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Specialty Blocks > 3. Paeds [Renal] > Flashcards

3. Paeds [Renal] Flashcards

1
Q

Top 5 renal disease presentations / symptoms:

A

Flank mass
Haematuria
Proteinuria _/- oedema
Oliguria / Polyuria
Hypertension

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2
Q

Top 5 urinary tract anomalies:

A

Renal agenesis (Potter sequence = bilateral renal agenesis and pulmonary hypoplasia)

Horseshoe / pelvic kidney

Obstruction e.g. posterior urethral valves, VUJ and PUJ obstruction

Multicystic dysplastic kidney disease (irregular cysts with no normal renal tissue)

Duplex - upper pole ureter tends to obstruct, and lower pole to reflux (VUR)

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3
Q

4 causes of oedema in children:

A

Nephrotic syndrome
Heart failure
Malnutrition
Liver failure

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4
Q

Proteinuria can either be benign or pathological; presence of which symptoms would lead you to think it was pathological?

A

Abnormal BP
Abnormal renal function
Macroscopic haematuria

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5
Q

State some causes of pathological proteinuria in children.

A

Glomerular disease e.g. glomerulosclerosis, glomerulonephritis, nephrotic syndrome, familial haematuria

Physiological stress .g. strenuous exercise, cold exposure, febrile illness, congestive cardiac failure

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6
Q

Describe the classification of nephrotic syndrome in children, including specific causes.

A

Idiopathic: Minimal Change Disease = 80-90%, FSGS 10-20%

Secondary: SLE, HSP

Congenital

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7
Q

Give the definition of nephrotic syndrome in children.

A

Proteinuria (>1g/m2/day)
Hypoalbuminaemia (25 g/L)
Oedema

High protein : creatinine ratio in one early morning urine sample (nephrotic range >150mg/mmol)

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8
Q

What is the treatment for nephrotic syndrome in children?

A

Prednisolone high dose reducing course (high dose for 4 weeks then gradually weaned over 8 weeks)

20% albumin infusion if severe hypoalbuminaemia

Furosemide for oedema

Low salt diet

Pneumococcal vaccination

Penicillin prophylaxis if severe

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9
Q

Haematuria can be macroscopic or microscopic. It is then also split into non-glomerular and glomerular causes. Give examples of each.

A

Non-glomerular:
Infection
Sickle cell
Trauma
Stones
Coagulopathy / bleeding disorder
Tumour
Renal vein thrombosis
Structural abnormalities

Glomerular:
Acute or chronic glomerulonephritis
IgA nephropathy
Familial nephritis

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10
Q

Ideally all patients presenting to paediatric services should have a BP measurement. Causes of hypertension in children can be split into 7 different categories. What are they?

A
  1. Renin-dependent e.g. renovascular disease, renal tumours, renal parenchymal disorders
  2. Pharmacological e.g. steroids, stimulants e.g. methylphenidate / dexamphetamine , cocaine, ketamine, methamphetamine, liquorice
  3. Endocrine e.g. Cushings, CAH, hyperthyroidism
  4. Catecholamine excess e.g. phaeochromocytoma, neuroblastoma
  5. Coarctation of the aorta
  6. Obesity
  7. Essential hypertension
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11
Q

5 indications for dialysis:

A

Severe volume overload e.g. pulmonary oedema, severe hypertension

Severe hyperkalaemia

Symptomatic uraemia

Severe metabolic acidosis

Toxin removal

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12
Q

Acute renal failure can be split into pre-renal, renal and post-renal causes. Give examples for each.

A

Pre-renal; hypovolaemia, cardiac failure

Renal; glomerulonephritis, HUS, tubular e.g. ATN, interstitial e.g. NSAIDs.

Post-renal; obstruction.

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13
Q

What is the treatment for a hypertensive crisis, and by how much should you aim to lower the BP / timeline of this?

A

Labetalol / Sodium Nitroprusside

Aim to lower by 1/3 every 12 hours for the first 24 hours, and the the 3rd 1/3 over 24 hours.

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14
Q

Discuss the top 5 renal imaging modalities.

A

US for renal anatomy, and vascular perfusion with doppler.

