Nephrology and Urogenital Flashcards
Give 2 reasons why UTIs in childhood is important?`
- 50% will have __
- pyelonephritis may __ predisposing to__
- up to 50% will have a structural abnormality of their urinary tract
- pyelonephritis may damage the growing kidney by forming a scar, p.disposes to HT and progressive CKD of bilateral
UTI symptoms vary with age.
Infants: symptoms are __..what can occur rapidly
(the classical symptoms are more common with increasing age)
- non-specific, +/- fever, vomiting, lethargy/irritable, poor feeding, jaundice, offensive urine, febrile seizure
- septicaemia can occur rapidly
Dysuria alone is often due to cystitis or ___ in girls or ____ in uncircumcised boys. What dipstick test is positive in both these conditions?
-vulvitis
-balanitis
Leukocyte will be postivie
If both leukocyte and nitrites are present on a dipstick regard and treat as UTI, if only one is positive what should you do?
- diagnosis depends on urine culture
- start Abx only if there is clinical evidence of UTI
Name 3 methods of urine sample collection in the young?
- “clean-catch” sample into pot when nappy removed
- adhesive plastic bag on perineum after careful washing
- urethral catheter (if need sample urgently)
- suprapubic aspiration (for severely ill, needing urgently)
What amount of CFU (colony-forming units) in a bacterial culture strongly suggest UTI
more than 10^5 CFU
What test should all infants with an unexplained fever >38degrees have done?
A urine sample tested
Name 3 common organisms causing UTIs and name one seen more commonly in boys from its presence under the prepuce.
- E.coli
- klebsiella
- Pseudomonas
- Strep. Faecalis
- Proteus
Name some contributing factors to incomplete bladder emptying in children:
- infrequent voiding –> bladder enlargement
- vulvitis, vesicoureteric reflux (VUR)
- incomplete micturition w residual volumes post micturition
- obstruction by a loaded rectum
- neuropathic bladder
Vesicoureteric reflux (VUR) is when the ureters are displaced ___ and enter __ into bladder (not at an __) It is __.
- laterally, directly (angle)
- familial
What association with VUR when urine flows back from renal pelvis to CDs can lead to severe renal scarring if UTIs occur.
-intrarenal reflux
Give 3 reasons why VUR-associated ureteric dilatation is importantly bad.
- if urine returns from ureters to bladder post-void, you get incomplete emptying and predisposition for infection
- pyelonephritis may develop esp with intrarenal reflux
- bladder voiding pressure is transmitted to the renal papillae which may contribute to renal damage if voiding pressures are high
VUR impacts on kidney mean infection can __ renal tissue leaving a __ of shrunken poorly functioning kidney ( __ ____). If scars are bilat and severe progressive ___ may develop. Also ~10% risk of childhood/early adult ___.
- destroy
- scar
- (reflux nephropathy)
- CKD
- hypertension
We do not need to investigate all children w UTIs only those with atypical UTIs, name some features that come under atypical UTIs:
e.g. non-ecoli organisms..
- seriously ill/septicaemia
- poor urine flow
- abdo/bladder mass
- raised creatinine
- not responding to abx in 48hrs
If a child with a UTI is found to be atypical and requiring investigation, what is the first line next step?
Ultrasound of kidneys and urinary tract
If urethral obstruction is identified as a probable cause for atypical UTIs in a boy with an abnormal bladder, what investigation should be carried out?
Clue: 4letters
MCUG: Micturating Cystourethrogram
What is the basis of UTI treatment in the following ages:
<3months
>3moths and children w pylonephritis
children with cystitis/lower UTI
<3mn: hospital for IV Abx (e.g. co-amoxiclav)
children: oral abx e.g. trimethoprim or IV abx followed by oral
lower UTI: oral abx short course
How can you try to prevent UTIs in children?
e.g. lactobacillus acidophilus probiotic
- high fluid intake
- regular voiding and/or double voiding
- treat/prevent constipation as it arises
- good perineal hygiene
In children with recurrent UTI/scarring/reflux what follow up should be arranged?
e.g. regular renal growth and function assessments if there are bilat defects bc of risk of CKD
- dipstick urine in any non-specific illness with MC&S
- long-term low dose abx prophylaxis
- circumcision
- anti-VUR surgery if scarring progresses with ongoing VUR
- check BP annually if renal defects present
- urinalysis to check for proteinuria as sign of CKD
What is a DMSA scan (it is used in the investigation of UTIs in young children <3yrs to look at the kidney’s and how they contribute to functioning;
Dimercaptosuccinic Acid scan
Nephrotic Syndrome = heavy proteinuria leading to low ____ and ____.
