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*Medicine: Paediatrics > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What are common symptoms of urinary tract and/or renal disease?

A
  • haematuria
  • proteinuria
  • hypertension
  • oedema
  • renal masses
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2
Q

In regards to urological imaging, what is ultrasound used for?

A
  • non-invasive anatomical assessment of the entire urinary tract
  • provides info about renal size
  • can identify most congenital abnormalities, renal calculi, hydonephrosis
  • indicates presence of obstruction or severe reflux
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3
Q

What is the DMSA scan?

A
  • isotope used in static nuclear medicine scans
  • particularly good (gold std) for detecting renal parenchyma defects + scars
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4
Q

What is the MAG3 scan?

A
  • isotope used in dynamic nuclear medicine scans
  • it is exerted in the glomerular filtrate + gives information about blood flow, renal function + drainage
  • good for detecting structural abnormalities
  • in older children who can stop and start voiding it can be used to detect vesicoureteric reflux
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5
Q

What is the MCUG scan?

A
  • micturating cystourethrography
  • the bladder is filled w/ contrast via a urethral catheter
  • contrast lines the bladder to show any vesicoureteric reflux (gold std)
  • uretheral obstruction can also be demonstrated if catheter removed + pt voids
  • invasive + requires catheterisation
  • prophylactic antibiotics are given to prevent iatrogenic infection
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6
Q

How common are urinary tract infections (UTIs) in children?

A

by age 7:

  • 7% of girls
  • 2% of boys

Evidently more common in girls, except in the first 6 months of life

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7
Q

What are the bacterial causes of UTI?

A
  • commonest → E. coli, from bowel flora
  • psueodomonas
  • proteus - splits urea into ammonia making the urine alkaline, which encourages the formation of phosphate stones
  • in the newborn, infection is most likely to be from haematogenous spread
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8
Q

Urinary stasis predisposes to UTIs as well as bacterial infections. What are the causes for this?

A
  • habitual infrequent voiding; vulvitis; constipation; obstructive uropathy eg. urethral valves; neuropathic bladder
  • vesicoureteric reflux:
    • some children are predisposed to this bc their ureters enter the bladder directly rather than at an angle, and the segment of ureter within the bladder is abnormally short
    • reflux into the kidneys can cause distension of ureter and renal pelvis and clubbed calyces
    • reflux increases the risk of renal scarring when a UTI is present
    • the reflux decreases as child gets older
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9
Q

How does the clinical presentation of UTI vary in children, depending on age?

A
  • often child is non-specifically ill
  • infants → fever, D+V, poor feeding, failure to thrive, collapse/septicaemia, neonatal jaundice, febrile convulsion (>6months), rarely any urine symptoms <2 y/o
  • childhood → LUTS: dysuria, frequency, wetting, haematuria, lower abdo pain
  • upper urinary tract symptoms → loin pain, fever, rigors, malaise
  • urinary tract is usually normal, byt 35% have vesico-ureteric reflux, 14% have renal scars (most having reflux too), 5% have stones, 3% develop hypertension

[*dysuria without a fever is often due to vulvitis or balanitis]

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10
Q

For all children present with a fever, it is important to measure: temp, HR, RR + CRT.

Acute pyelonephritis/upper UTI should be suspected in children with what features?

A
  • temp of 38oC or higher + bacteriuria
  • temp < 38oC + loin pain/tenderness + bacteriuria

If no systemic symptoms but bacteruria is present then → cystitis/lower UTI considered

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11
Q

It is rare but healthcare professionals should be aware that urinary symptoms could be due to child abuse. Consider if a child has dysuria or ano-genital discomfort that is persistent or recurrent and has no medical explanation.

What investigations should be done for UTI in children?

A
  • Urine Sample → all infants w/ unexplained temp of 38oC or higher should have urine sent for M+C within 24hrs
    1. clean catch urine sample ⇒ ready w/ pot for baby to pee into
    2. urine collection pads (+ not cotton, gauze, sanitary towels)
    3. catheter or suprapubic aspiration
  • Urine dipstick → leukocyte + nitrites +ve? → M+C
    • E.Coli ⇒ gram negative rods
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12
Q

What are features of an atypical UTI?

A
  • poor urine flow
  • abdominal or bladder mass
  • raised creatinine
  • sepsis
  • failure to respond to treatment within 48 hrs
  • non-E.coli organism
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13
Q

What is the definition of recurrent UTI?

A
  • two or more episodes of upper UTI (pyelonephritis)
  • one episode of upper UTI + one episode of lower UTI
  • three episodes of lower UTI
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14
Q

What is the role of imaging for UTI in infants under 6 months?

A
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15
Q

What is the role of imaging for UTI in childreen between 6 months and 3 years?

A
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16
Q

What is the role of imaging for UTI in children over 3 years?

