Nephrology Flashcards

Enuresis, haematuria, HSP, nephrotic syndrome, UTIs, VUR, AKI, CKD, tract abnormalities

1
Q

Daytime enuresis

A

Lack of bladder control in a child over 3-5y, usually also nocturnal

Causes: lack of attention to full bladder (developmental/psychogenic/preoccupied child), detrusor instability, bladder neck weakness, neuropathic bladder e.g. spina bifida, UTI, constipation, ectopic ureter

Ix: urine for MCS, US if indicated, exclude neurological cause (different management)

M: look for underlying cause, adv on fluid intake/diet/toileting, reward systems e.g. star chart (for agreed behaviours e.g. using toilet when get up), enuresis alarm (if <7 is first line), desmopressin (may be first line for >7 esp if need short term relief like for a sleepover, this is an anti-diuretic for overnight), daytime may need antimuscarinics like oxybutynin or TCA like imipramine (2ndary care)

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2
Q

Causes of haematuria

A

Non-glomerular: infection, trauma to renal tract, stones, tumours, sickle cell, bleeding disorders, renal vein thrombosis, hypercalciuria

Glomerular: acute glomerulonephritis, IgA nephropathy, familial nephritis (eg Alport syndrome-X linked, progress to end stage RF by early adult life in males, a/w sensorineural deafness + eye abnormalities), thin basement membrane disease

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3
Q

Acute glomerulonephritis

A

Causes: post-infectious (e.g. strep throat/skin), vasculitis (HSP, SLE etc), IgA nephropathy, mesangiocapilary glomerulonephritis, anti-GBM disease (Goodpasture syndrome)

CF: reduced urine output, volume overload, HTN, seizures, periorbital oedema, haematuria + proteinuria

M: water + electrolyte balance (diuretics if needed). If rapidly progressive need renal biopsy + immunosuppression +/- plasma exchange

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4
Q

Henoch-Schonlein purpura

A

IgA-mediated vasculitis that affects the kidney, peaks in winter, often preceded by URTI but cause unknown

CF:

  • Rash: symmetrical over buttocks, extensor surfaces (trunk usually spared). May progress from urticarial - maculopapular - purpuric, usually palpable
  • Joint pain: in 2/3 joints esp knees + ankles, peri-articular oedema, doesn’t cause long term issues
  • Colicky abdomen pain: common
  • Renal involvement: majority get micro/macroscopic haematuria, or mild proteinuria

M: should follow up all for a year to detect persisting haematuria/proteinuria. Give steroids if severe CF

Comps: haematemesis/melaena/intussusception, nephrotic syndrome, progressive CKD (more likely if lots of proteinuria, oedema, HTN and deteriorating renal function)

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5
Q

Causes of proteinuria

A
Transient from febrile illness/exercise
Orthostatic: only when stand up
Increased glomerular filtration pressure
Reduced renal mass in CKD
HTN
Tubular proteinuria
Glomerular abnormalities: minimal change disease, glomerulonephritis, abnormal GBM
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6
Q

What is nephrotic syndrome?

A

Heavy proteinuria of unknown cause - leads to low plasma albumin + oedema
(sometimes secondary to systemic disease like HSP, SLE, infections)

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7
Q

CF of nephrotic syndrome

A

Periorbital oedema esp on waking
Scrotal/vulval/leg oedema
Ascites
Breathlessness from pleural effusions/abdo distension
Infection due to loss of protective immunoglobulins in urine

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8
Q

What are the types of nephrotic syndrome?

A

Steroid-sensitive: most common group + don’t progress to CKD. A/w atopy, often URTI precipitates, mostly in 1-10y.