DMSA to evaluate renal function and structure. Particularly useful for renal scarring, congenital abnormalities, renal tumours and differential renal function. Must be done 3 months post UTI if one present.

DTPA for drainage and obstruction assessment.

MCUG for lower UT abnormalities. Contrast into bladder through catheter then imaging during voiding. Helps diagnose VUR, posterior urethral valves, urethral strictures.

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15
Q

What is the triad of HUS?

A

Acute renal failure
Microangiopathic haemolytic anaemia
Thrombocytopenia

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16
Q

Give some clinical features of HUS and the physiological causes of them (8).

A

Bruising (thrombocytopenia)
Abdominal pain
Hypertension (renal failure)
Confusion (uraemia)
Oliguria (renal failure)
Haematuria
Lethargy and pallor (anaemia)

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17
Q

What increases the risk of HUS post gastroenteritis?

A

Use of antibiotics and antimotility agents e.g. loperamide during gastroenteritis episode

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18
Q

What is the most common cause of HUS?

A

Gastroenteritis (prodrome of bloody diarrhoea) from E.coli 0157 or Shigella with shiga toxin production.

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19
Q

What management plan would be suitable for a patient with HUS?

A

Supportive management:

IV fluids

Hypertension management (if crisis, bb and sodium nitroprusside)

Severe anaemia correction with blood transfusion

Dialysis if severe renal failure

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20
Q

What are the consequences of posterior urethral valves?

A

Bladder hypertrophy leading to uni or bilateral hydronephrosis and renal failure.

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21
Q

Give 4 complications of nephrotic syndrome in children.

A

Hypovolaemia - fluid leaks from the intravascular space to the interstitial space causing oedema and low BP.

Infections due to loss of complement and Ig in urine. Exacerbated by treatment with steroids.

Thrombosis - proteins that normal prevent clotting are lost in the kidneys, and because the liver responds to the low albumin by producing pro-thrombotic proteins.

Also, hypocalcaemia as vitamin D and binding protein is lost in urine.

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22
Q

What is the difference between acute tubular necrosis and acute interstitial nephritis?

A

ATN is the most common cause of AKI, and its pathophysiology is either ischaemic or pharmacological insult. Necrosis of tubular epithelial cells severely affects functioning.
Ischaemic causes: hypovolaemia / shock / sepsis
Drugs; aminoglycosides, lead, radiocontrast, myoglobin secondary to rhabdo.
Muddy cell casts are present.

Acute Interstitial Nephritis is the presence of interstitial oedema between tubules. Results in fever, rash, hypertension, arthralgia and eosinophilia. Mild renal impairment. White cell casts are present.
Causes include antibiotics, rifampicin, NSAIDs, allopurinol and furosemide. SLE, sjogren’s also.

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23
Q

In an AKI, which biochemical markers can be used to differentiate between acute tubular necrosis or a pre-renal uraemia?

A

Pre-renal uraemia; kidneys hold onto sodium to preserve volume, leading to low urinary sodium <20, high urine osmolality >500 and a good response to fluid challenge.

ATN has a raised urine sodium excretion >40, urine osmolality of <350 and a poor response to fluid challenge.

24
Q

Describe the first line investigations for patients with hypertension in all cases.

A

FBC, U&Es, creatinine, albumin, bicarb, calcium, phosphate, LFTs.

Plasma renin levels, aldosterone and catecholamines.

Urinalysis, microscopy and culture, urinary catecholamines, urinary protein : creatinine ratio.

CXR, Echo, ECG.

Renal US + doppler of the renal vessels, ?DMSA to look for scarring.

25
Q

The classic triad of nephrotic syndrome is proteinuria, hypoalbuminaemia and oedema. What other 3 features can occur in patients with nephrotic syndrome?

A

Hyperlipidaemia
Hypercoagulable state (due to loss of antithrombin III)
Hypertension
Predisposition to infection

26
Q

Minimal change disease is the most common cause of nephrotic syndrome in children, accounting for 80-90% of cases. Give some intrinsic kidney diseases and also systemic illnesses that can also cause nephrotic syndrome in children.

A

Intrinsic: FSGS, Membranoproliferative

Systemic: HSP, Infections e.g. HIV, hepatitis, malaria, Diabetes

27
Q

80% of children with minimal change disease are steroid responsive. What are the next options if a patient is steroid resistant?