A
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17
Q

What is the management of UTI in children?

A
  1. All infants < 3 months w/ suspected UTI → refer immediately to care of a paediatric specialist for urine analysis + treatment w/ parenteral antibiotics
  2. For all infants + children 3 months or older w/ cystitis/lower UTI →
    • treat w/ oral antibiotics for 3 days ⇒ trimethoprim, nitrofurantoin, a cephalosporin or amoxicillin may be suitable (refer to guidelines + results of urine culture)
    • advise parents + carers to bring child back to GP if still unwell 24-48hrs later
  3. For infants + children 3 months or older w/ acute pyelonephritis or upper UTI →
    • consider referral to paed specialist ?(age, vomming, fluids, carer)
    • if referral not appt ⇒ treat w/ oral abx ⇒ ciprofloxacin or co-amoxiclav 7-10 days
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18
Q

What is the use of prophylactic antibiotics for UTI?

A
  • consider if recurrent UTI or significant GU anomaly/renal damage
  • eg. trimethoprim prophylaxis (2mg/kg at night, max 100mg)
  • eg. while awaiting imaging - and sometimes indefinitiely (optimum duration is unknown, but may be after 2 negative cystograms, if indication is reflux)
  • consider screening siblings for reflux
  • prophylaxis can be ruled out if there is no scarring
  • recurrence of UTIs are more likely in:
    • younger children - <6months
    • girls over boys
    • VUR grade 3-5
    • voiding abnormalities
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19
Q

AKI/acute renal failure can be defined as a sudden decrease in renal function; elevated urea is followed by an elevated creatinine and a resulting decreasing GFR. There are often associated difficulties in fluid + electrolyte regulation as well as with BP control.

What are pre-renal (hypoperfusion of kidney) causes of acute renal failure?

A
  • hypovolaemic shock (eg. gastroenteritis, burns, nephrotic syndrome)
  • septic shock
  • cardiogenic shock

Important to replace intravascular fluid in these pts, but if more severe -> specialist input

20
Q

What are renal (intrinsic renal pathology) causes of acute renal failure?

A
  • vasculitis
  • renal vein thrombosis
  • glomerulonephritis
  • acute tubular necrosis
  • interstitial nephritis
  • pyelonephritis
  • acute-on-chronic renal failure

Management complex requiring specialist input, fluid restriction may be necessary to avoid overload and a renal biopsy may be required

21
Q

What are the post-renal (outflow tract obstruction) causes of acute renal failure?

A
  • congenital eg. posterior urethral valves
  • acquired eg. abdominal mass obstructing ureter

Treatment requires identification of site of obstruction + targeted therapy, this may mean a urinary catheter is required or a nephrostomy

22
Q

What is haemolytic uraemic syndrome (HUS)?

A
  • thought to be due to the activation of neutrophils which damage endothelium
  • normally secondary to gastrointestinal infection w/ verocytotoxin-producing E.Coli or shigella
  • the syndroem follows a bout of bloody diarrhoea
  • other involved organs: pancreas, brain, heart
  • characterised by presence of acute renal failure, microangiographic haemolytic anaemia + thrombocytopenia
  • management is with supportive therapy
23
Q

Acute renal failure can present non-specifically, particularly in neonates w/ symptoms such as unexplained crying, restlessness, lethargy, vomiting or poor feeding. Other features may include reduced urine output and pallor.

What features can more severe AKI present with?

A
  • haematuria
  • rash → may be purpuric as found in HUS + HSP
  • bloody diarrhoea → only found if AKI is caused by HUS
  • confusion → normally due to uraemia
  • abdo pain
  • oliguria
  • oedema → particularly in periorbital region
  • abdo mass → may be due to PKD or urinary retention
  • hypertension
  • arrhythmia → usually secondary to hyperkalaemia
24
Q

What investigations can be done for those who have a very mild AKI with a known cause such as sepsis or dehydration?

A
  • U+Es → quantify renal dysfunction + identify electrolyte disturbance
  • venous blood gas → allow rapid assessment of acid-base balance
  • urine dipstick → identify proteinuria + haematuria
  • MC+S → to exclude infection + to look for red cells in context of glomerulonephritis
25
Q

What additional investigations can be done in those with more severe AKI or where the cause is unknown?

A
  • FBC + blood film → anaemia if renal dysfunction longstanding, anaemia part of HUS
  • early morning urine protein:creatinine → look for proteinuria, more sensitive
  • urinary sodium → look for IV fluid depletion
  • blood + stool cultures → identify infective causes
  • throat swab → post-streptococcal glomerulonephritis
  • urate → identify urate nephropathy
  • CXR → pulmonary oedema secondary to AKI
  • renal USS → identify a cause for renal failure eg. hydronephrosis
26
Q

Treatment of acute renal failure depends on the underlying cause.

