Kidneys Flashcards
What is Potter’s syndrome?
A result of renal agenesis causing oligohydramnios
Features: Facies: • Low-set ears • Beaked nose • Downward slanted eyes Pulmonary hypoplasia Limb deformity
What are the features of UTI in an infant?
Fever Jaundice Poor feeding Febrile convulsions Vomiting Offensive urine
What are the features of UTI in a child?
Frequency Dysuria Urgency Abdominal pain D&V Haematuria Febrile convulsions Enuresis
What is vesicoureteric reflux and why is it important?
The ureters are displaced laterally and enter directly into the bladder, rather than an angle.
This can lead to backflow of urine from the bladder, back into the ureters
This is problematic because:
1) After voiding, the urine in the ureter will return to the bladder, leading to incomplete bladder emptying
2) If the child has a UTI, the infected urine may backflow to the kidney, leading to kidney damage and scarring
How is vesicoureteric reflux investigated?
Initial ultrasound to identify potential obstruction or renal defects Micturating cystourethrogram (MCUG) is best investigation
What are features of atypical UTIs?
Sepsis Crap urine flow Abdominal mass Raised creatinine Repeated UTI Failure of Abx
What are the investigations for UTI?
Urine dipstick if clinical suspicion
Urine culture if:
• Urine dipstick is leukocyte esterase or nitrite positive
○ If Nitrite +ve and leukocyte -ve, don’t start antibiotics unless there is good clinical evidence
• Child is <3 months
• Suspected upper UTI
• Risk of serious infection
• Recurrent infection
What is the management of UTI in infants <3 months?
REFERRAL TO HOSPITAL
IV Antibiotics (Co-amoxiclav) for 5-7 days
Followed by oral prophylaxis
What is the management of UTI in children >3 months?
If suspected upper UTI (Fever or loin pain):
Trimethoprim (PO) for 7 days
If suspected lower UTI:
Trimethoprim (PO) for 3 days
What are the investigations for atypical UTIs?
- Ultrasound of the urinary tract to identify structural abnormalities
- DMSA and MCUG may also be performed in children < 6 months presenting
What is daytime enuresis?
This is lack of bladder control during the day in a child old enough to be continent (over the age of 3-5). Daytime enuresis may also be accompanied by nocturnal enuresis.
What are the causes of daytime enuresis?
Causes include:
- Lack of attention to the bladder.
- Detrusor instability - Sudden bladder contractions leading to feeling of urgency and enuresis.
- Neuropathic bladder - Enlarged bladder that fails to empty properly. Associated with spina bifida and other neurologic problems. There may be abnormal perianal sensation and anal tone, abnormal leg reflexes and gait.
- UTI (rarely in the absence of other symptoms)
- Constipation
- Ectopic ureter - Causes constant dribbling, and the child is always damp. Girls may be dry all night, but wet themselves when waking due to pooling of the urine in the vagina, secondary to ectopic ureter.
How should daytime enuresis be investigated?
A urine sample should be examined for MC&S. Perform an examination to exclude neurologic causes.
Further investigations may be indicated, including urodynamic studies, ultrasound of bladder, X-ray of spine or MRI.
What is the management of daytime enuresis?
○ Children in whom a neurological cause has been excluded, may benefit from:
§ Star charts
§ Bladder training
§ Pelvic floor exercises
○ Anticholinergic drugs (e.g. oxybutynin), which reduces bladder contractions, may be useful
What is the most common cause of secondary enuresis?
Loss of previously attained bladder control
Most common cause is emotional upset
Other causes include UTI and polyuria from diabetes
When is nocturnal enuresis a disorder?
Treatment is rarely undertaken for children younger than 5 years; at 5 years of age most children should be continent. Infrequent bedwetting is common in children. Bedwetting becomes a disorder when it is more frequent (2 or more times a week), which is present in 6% of 5 year olds, and 1.5% of 10 year olds
What tends to cause primary nocturnal enuresis?
Rarely medical
Mixture of developmental delay and genetic factors which determine bladder control
2/3 of children with enuresis have a first-degree relative who has shared the issue.
What is the management of nocturnal enuresis?
If child is <5 = Reassure that it should stop by the time they’re 5
If child is >5 and infrequent bedwetting (<2 times a week) = Watchful waiting, provide advice on reducing fluid intake before sleep, increase access to toilets, pee before sleep etc
If child is >5 and frequent bedwetting (>2/week) =
• Enuresis alarm with positive reward system
• Desmopressin
If short term relief is needed, prescribe desmopressin
If after 2 courses of treatment there is no response, refer to specialist
If there is nocturnal enuresis with daytime enuresis too, refer to secondary care
What are causes of transient proteinuria?
Febrile illness
Exercise
Orthostatic (postural) proteinuria - Normally the result of a child being upright all day
Does not require investigation
What are the causes of pathological proteinuria?
Minimal change glomerulonephritis
Glomerulonephritides
Increased GFR
Hypertension
What are the clinical features of nephrotic syndrome?
Triad:
• Proteinuria
• Hypoalbuminaemia
• Oedema
Hyperlipidaemia and lipiduria
Earliest sign is periorbital oedema on waking
Breathlessness due to pleural effusion
Ascites
Secondary causes: HSP, SLE, infections (e.g. malaria) or allergens (e.g. bee stings
NOTE: Same presentation for minimal change nephropathy
What is the management of nephrotic syndrome?
