Nephrology and genitourinary 3 (important) Flashcards
What is the treatment of pyelonephritis in <3 months old infants
Infant < 3 months:
Refer to paediatric specialist.
PO antibiotics 7-10 days (eg. cephalosporin or co-amoxiclav have low resistance patterns)
If IV has to be used, then cefotaxime or ceftriaxone for 2-4 days followed by oral until 10 days of abx
What is the treatment of pyelonephritis in >3 months old infants and children
Oral antibiotics for 3 days. Trimethoprim, nitrofurantoin, cephalosporin or amoxicillin
Advise parent to bring back child if still unwell after 24-48 hours
Features of AKI in children
Renal failure is most severe: oliguria (<0.5ml/kg/h)
AKI is a sudden reduction in glomerular filtration rate, resulting in increased blood concentration of urea and creatinine nad disturbed fluid and electrolyte homeostasis
Classify AKI
Pre-renal: commonest cause in children
Renal: salt and water retention; blood and protein in urine, symptoms of specific disease? (eg. HUS)
Postrenal - urinary obstruction (eg. posterior urethral valves or blocked urinary catheter)
Prerenal causes of AKI
Hypovolaemia: D+V Burns Sepsis Haemorrhage Nephrotic syndrome
Circulatory failure
Renal causes of AKI
Vascular:
HUS
Vasculitis
Embolus
Tubular:
Acute tubular necrosis
Ischaemic
Toxic
Glomerulonephritis
Interstitial nephritis
Pyelonephritis
Management of prerenal AKI
Usually there is hypovolaemia (with sodium depletion):
fluid replacement and circulatory support to avoid tubular necrosis
Management of renal AKI
If there is circulatory overload: may restrict fluid and challenge with a diuretic
High-calorie, normal protein feed to decrease catabolism, uraemia and hyperkalaemia
Emergency management of metabolic acidosis, hyperkalaemia and hyperphosphataemia
Renal biopsy if the cause of renal failure not obvious (can identify rapidly progressing glomerulonephritis (needs immediate immunosuppression))
What are the commonest renal causes of acute renal failure in children in the UK
HUS
Acute tubular necrosis (usually in multisystem failure)
Management of post-renal renal failure
assess site of obstruction
relieve by nephrostomy or bladder catheterisation
Surgery, once fluid volume and electrolyte abnormalities corrected
The triad of abnormalities which define HUS
Acute renal failure
Haemolytic anaemia
Thrombocytopenia
Commonest organisms causing diarrhoea associated HUS in childhood
Typically secondary to gastrointestinal infection with verocytotoxin-producing E.coli (acquired through contact with farm animals or eating uncooked beef..
Less often Shigella
Features of verocytotoxin-producing E.coli causing diarrhoea leading to HUS (pathophysiology)
Prodrome of bloody diarrhoea
Toxin localises to enothelial cells of kidney - causes intravascular thrombocytogenesis
Coagulation cascade is activated and platelets become consumed. Microangiopathic haemolytic anaemia results from damage to RBCs as they circulate through the microcirculation (occluded)
Brain, pancreas and heart may also be involved
Prognosis of diarrhoea associated HUS
With early supportive therapy, including dialysis - good prognosis
Folow-up for persistent proteinuria/HTN/declining renal function in following years
Prognosis of non-diarrhoea associated HUS (atypical)
Familial?
Frequent relapse
High risk of HTN and chronic renal failure in later life
High mortality
Children with intracerebraö involvement or atypical HUS may be treated with plasma exchange, but efficacy is unproven
What is chronic renal failure (stages)
GFR < 15ml/min per 1.73m^2
Quite rare in children. Usually congenital (structural, glomerulonpehritis, hereditary nephropathies, systemic disease).
1: normal GFR>90ml/min1.73m^2 and persistent albuminuria
2: GFR 60-89 and persistent albuminuria
3: GFR 30-59
4: GFR 15-30
5: GFR < 15 or end-stage renal disease
Clinical features of chronic kidney disease
Anorexia
Lethargy
Polydypsia
Polyuria
FTT Bone deformities HTN Acute-on-chronic renal failure Proteinuria Normochronic, normocytic anaemia
Symptoms rarely develop before GFR <30.
Most picked up antenatally on US
Which aspects of chronic renal failure need to be managed? (think MDT)
Diet Prevent renal osteodystrophy Control of salt and water balance Control acidosis Anaemia Hormonal abnormalities Dialysis and transplantation
Dietary management pf CKD
Calorie supplements and NG or gastrostomy feeding often necessary to optimise growth
(anorexia and vomiting common)
Protein intake sufficient for growth and albumin, but low enough to prevent accumulation of toxic metabolic products
Prevention of renal osteodystrophy in CKD
Decreased activation of Vit D leads to Phosphate retention and hypocalcaemia.