  • CF: no macroscopic haematuria, normal BP, normal complement + renal function
  • Causes: minimal change disease (commonest), focal segmental glomerulosclerosis (more likely to cause ESRD), mesangiocapillary glomerulonephritis (more in older kids, low complement, decline in renal function over many years), membranous nephropathy (a/w Hep B, may precede SLE, most resolves within 5y)
  • M: oral corticosteroids (unless atypical), taper after 4w and end after 6w

Steroid-resistant: refer to nephrology. M: diuretics, salt restriction, ACEi, sometimes NSAIDs

Congenital: rare, in first 3m, most common in Finnish people. High mortality cos of low albumin, may need nephrectomy + dialysis + transplant

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9
Q

Complications of nephrotic syndrome

A

Hypovolaemia: volume depletion of intravascular compartment, CF abdo pain/faint feeling/peripheral vasoconstriction/shock (need IV fluids before shocked)

Thrombosis: hyper coagulable state as lose anti-thrombin III, exacerbated by steroids. In any circulation tbh

Infection: encapsulated bacteria e.g. Pneumococcus. E.g. spontaneous bacterial peritonitis.

Hypercholesterolaemia

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10
Q

RF for UTI in children?

A
  • Congenital renal tract abnormality: in up to half
  • Vesicoureteric reflux (35%)
  • Incomplete voiding: e.g. obstructed from loaded rectum, neuropathic bladder, VUR, hurried micturition, infrequent voiding
  • Poor hygiene
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11
Q

UTI presentation + Ix

A

CF:

  • infants: usually non-specific like fever, vomiting, lethargy, poor feeding, jaundice, sepsis, offensive urine, febrile convulsion
  • children: dysuria/frequency/urgency [these alone usually cystitis, or vulvitis/balanitis], abdo pain/loin tenderness, fever +/- riggers, lethargy, anorexia, D+V, haematuria, offensive/cloudy urine, febrile seizure, enuresis – basically so many so commonly need to check kids urine
  • Pyelo suggested when bacteria + fever >38, or bacteria + loin pain/tenderness

Ix: clean catch urine sample if poss (e.g. when nappy removed), catheter if urgent, in older children MSU

  • Nitrite pos likely a true UTI, but some UTI are nitrite neg
  • leucocytes may be there or not and are common in any febrile illness
  • L+N+ = UTI, L-N+ = start Abx if CF of UTI + send culture, L+ N- = only Abx if convincing CF, L- N- = UTI unlikely
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12
Q

Management of UTIs

A

<3m old with suspected UTI: immediately refer for IV Abx e.g. co-amoxiclav for 5-7d, then oral

> 3m + children with acute pyelonephritis: oral Abs e.g. TMP for 7d, or if severe IV co-amox then oral

Cystitis/lower UTI (no systemic CF): oral TMP/nitrofurantoin for 3d

Adv high fluid + regular voiding to completion to wash out aggressive organisms (they enter from perineum/stool etc), treat/prevent constipation, hygiene, probiotic to encourage gut colonisation. Abx prophylaxis is controversial

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13
Q

Vesicoureteric reflux

A

Developmental abnormality of the VUJ - ureters displaced and have shortened intramural course

Causes: familial, from bladder pathology like neuropathic bladder or temporary after UTI

Severe cases cause gross dilation of ureter + RP + calyces - predisposes to intra-renal reflux (back flow into the collecting ducts) + renal scarring if a UTI occurs; infection may destroy renal tissue causing a shrunken poorly-formed section of kidney (reflux nephropathy); if B/L can cause CKD

M: lower grades tend to resolve with age

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14
Q

Acute kidney injury

A

Sudden, potentially reversible reduction in renal function, usually p/w oliguria

Causes:

  • pre renal: commonest in kids, due to hypovolaemia (gastro, burns, sepsis, haemorrhage, nephrotic syndrome) or circulatory failure
  • renal: salt + water retention, blood/protein/casts in urine. may be due to HUS, ATN, ischaemia, glomerulonephritis, interstitial nephritis
  • post-renal: obstruction, either congenital e.g. posterior urethral valves or acquired e.g. a blocked catheter
  • acute on chronic RF: suggested in a child with growth failure, anaemia + disordered bone mineralisation

M:

  • pre-reanl: fluids!
  • Renal: diuretic/fluid restriction if overloaded, high calorie normal protein feed to reduce catabolism/uraemia/hyperkalaemia
  • post-renal: relieve obstruction
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15
Q