Oral steroids (Prednisolone) After 4 weeks, beginning reducing dose If after 6 weeks, no improvement, renal biopsy is necessary
NOTE: Same management for minimal change nephropathy
What are the complications of nephrotic syndrome?
• Hypovolaemia
○ Abdominal pain/Feeling faint
○ Treat with IV saline
• Thrombosis
○ Urinary loss of antithrombin III
○ Steroid therapy can worsen thrombocytosis
• Infection
○ Vaccinations against pneumococcus/ influenza recommended
○ Aciclovir treatment of chicken pox
• Hypercholesterolaemia
○ Inversely proportional to serum albumin
What is the management of steroid-resistant nephrotic syndrome?
Oedema is managed with diuretics, salt restriction and ACE inhibitors
Unlike steroid sensitive, haematuria would be seen
Most common cause is focal segmental glomerulosclerosis
How do you differentiate glomerular and lower urinary tract haematuria?
Glomerular - LUT
Brown urine - Red urine
Proteinuria - No proteinuria
Glomerular has deformed cells
LUT haematuria seen at start or end of urine stream
What are the symptoms of Alport syndrome?
Kidney disease
Hearing loss
Eye abnormality
X-linked recessive
What investigations are conducted for haematuria?
○ ALL patients § Urine MC&S § Protein and calcium excretion § Kidney and urinary tract ultrasound § U&Es, albumin § FBC, platelets, coagulation, sickle cell screen
○ If suggestive of GLOMERULAR haematuria
§ ESR, complement and anti-dsDNA antibodies
§ Throat swab, antistreptolysin O/anti-DNAse B titres
§ Hepatitis B and C screen
§ Renal biopsy
§ Test mother’s urine for blood (if Alport syndrome is suspected)
§ Hearing test (if Alport syndrome is suspected)
○ NOTE: indications for renal biopsy:
§ Significant persistent proteinuria
§ Recurrent macroscopic haematuria
§ Renal function is abnormal
§ Complement levels are persistently abnormal
What are signs of acute nephritis?
In acute nephritis, increased glomerular cellularity restricts glomerular blood flow, and therefore GFR is decreased. This leads to:
○ Decreased urine output and volume overload
○ Hypertension (may cause seizures)
○ Oedema (initially periorbital)
○ Haematuria + proteinuria
What are the features of post-streptococcal glomerulonephritis?
Develops 1-2 weeks after URTI infection (IgA nephropathy is 1-2 days)
Diagnosed by evidence of recent streptococcal infection:
• Anti-streptolysin O titre
• Anti-DNAse B titres
What are the clinical features of Henoch-Schonlein purpura?
• Purpuric & petechial rash over extensor surfaces
○ Most commonly the buttocks/legs
○ Symmetrical distribution
• Joint pain and swelling (periarticular oedema)
• Abdominal pain
○ Can cause melaena or haematemesis
• Haematuria
What is the management of Henoch-Schonlein purpura?
Spontaneously resolves after 4 weeks
Joint pain managed with paracetamol/ibuprofen
Severe oedema managed with oral prednisolone
IV corticosteroids in those with nephrotic syndrome levels of proteinuria or declining renal function
What are the features of IgA nephropathy?
Macroscopic haematuria
Develops 1-2 days after URTI infection (Compared to post-strep which develops after 1-2 weeks)
Managed the same as HSP
What are the clinical features of haemolytic-uraemic syndrome?
Acute renal failure
MAHA
Thrombocytopaenia
Typically triggered by gastrointestinal infection, most commonly E.coli infection. This normally presents with bloody diarrhoea
The toxins from this infection travels directly to kidney endothelium, resulting in intravascular thrombogenesis.
The coagulation cascade is activated, leading to platelet consumption.
There is haemolysis due to the RBCs coming in contact with the thrombuses and breaking
What is the management of haemolytic uraemic syndrome?
Hospitalisation
Monitor urine output and hydration status
Avoid antibiotics, anti-diarrhoeals, narcotic opioids and NSAIDs
Monitor BP, treat with CCBs if elevated
What are the clinical features of chronic kidney disease?
○ Anorexia and lethargy
○ Polydipsia and polyuria
○ Faltering growth/growth failure
○ Bony deformities from renal osteodystrophy
○ Hypertension
○ Acute-on-chronic renal failure (precipitated by infection or dehydration)
○ Incidental finding of proteinuria
○ Unexplained normochromic, normocytic anaemia
What is the management of chronic kidney disease?
• Diet
○ Anorexia and vomiting are common
○ Calorie supplements or NG/gastrostomy feeding
○ Protein intake enough to maintain growth and albumin but preventing accumulation of toxic metabolic by-products
• Prevention of renal osteodystrophy
○ Decreased activation of vitamin D leads to phosphate retention and hypocalcaemia. Leads to hyperparathyroidism and eventually osteitis fibrosa cystica and osteomalacia
○ Phosphate restriction (by reducing milk), using calcium carbonate as a phosphate binder and activated vitamin D supplements can help
• Control of salt and water balance, and acidosis
○ Salt supplements and a lot of water
○ Treatment with bicarbonate supplements is needed to prevent acidosis
• Acidosis
○ Reduced EPO production and circulation of marrow-toxic metabolites leads to anaemia
○ Responds well to the administration of SC recombinant human erythropoietin
• Hormonal abnormalities
○ Growth hormone resistance, characterised by a high GH level but poor growth, is a feature of CKD
○ Recombinant human GH is effective in improving growth for up to 5 years of us
○ Many children with stage 4/5 CKD will have delayed puberty or subnormal pubertal growth spurt