A

Immunosuppressants such as cyclosporine, tacrolimus or rituximab.

ACE inhibitors.

28
Q

Triad / features of nephritic syndrome:

A

Acute renal failure / reduced renal function
Haematuria
Proteinuria (less so than nephrotic syndrome)

29
Q

2 most common causes of nephritic syndrome in children:

A

Post-streptococcal glomerulonephritis

IgA nephropathy (Berger’s disease)

Other causes include HSP vasculitis, SLE, microscopic polyarteritis, polyarteritis nodosa, anti-GBM disease (Goodpasture’s, very rare).

30
Q

What is post-streptococcal glomerulonephritis, how would you diagnose it and what do you do for the patient?

A

Occur 1-3 weeks post streptococcal infection, often tonsillitis. IgG, IgM and C3 deposition in the glomeruli.

Features include general headache and malaise, visible haematuria, proteinuria (maybe resulting in oedema), hypertension and oliguria.

Diagnosis confirmed with anti-streptolysin O titres and low C3 in bloods. Renal biopsy is done.

31
Q

What is IgA nephropathy related to, what is seen on a renal biopsy, who tends to present with it, and how is it managed?

A

Related to HSP, which is an IgA vasculitis.

Commonly presents in young people following and URTI, but usually 1-2 days rather than weeks with post-strep.
Recurrent episodes of macroscopic haematuria, rarely nephrotic range proteinuria and renal failure is actually unusual.

IgA deposits in the nephrons causing inflammation.
Renal biopsy shows IgA deposits and glomerular mesangial proliferation.

Supportive treatment of the renal failure and immunosuppressant meds e.g. steroids and cyclophosphamide to slow progression.

32
Q

How to differentiate between post-strep GN and IgA nephropathy?

A

Post-strep is associated with low complement levels e.g. low C3.

Time of onset is different; IgA presents 1-2 days post URTI infection, whereas post-strep GN is more likely 1-2 weeks.

Main symptom in post-strep GN is proteinuria, as opposed to IgA where haematuria is more dominant over proteinuria.

33
Q

[ADULT] In some cases of IgA nephropathy, no management is required, only follow up. When would this be warranted, and when would more active treatment be needed and with what?

A

Isolated haematuria, no or minimal proteinuria (<500-1000mg/day) and normal GFR = only follow up.

Persistent proteinuria >500-1000mg/day and normal / slightly reduced GFR = ACE inhibitor is first line.

Active disease e.g. falling GFR, or failure to respond to ACEi, then corticosteroids.

34
Q

Give one marker of good prognosis and 5 markers of poor prognosis for IgA nephropathy.

A

Good: frank haematuria

Poor: smoker, male, hypertension, proteinuria esp >2g /day, hyperlipidaemia

35
Q

[ADULT] Give 3 conditions associated with IgA nephropathy.

A

HSP
Alcoholic cirrhosis
Coeliac disease / dermatitis herpetiformis

36
Q

Describe the pathophysiology of acute glomerulonephritis, and give causes.

A

Increased glomerular cellularity restricts glomerular blood flow, and therefore glomerular filtration.
This leads to decreased urine output and fluid overload, oedema (initially periorbital), hypertension and haematuria and proteinuria.

37
Q

[ADULT] What criteria is used to stage AKI and describe the stages.

A

KDIGO

Stage 1
Urine output <0.5ml/kg/hr for >=6 hours
Creatinine increase to 1.5-1.9x baseline
Creatinine increased by 26.5

Stage 2
Urine output <0.5ml/kg/hr for >=12 hours
Creatinine 2.0-2.9x baseline

Stage 3
Urine output <0.3ml/kg/hr for >=24 hours
Creatinine >=353
Creatinine >3x baseline
RRT started
If under 18, eGFR of <35

38
Q

When to refer to a nephrologist in AKI:

A

Stage 3 AKI
Renal transplant
ITU patient with unknown cause
Vasculitis, GN, tubulointerstitial nephritis, myeloma
Unknown cause of AKI
Inadequate response to treatment
CKD 4 / 5
RRT qualify, hyperkalaemia, metabolic acidosis, complications of uraemia, fluid overload e.g. pulmonary oedema

39
Q

At what age do most children achieve day and night time continence, and therefore at what age can nocturnal enuresis be reasonably diagnosed?