Chronic kidney disease

A

Progressive loss of renal function, in 5 stages, stage 5 eGFR <15

CF (apparently in stage 4-5): anorexia, lethargy, polydipsia+uria, faltering growth, renal osteodystrophy, HTN, acute on chronic renal failure, proteinuria, normochromic normocytic anaemia

M: supplements (as anorexia/vomiting common), prevent renal osteodystrophy (calcium + vid D), salt + bicarb supplements, SC EPO for anaemia, may need GH treatment. May need dialysis or transplant

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16
Q

Urinary tract abnormlaities

A

May lead to CKD, infections or cause urinary obstruction. Can have antenatal detection + treatment

  • renal ageneiss (no kidneys, severe oligohydramnios, Potter syndrome-fatal pulmonary hypotension)
  • multicystic dysplastic kidney: non functioning large cysts with no renal tissue, if b/l can cause potter syndrome
  • ARPKD (diffuse b/l enlargement)/ ADPKD (cysts baying size between normal parenchyma)/tuberous sclerosis : these are all b/l but there is some renal function maintained. In chidden ADPKD commonest and causes HTN, a/w cysts in liver + pancreas, cerebral aneurysms + MV prolapse
  • pelvic/horseshoe kidneys from abnormal migration
  • duplex system: premature division of ureteric bud
  • bladder exstrophy: exposure of bladder mucosa
  • Prune-belly syndrome absent musculature so large dilated bladder, wrinkled abdomen
  • Obstruction at PUJ/VUJ, posterior urethral valves (in males due to mucosal folds)
17
Q

Hypertension

A

Increases with height, is BP >95th gentile for age height + sex

RF: overweight

Sx: vomiting, headache, facial palsy, hypertensive retinopathy, convulsions, proteinuria

If have paroxysmal palpitations + sweating consider phaeochromocytoma

18
Q

Renal tubular disorders

A

Generalised proximal tubule dysfunction - Fanconi syndrome. get excessive losses of amino acids, glucose, phosphate, bicarb, sodium potassium, magnesium. Can be idiopathic, from IEMs or acquired like heavy metals. Consider in a child with polydipsia+uria, salt depletion, dehydration, hyperchloraemic metabolic acidosis, rickets, faltering growth

Specific transport defects in transporters

19
Q

Haemolytic uraemic syndrome

A

Acute renal failure + microangiopathic haemolytic anaemia + thrombocytopenia

Cause: often toxin produced by E coli infection - it preferentially goes to the kidneys forming clots - coagulating cascade activated but clotting normal so plts consumed so u get MHA from RBC damage

M: supportive, may need dialysis
FU for proteinuria/HTN/CKD

20
Q

What is secondary onset enuresis?

A

Loss of previously-achieved continence

Causes: emotional upset, UTI, polyuria

Ix: urine dip for glucose/protein, can measure osmolality of early morning urine sample to test kidney concentrating ability, US renal tract

21
Q

How may the colour of haematuria indicate the aetiology?

A

Brown - glomerular cause (also deformed red cells + casts + often proteinuria), myoglobinuria

Red - lower urinary tract. Unusual in kids, usually at beginning/end of stream, no proteinuria

Microscopic - any just less blood

22
Q

IgA nephropathy

A

A common nephritic syndrome causing macroscopic haematuria, often a/w URTI. Histology + management the same as HSP. Childhood prognosis is better than in adults

23
Q

What causes UTI in children?

A
  • Bowel flora enter urethra - E coli, Klebsiella, Proteus, Strep faecalis
  • Haematogenous e.g. in newborn
24
Q

When would you check a urine sample in children?

A

*symptoms or signs suggestive or a UTI
with unexplained fever of 38°C or higher (test urine after 24 hours at the latest)
*with an alternative site of infection but who remain unwell (consider urine test after 24 hours at the latest)

25
Q

What are the signs of an atypical UTI?

A
Seriously ill/sepsis
Poor urine flow
Abdo/bladder mass
Raised creatinine
Failure to respond to suitable Abx within 48h
Infection with non-E coli organisms

Do US

26
Q

How is vesicoureteric reflux diagnosed?

A
  • Micturating cystourethrogram

* DMSA scan may also be done to look for renal scarring