What might treatment include?

A
  • hospitalisation
  • administration of IV fluids in large volumes
  • diuretic therapy or medications to inc urine output
  • close monitoring of important electrolytes such as potassium, sodium + calcium
  • anti-hypertensives
  • specific diet requirements
  • dialysis if above fails or severe electrolyte imbalances or pulmonary/multisystem failure
27
Q

Nephrotic syndrome is a glomerular disorder which presents as a classic triad of what?

A
  • generalised oedema
  • heavy proteinuria (>200mg/mmol or 3+ on dipstix)
  • hypoalbuminaemia (<25g/L)
28
Q

What is the pathophysiology of nephrotic syndrome?

A
  • nephrosis is the process of leaking protein from a damaged glomerulus
  • distinguishing it from nephritis, which is inflammation that can involve any part of the nephron or interstitium
  • the glomerular basement membane is made of specialised epithelial cells ⇒ podocytes
  • they normally fuse together + prevent proteins albumin-sized or larger from being filtered
  • in nephrotic syndrome, they become flattened + start to allow the leaking of these proteins
  • the most common cause of nephrotic syndrome in children is minimal change disease, so-named bc on biopsy there is little change to see
  • other, rarer causes include congenital nephrotic syndromes, focal segmental glomerulosclerosis + mesangiocapillary glomerulonephritis
29
Q

Symptoms of nephrotic syndrome vary depending on the underlying aetiology and severity of the condition. What might patients present with?

A
  • periorbital oedema (often earliest sign)
  • discomfort relating to swelling or skin breakdown
  • weight gain
  • abdo distension
  • tiredness
  • foamy urine
  • increased infections
  • poor growth + development
30
Q

First line investigations aim to confirm the diagnosis of nephrotic syndrome and to rule out any atypical features.

What investigations should be done for children presenting for the first time with typical nephrotic syndrome?

A
  • urine dip
  • urinary protein:creatinine ratio
  • U+Es
  • FBC
  • serum albumin
  • varicella zoster + hepatitis serology
  • complement levels
  • anti-streptolysin O Titre (ASOT)
  • autoimmune → ANA, ANCA + anti-dsDNA
31
Q

Children with typical nephrotic syndrome are usually managed with steroids, without the need for a diagnostic renal biopsy.

There are some atypical features which would prompt discussion with a nephrologist and consideration of renal biopsy. What are said atypical features?

A
  • age <1yr or >12yrs
  • hypertension
  • impaired renal function
  • frank haematuria
  • steroid resistant nephrotic syndrome
32
Q

What is the management of nephrotic syndrome?

A
  1. high-dose steroids → majority of children w/ minimal change disease will respond (steroid-sensitive nephrotic syndrome) but most will have a relapse ⇒ if they respond to further course of steroids + enter remission then prognosis favourable
    • some will have frequent relapse or steroid-resistant ⇒ low-dose maintenance steroid therapy or immunomodulatory drugs (eg. levamisole, cyclophosphamide, ciclosporin or tacrolimus)
  2. low salt diet → to avoid worsening oedema
  3. prophylactic antibiotics → these children leak immunoglobulins through their kidneys + therefore at high risk of infection, so also consider vaccination against pneumococcal + varicella
33
Q

What is characteristic of nephritic syndrome?

A
  • microscopic haematuria is the main feature
  • also may be proteinuria, oedema and hypertension
  • caused by fluid retention due to oliguria
  • nephritic syndrome is not a diagnosis but a clinical syndrome
  • several underlying causes
34
Q

What are the differentials for haematuria in children?

A
  • infecton → cystitis, TB, infective endocarditis, schistosomiasis
  • tumours → renal or bladder
  • trauma
  • inflammation → glomerulonephritis, IgA vasculitis, Alport syndrome
  • haematological → sickle cell anaemia
  • medications → NSAIDs, sulphonamides
35
Q

What is post-infectious glomerulonephritis?

A
  • commonest cause of nephritic syndrome
  • mixed nephritic-nephrotic
  • often caused by group A streptococcus
  • typically present 1-2 weeks after a streptococcal throat infection
  • diagnosis is based on clinical history, positive antistreptolysin O antibody titre (ASOT) and anti-DNase B titres, plus reduced complement C3 + C4
36
Q

What is IgA nephropathy?

A
  • usually presents as macroscopic haematuria in association w/ URTI when IgA levels may be elevated
  • only definitive way to diagnose is via percutaneous renal biopsy, but rarely required
  • prognosis in children is better than in adults
37
Q

What are the relevant investigations for nephritic syndrome?