Leads to secondary hyperparathyroidism - causes osteitis fibrosis and osteomalacia
Thus, phosphate restriction (few milk products) Calcium carbonate (bind phosphate) Activated vit D supplements
Control of salt and water balance and acidosis in CKD
Many children with CKD caused by congenital malformationss and renal dysplasia have obligatory loss of salt and water.
Salt supplements and free access to water.
Bicarbonate supplements to prevenet acidosis
Managing anaemia in CKD
Due to reduced EPO production of circulation of metabolites that are toxic to bone marrow..
Administer recombinant human EPO
Manage hormonal abnormalities in CKD
GH resistance with high GH levels but poor growth
recombinant human GH can improve growth for up to 5 years of treatment.. But whether it improves final height is unknown
Many children with CKD have delayed puberty and subnormal pubertal growth spurt
Role of dialysis and transplant in CKD
All children can enter renal replacement programme when in end-stage renal failure
> 10kg is necessary though, to avoid renal vein thrombosis
Best chance with kidney from related (living) donor
There are graft losses even with living donor. (acute rejection)
Immunosuppression with combo of prednisolone, tacrolimus and azathrioprine
Ideally transplant should occur before dialysis is needed. Otherwise, dialysis can be started.
Peritoneal dialysis: cycling overnight woth a machine (continuous cycling peritoneal dialysis)
or
manual exchanges over 24 h (continuous ambulatory peritoneal dialysis) which can be done by the parents at home and is therefore less disruptive
Haemodialysis can be done in hospitals (3-4 per week)
General trend in BP throughout childhood? How is it compared? What is HTN
increases with age and height
Reading should be plotted on a centile chart. (SBP vs age or height)
HTN is BP >95th percentile for height, age and sex
What are the commonest causes of HTN in children
Renal, cardiac or endocrine
Renal: Parenchymal disease Renal artery stenosis Polycystic kidney disease Renal tumours
Coarctation of the aorta
Endocrine:
CAH
Cushing syndrome or corticosteroid therapy
Hyperthyroidism
Catecholamine excess:
phaeochromocytoma
neuroblastoma
Essential HTN is a diagnosis of exclusion
Presentation of HTN in children
Vomiting Headaches Facial palsy HTN Retinopathy Convulsion proteinuria
FTT and cardiac failure in infants (paroxysmal palpitations/sweating with phaeochromocytoma)
Investigations in children with HTN and their importance
Some causes are correctable:
Nephrectomy for unilateral scarring (DMSA)
Angioplasty for renal artery stenosis
Surgical repair of coarctation of the aorta
Resection of phaeochromocytoma
In most cases, however antihypertensives have to be taken
HTN can cause serious damage to organs and bleeds
-cause needs to be found and managed.
Early detection of HTN is very important - any child with renal abnormality should have yearly checks.
Children with a FH of essential HTN should be encouraged to restrict salt intake, avoid obesity and regularly check BP
What are the presenting features of urinary tract abnormalities
Most identified on US scan (1 in every 200-400)
Abnormal renal development or function
Postnatal infection
Can involve urinary obstruction which needs surgery
Which anomalies can present on antenatal ultrasound
Absence of both kidneys (renal agenesis) - severe oligohydramnios which results in Potter syndrome
Multicystic dysplastic kidney - non-functioning structure with large fluid-filled cysts and no renal tissue or connection to bladder
Autosomal dominant or recessive polycystic kidney disease: some renal function is maintained, but both kidney affected
Pelvic or horseshoe shaped kidney - predispose to infection or obstructs drainage
Posterior urethral valves (leads to urinary outflow obstruction)
Hydronephrosis
Which investigations are used for diagnosing antenatal urinary tract abnormalities?
GFR is low in a newborn, especially in a premature infant! (15-20ml/min)
Rises to normal adult rate by 2 years
Ultrasound - anatomical assessment
DMSA scan - functional defects
MCUG/VCUG - visualise bladder and urethral anatomy and can detect both reflux and obstruction
MAG3 isotope scan - isotopes excreted from the blood into the urine
Plain abdo X ray - spinal abnormalities and potentially renal stones
Managing bilateral hydronephrosis in a male infant?
Usually picked up on antenatal scan
Start prophylactic antibiotics at birth
Ultrasound shortly after birth (within 48h)! To exclude posterior urethral valves which ALWAYS require urological intervention (eg. cystoscopic ablation)
If negative, then stop antibiotics and repeat US after 2-3 months
Protocol for antenatally found unilateral hydronephrosis or any anomaly in a female?
Start prophylactic antibiotics at birth
Do an ultrasound at 4-6 weeks. If normal, stop abx.
Otherwise do more investigations (eg. micturating cystourethrogram (MCUG))