Cause often unknown but suggest 2 systemic things it can be secondary to.
- low plasma albumin, and oedema
- 2dry to: Henloch-Schonlien Purpura, SLE, infection like malaria, allergens like bee sting
Give 3 clinical signs of nephrotic syndrome:
NB: infection e.g. peritonitis, septic arthritis or sepsis can occur, why?
- periorbital oedema 1st sign (often on waking)
- scrotal, vulval/leg/ankle oedema
- ascites
- SOB due to pleural effusions + abdo distension
- infection due to loss of protective Igs in the urine
In 90% children with nephrotic syndrome, what does is resolve with and hence won’t progress to CKD
NB: children more commonly 1-10yrs, Asian, male, often precipitated by resp tract infection
how will these children be generally?
On biopsy due to findings on EM, what is this disease called?
Steroid therapy (‘steroid-sensitive nephrotic syndrome)
- associated with atopy
- well (normal BP, normal complement level, normal renal function)
- fusion of podocytes so called minimal change disease
Give 3 complications of nephrotic syndrome:
clue: one issue correlates inversely with serum albumin, cause unknown, hyper______
- hypovolaemia (c/o abdo pain and feel faint, give saline or albumin)
- thrombosis due to urinary losses of antithrombin III, increased viscosity and steroid therapy
- infection esp. capsulated bacterial e.g. pneumococcus (give flu and pneumococcal vaccine)
- hypercholesterolaemia
How is the oedema of steroid-resistant nephrotic syndrome managed in children ? (NB: would be referred to a paediatric nephrologist for management)
-manage oedema w diuretics, salt restriction and ACEi +/-NSAIDS
(also note: Genetic testing can help manage if clear cause found e.g. replace missing defect)
Prognosis for Steroid-Sensitive Nephrotic Syndrome?
1/3
1/3
1/3
1/3 resolve directly
1/3 infrequent relapses
1/3 frequent relapses, steroid dependent
Haematuria causative location?
- brown urine with deformed red cells and casts +/- proteinuria
- vs: more rare presentation, red blood, occurring at beginning/end of stream, no proteinuria
- brown w casts suggests glomerular origin
- red is lower urinary tract haematuria
If glomerular haematuria is suspected what extra investigations would you consider (on top of: MC&S, US, U&Es, FBC, clotting and sickle screen)
- ESR, complement, anti-DNA antibodies
- throat swab, antistreptolysin O/anti-DNAse B titres
- Heb B and C screen
- hearing test and test mother’s urine in Alport S. suspected
- +/-renal biopsy
When in haematuria presentations would a renal biopsy be indicated? Give 2
- there’s significant persistent proteinuria
- recurrent macroscopic haematuria
- renal function is abnormal
- complement levels are persistently abnormal
Acute nephritis: increased glomerular cellularity restricts glomerular blood flow so GFR decreases, what features arise as a result, name 2:
- decreased urine output, volume overload
- hypertension, can -> seizures
- oedema (starts periorbital)
- haematuria
- proteinuria
Give 4 causes of acute nephritis in children:
- Post infections (e.g. streptococcus)
- Vasculitis: Henoch-Schonlein Purpura, Wegener Granulomatosis, Microscopic Polyarteritis, Polyarteritis Nodosa
- IgA Nephropathy, mesangiocapillary glomerulonephritis
- Anti-glomerular basement membrane disease
How is post-streptococcal/infectinous nephritis diagnosed? (rare in developed countries, good prognosis)
- evidence or recent strep infection e.g. culture, raised ASO/anti-DNAse B titres
- low C3 levels that return to normal after few weeks
What condition do the following features belong to?
- skin rash on extensors, arthralgia, periarticular oedema, abdo pain, glomerulonephritis
- 3-10yrs old, more in boys and peaks in winter months
- precipitated by URTI often
Henoch-Schonlein Purpura (activated complement are deposited in organs, precipitating an inflamm response with vasculitis)
What is the characteristic rash of Henoch-Schonlein Purpura (activated complement are deposited in organs, precipitating an inflamm response with vasculitis)
- presents w fever
- symmetrically distributed
- over buttocks and extensor surfaces of limbs and ankles
- trunk often spared
- rash initially urticarial then maculopapular and purpuric
- palpable rash, can recur over several weeks
What disease is this describing?