A
  • urine → dipstick, MC+S (red cell casts), early morning urine albumin:creat ratio
  • U+Es, LFTs, albumin → identify AKI, electrolyte imbalance
  • ASOT → specific streptococcal exposure
  • FBC → anaemia? thrombocytopaenia?
  • ESR → SLE? infection?
  • auto-antibody tests → inc ANA and dsDNA may suggest autoimmune disorders eg SLE, anti-glomerular basement membrane (GMB) antibodies are +ve in Goodpasture syndrome
  • throat swabs → strep infections
  • renal USS → identify parenchymal abnormalities
38
Q

Management of nephritic syndrome should be tailored to the likely cause, but is generally supportive therapy, including fluid + electrolyte monitoring.

It may be rapidly progessive glomerulonephritis, which is characterised by rapid deterioration of GFR rate and usually associated w/ crescent formation (fibrin deposition in the shape of crescents) on percutaneous renal biopsy.

What would be the treatment?

A
  • requires immunosuppression → corticosteroids w/ IV methylprednisolone
  • may require dialysis and/or plasmapheresis
39
Q

Cryptorchidism is a congenital absence of one or both testes in the scrotum due to a failure of the testes to descend during development.

It’s found in 6% of newborns, but drops to 1.5-3.5% of males at 3 months.

What 3 broad groups can crytoporchidsm be divided into?

A
  • true undescended testis: where testis is absent from scrotum but lies along the line of testicular descent
  • ectopic testis: where testis is found away from the normal path of decent
  • ascending testis: where testis previously identified in the scrotum undergoes a secondary ascent out of the scrotum
40
Q

What are the stages of testicular descent in foetal development?

A
  1. trans-abdominal phase: occurs in 1st trimester and is dependent on mullerian-inhibiting substances (MIS) + insulin related growth factor (IRGF), descent occurs from kidneys down to the inguinal ring
  2. inguino-scrota stage: occurs in 3rd trimester + depends on testosterone, this in turn depends on a functional HPA, descent occurs through inguinal canal down to bottom of scrotum

Risk factors for undescended testes include: prematurity, low birth weight, having other genitalia abnormalities + first degree relative w/ cryptorchidsm

41
Q

What is the difference between palpable and impalpable undescended testis?

A
  • key element in history is to clarify if testis has ever been seen or palpated within scrotum (such as @ newborn check)
  • initial inspection may reveal testes within scrotum, therefore a dx of retractile or normal descended testis can be made
  • around 80% of undescended testis are palpable
    • imperfectly descended → external inguinal ring, superficial inguinal pouch, gliding testis
    • ectopic → lateral abdo wall, femoral, base of penis, perineal
  • around 20% of undescended testis are impalpable
    • absent → primary failure, vascular injury
    • high location → intra-abdominal
    • ectopic
42
Q

How do you examine for undescended testis?

A
  • have infant/child lay flat on bed
  • aim to keep child relaxed + comfortable
  • w/ warm hands, palpate laterally w/ left hand from inguinal ring + work along inguinal canal to pubic symphysis
  • from there, use other hand to palpate testis in scrotum
  • if found, one should attempt to see if testes can be gently milked down to base of scrotum, if so → retractile testis
  • if it is pulled down but under tension in base → high scrotal/testis
  • sometimes found in groin along inguinal canal but won’t move further → inguinal undescended testis
  • if having difficulties finding testis during examination, add a little soap to finger tips to remove friction, it will feel like an enlarged lymph node
43
Q

What should you do if disorder of sexual development (DSD), undescended testis assocatied w/ ambiguous genitalia or hypospadias or bilateral undescended testis are suspected?

A
  • urgent referral to senior paeditrician within 24hrs
  • ideally w/ access to paed endocrinology + urology services
  • this may be a presentation of congenital adrenal hyperplasia
  • therefore at risk of salt-losing crisis
  • requiring high dose sodium chloride therapy + careful glucose monitoring followed by steroid replacement
44
Q

For undescended testis in the newborn, what would you do (in terms of time-scale and when to review)?

A
  • at birth → review @ 6-8wks of age
  • at 6-8wks → if fully descended ⇒ no further action, if unilateral ⇒ re-examine @ 3 months
  • at 3 months → if testis is retractile then advise annual follow up (due to risk of ascending testis), if undescended ⇒ refer to paed surg/urology for definitive intervention, ideally occurring 6-12months of age
45
Q

What is the intervention for undescended testes?

A

Intervention is dependent on clinical findings + suspected position of undescended testis. If unable to find testis on examination it is important to identify if the testis is absent or intra-abdominal. Therefore, an examination under anaesthesia followed by laparoscopy remains the mainstay of intervention in order to locate an impalpable testis.

  • if testis palpable → open orchidopexy
  • if testis intra-abdominal → a single or 2-stage procedure (Fowler-Stephens) can be adopted
  • alternative findings at laparoscopy may be an atrophic testis, which should be removed or an absent testis → groin exploration

*Medicine: Paediatrics (14 decks)

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