clotting screen, U+Es, IgA* [increased IgA, normal coagulation]
  • Urinalysis (RBCs, proteinuria, casts, urea, Cr, 24h protein) - to rule out meningococcal sepsis
  • F/u weekly for 1m, then 2-weekly for 2m, 3m etc till 12m for BP measurements and haematuria
37
Q

What is the management for HSP? What are some complications?

A

Mx:
> Most cases spontaneously resolve within 4w
> Symptomatic mangement i.e.:
–> Paracetamol/NSAIDs for joint pain
–> Oral prednisolone for scrotal involvement, severe oedema or severe abdominal pain
–> IV CS for those with nephrotic-range proteinuria (>3.5g) or rapidly declining renal function
–> Renal transplant may be considered if ESRD
–> F/u checks of BP and renal function

Complications:

  • ARF/CRF as an adult
  • Arthritis of knees
  • Intussusception
  • Pancreatitis
  • Testicular pain (rare)