“episodes of macroscopic haematuria commonly in association with URTIs”
NB: prognosis in children is better vs adults
IgA nephropathy
what follow up and why is required for Henoch-Schonlein Purpura and IgA Nephropathy in children? (same follow up for both conditions)
- follow for a year, check for persisting haematuria or proteinuria
- if + may need longer term follow up
- due to risk of HT and progressive CKD developing
What X-linked disorder is the most common form of familial nephritis? (associated with nerve deafness and ocular defects)
-Alport Syndrome: progresses to end-stage CKD by early adulthood in males
Other vasculitis that cause nephritis (Henoch-Schonlein Purpura) are: polyarterits nodosa, microscopic poluarteritis,, granulomatosis with polyangiitis…
- what blood test is done?
- suggest 2 rx options (may need to continue for months)
- ANCA blood test +
- rx: e.g. steroids, plasma exchange, IV cyclophosphamide
Young girls esp Asian/Black may develop what condition that has low complement C3 and C4 esp in active disease? What other blood result may be +? Give an indication for renal biopsy in these pts?
- SLE
- ds-DNA + autoantibodies
- haematuria or proteinuria are indications for biopsy
Generalized proximal tubular dysfunction aka Fanconi syndrome leads to urinary losses of what?
and why are these proximal tubular cells vulnerable to damage?
-fts: excessive urinary loss of amino acids, glucose, phosphate, bicarbonate, sodium, calcium, potassium & magnesium
–proximal tubule cells are v metabolically active
-
In a child presenting with: polydipsia, polyuria, salt depletion, dehydration, hyperchloremic metabolic acidosis, rickets, faltering or poor growth
-what syndrome would you suspect? give 2 acquired causes of this?
- Fanconi Syndrome (Generalised Proxima Tubular Dysfunction)
- cause: heavy metals, drugs, toxins, vit D deficiency
Fanconi syndrome (Generalised Proxima Tubular Dysfunction) can be 2ndry to inborn errors of metabolism such as? name 2+
- cystinosis
- glycogen storage disease
- lowe syndrome
- galactosaemia
- fructose intolerance
- tryosinaemia
- Wilson’s disease
Most common cause of AKI in children is pre-renal failure, what is the sign of this? What fraction of sodium will be excreted and why?
-Urgent fluid replacement to avoid what complication affecting tubules?
- sign is hypovolaemia
- very low Na+ excretion as body tries to retain volume
- avoid acute tubular injury and necrosis
How is post-renal failure managed in children after assessment of the site of obstruction?
relief by nephrostomy or bladder catheterisation
Suggest 3 indications for dialysis in AKI:
- failure of conservative rx measures
- hyperK+
- severe hypo/hyper Na+
- pulmonary oedema or severe HT due to volume overload
- severe metabolic acidosis
- multisystem failure
Haemolytic syndrome is a common cause of renal AKI in children, it is a triad of:
-AKI
-__… ___..___..
-______
typical HUS is secondary to what? caused by.. hence the prodrome is
- AKI, microangiopathic haemolytic anaemia, thrombocytopaenia
- 2ndry to GI infection w E coli 0157:H7 (or Shigella) hence prodrome of bloody diarrhoea
Typical HUS (triad: AKI, microangiopathic haemolytic anaemia, thrombocytopaenia) is 2dry to GI infection with good prognosis, vs the more rare typical HUS which has no diarrhoea prodrome and risk of what? Mainstay of rx?
- familial, frequent relapses
- risk of HT and progressive CKD with high mortality
- rx with plasma exchange mainly
Undescended testes affect 5% newborns, more common in premature babies, by 3 months 99% will have descended, for undescended still,
- how should you examine?
- what surgery is done (about 1yr of age)? And suggest 3 reasons this is needed/favourable
- examine in warm place w warm hands (retractile testes will hide otherwise) gentle pressure along line on inguinal canal
- orchiopexy
- cosmetic (+psychological, boy feels same as peers, if absent prosthesis can be put in when older)
- reduced risk of torsion/trauma vs. typically groin location
- fertility (esp. if bilateral as spermatogenesis best below body temp)
- malignancy (in scrotum facilitates self-examination hence lumps felt earlier)