A

Most children by age 3/4.

Can be diagnosed in a child 5 years or older, in the absence of congenital or acquired defects of the nervous system or urinary tract.
Primary or secondary (has been dry for at least 6 months before).

40
Q

Give 3 underlying causes / triggers for nocturnal enuresis.

A

Constipation
Diabetes mellitus
UTI if recent onset

41
Q

Give 2 management options outwith behavioural advice to treat nocturnal enuresis.

A

Enuresis alarm

Desmopressin if short term control is needed e.g. sleepovers, or enuresis alarm not acceptable to family. It is also known as ADH, and is taken at night to reduce the volume of urine produced by the kidneys.

42
Q

Causes of primary nocturnal enuresis:

A

Family history of delayed dry nights
Overactive bladder
Fluid intake prior to bedtime
Failure to wake due to particularly deep sleep and underdeveloped bladder signals
Psychological stress

43
Q

Give some secondary causes of nocturnal enuresis.

A

UTI
Constipation
Type 1 Diabetes
New psychosocial problems e.g. family stress
Maltreatment

44
Q

Which type of polycystic kidney disease presents in neonates?

A

Autosomal recessive

45
Q

What is the underlying pathophysiology / mutation in ARPKD?

A

Mutation in the PKHD1 gene on chromosome 6.
This gene codes for a protein that is responsible for the creation of tubules and maintenance of healthy epithelial tissue in the kidneys, liver and pancreas.

46
Q

The underlying pathology of ARPKD also causes other issues including:

A

Cystic enlargement of renal collecting ducts

Oligohydramnios, pulmonary hypoplasia and Potter syndrome

Congenital liver fibrosis

47
Q

When is ARPKD usually picked up?

A

Antenatal period with oligohydramnios and polycystic kidneys seen on antenatal scans.

Oligohydramnios can lead to Potter syndrome (dysmorphic features and skeletal abnormalities).

48
Q

What would happen to a neonate in the early stages of life born with ARPKD?

A

Pulmonary hypoplasia from oligohydramnios would result in respiratory failure shortly after birth, additionally impeded by large polycystic kidneys.

Patients may require renal dialysis in the early stages of life.

Most patients develop end stage renal failure by the time they reach adulthood.

49
Q

Patients with ARPKD have a number of ongoing problems throughout life. State 5.

A

Liver failure due to liver fibrosis.
Portal hypertension leading to oesophageal varices.
Chronic lung disease
Progressive renal failure.
Hypertension due to renal failure.

50
Q

Babies and older children with a UTI will present differently. Give clinical signs and symptoms of a baby vs an older child with a suspected UTI.

A

Baby:
Fever
Lethargy
Irritability
Vomiting
Poor feeding
Urinary frequency

Child:
Urinary frequency
Dysuria
Abdo pain esp suprapubic
Fever
Vomiting
Incontinence

51
Q

How should all children under 3 months with a fever be managed?

A

IV antibiotics e.g. ceftriaxone
Full septic screen
LP considered

52
Q

What are the top 3 organisms that can cause UTI in children?

A

E.coli in 80%
Proteus
Pseudomonas

53
Q

Give 3 predisposing factors for UTI in children.

A

Incomplete bladder emptying; infrequent voiding, hurried micturition, chronic constipation causing obstruction, neuropathic bladder.

Vesicoureteric reflux; a developmental anomaly present in 35% of children who present with a UTI.

Poor hygiene e.g. girls not wiping front to back

54
Q

What is VUR, how is it diagnosed and what is the management of it?

A

Vesicoureteric reflux is where urine has a tendency to flow from the bladder back into the ureters.
Diagnosed with a MCUG.

Avoid constipation, avoid excessively full bladder, prophylactic antibiotics and surgical input from paediatric urology.

55
Q

When should US scans be performed on children to investigate a UTI?

A

Children < 6 months with their first UTI; within 6 weeks, or during illness if recurrent UTIs or atypical bacteria.

Children with recurrent UTI should have US within 6 weeks.

Children with atypical UTIs should have US during the illness.

Specialty Blocks (27 decks)

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