Nephrology Flashcards
Enuresis, haematuria, HSP, nephrotic syndrome, UTIs, VUR, AKI, CKD, tract abnormalities
Daytime enuresis
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)
Causes of haematuria
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
Acute glomerulonephritis
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
Henoch-Schonlein purpura
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)
Causes of proteinuria
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
What is nephrotic syndrome?
Heavy proteinuria of unknown cause - leads to low plasma albumin + oedema
(sometimes secondary to systemic disease like HSP, SLE, infections)
CF of nephrotic syndrome
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
What are the types of nephrotic syndrome?
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
Complications of nephrotic syndrome
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
RF for UTI in children?
- 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
UTI presentation + Ix
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
Management of UTIs
<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
Vesicoureteric reflux
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
Acute kidney injury
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
Chronic kidney disease
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
Urinary tract abnormlaities
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)
Hypertension
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
Renal tubular disorders
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
Haemolytic uraemic syndrome
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
What is secondary onset enuresis?
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
How may the colour of haematuria indicate the aetiology?
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
IgA nephropathy
A common nephritic syndrome causing macroscopic haematuria, often a/w URTI. Histology + management the same as HSP. Childhood prognosis is better than in adults
What causes UTI in children?
- Bowel flora enter urethra - E coli, Klebsiella, Proteus, Strep faecalis
- Haematogenous e.g. in newborn
When would you check a urine sample in children?
*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)
What are the signs of an atypical UTI?
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
How is vesicoureteric reflux diagnosed?
- Micturating cystourethrogram
* DMSA scan may also be done to look for renal scarring
