Paediatric Renal and Urology Flashcards
Urinary tract infections
The urinary tract includes the urethra, bladder, ureters and kidneys. Urinary tract infections are infections anywhere along this pathway.
Acute pyelonephritis is when the infection affects the tissue of the kidney. It can lead to scarring in the tissue and consequently a reduction in kidney function.
Cystitis means inflammation of the bladder, and can be the result of a bladder infection.
Signs and symptoms of UTIs
Fever may be the only symptom of a urinary tract infection, especially in young children. Always consider (and exclude) a urinary tract infection in a child with a temperature, unless there is a clear alternative source of infection.
Babies will present with very non-specific symptoms:
Fever
Lethargy
Irritability
Vomiting
Poor feeding
Urinary frequency
Signs and symptoms in older infants and children are more specific:
Fever
Abdominal pain, particularly suprapubic pain
Vomiting
Dysuria (painful urination)
Urinary frequency
Incontinence
Acute pyelonephritis
The diagnosis of acute pyelonephritis is made if either there is:
A temperature greater than 38°C
Loin pain or tenderness
This is a very important point to note, as it affects the way you would investigate the child for recurrent infections.
Urine dipstick
The ideal urine sample is a clean catch sample, avoiding contamination. This can be tricky in younger children and babies, particularly girls. This often involves the parent sat with the infant without a nappy and a urine pot held ready to catch the sample if it occurs. A clean catch sample is important to avoid contamination and unreliable microbiology results.
Nitrites – gram negative bacteria (such as E. coli) break down nitrates, a normal waste product in urine, into nitrites. The presence of nitrites suggest bacteria in the urine.
Leukocytes – leukocytes are white blood cells. There are normally a small number of leukocytes in the urine, however a significant rise can be the result of an infection or another cause of inflammation. A urine dipstick tests for leukocyte esterase, a product of leukocytes that give an indication about the number of leukocytes in the urine.
Nitrites are a better indication of infection than leukocytes. If both are present the patient should be treated as a UTI. If only nitrites are present it is worth treating as a UTI. If only leukocytes are present the patient should not be treated as a UTI unless there is clinical evidence they have one.
If nitrites or leukocytes are present, the urine should be sent to the microbiology lab. If neither are present the patient is unlikely to have a UTI.
Send a midstream urine (MSU) sample to the microbiology lab to be cultured and have sensitivity testing.
Managing UTIs
All children under 3 months with a fever should start immediate IV antibiotics (e.g. ceftriaxone) and have a full septic screen, including blood cultures, bloods and lactate. A lumbar puncture should also be considered.
Oral antibiotics can be considered in children over 3 months if they are otherwise well. Children with features of sepsis or pyelonephritis will require inpatient treatment with IV antibiotics. Always follow local guidelines. Typical antibiotic choices in urinary tract infections in children are:
Trimethoprim
Nitrofurantoin
Cefalexin
Amoxicillin
Investigating recurrent UTIs
Recurrent UTIs should be investigated for an underlying cause and renal damage. This is a summary of the NICE guidelines on urinary tract infections in under 16s. Please read the full guidelines before treating patients.
Ultrasound Scans
All children under 6 months with their first UTI should have an abdominal ultrasound within 6 weeks, or during the illness if there are recurrent UTIs or atypical bacteria
Children with recurrent UTIs should have an abdominal ultrasound within 6 weeks
Children with atypical UTIs should have an abdominal ultrasound during the illness
DMSA (Dimercaptosuccinic Acid) Scan
DMSA scans should be used 4 – 6 months after the illness to assess for damage from recurrent or atypical UTIs. This involves injecting a radioactive material (DMSA) and using a gamma camera to assess how well the material is taken up by the kidneys. Where there are patches of kidney that have not taken up the material, this indicates scarring that may be the result of previous infection.
Vesico-Ureteric Reflux (VUR)
Vesico-ureteric reflux (VUR) is where urine has a tendency to flow from the bladder back into the ureters. This predisposes patients to developing upper urinary tract infections and subsequent renal scarring. This is diagnosed using a micturating cystourethrogram (MCUG).
Management of vesico-ureteric reflux depends on the severity:
Avoid constipation
Avoid an excessively full bladder
Prophylactic antibiotics
Surgical input from paediatric urology
Micturating Cystourethrogram (MCUG)
Micturating cystourethrogram (MCUG) should be used to investigate atypical or recurrent UTIs in children under 6 months. It is also used where there is a family history of vesico-ureteric reflux, dilatation of the ureter on ultrasound or poor urinary flow. A MCUG is used to diagnose VUR.
It involves catheterising the child, injecting contrast into the bladder and taking a series of xray films to determine whether the contrast is refluxing into the ureters. Children are usually given prophylactic antibiotics for 3 days around the time of the investigation.
Vulvovaginitis
Vulvovaginitis refers to inflammation and irritation of the vulva and vagina. It is a common condition often affecting girls between the ages of 3 and 10 years.
This irritation is caused by sensitive and thin skin and mucosa around the vulva and vagina in young girls. The vagina is more prone to colonisation and infection with bacteria spread from faeces. It can be exacerbated by:
Wet nappies
Use of chemicals or soaps in cleaning the area
Tight clothing that traps moisture or sweat in the area
Poor toilet hygiene
Constipation
Threadworms
Pressure on the area, for example horse riding
Heavily chlorinated pools
Vulvovaginitis improves and is much less common after puberty, as oestrogen helps keep the skin and vaginal mucosa healthy and resistant to infection.
Presentation of vulvovaginitis
Vulvovaginitis is a common presentation in young girls before puberty. It presents with:
Soreness
Itching
Erythema around the labia
Vaginal discharge
Dysuria (burning or stinging on urination)
Constipation
A urine dipstick may show leukocytes but no nitrites. This will often result in misdiagnosis as a urinary tract infection.
Managing vulvovaginitis
Often patients have already been treated for urinary tract infections and thrush, usually with little improvement in symptoms. It is unusual for girls to develop thrush before puberty.
Generally no medical treatment is required and management focuses on simple measures to improve symptoms:
Avoid washing with soap and chemicals
Avoid perfumed or antiseptic products
Good toilet hygiene, wipe from front to back
Keeping the area dry
Emollients, such as sudacrem can sooth the area
Loose cotton clothing
Treating constipation and worms where applicable
Avoiding activities that exacerbate the problem
In severe cases an experienced paediatrician may recommend oestrogen cream to improve symptoms.
Nephrotic syndrome
Nephrotic syndrome occurs when the basement membrane in the glomerulus becomes highly permeable to protein, allowing proteins to leak from the blood into the urine. It is most common between the ages of 2 and 5 years. It presents with frothy urine, generalised oedema and pallor.
Nephrotic syndrome features a classic triad of:
Low serum albumin
High urine protein content (>3+ protein on urine dipstick)
Oedema
There are three other features that occur in patients with nephrotic syndrome:
Deranged lipid profile, with high levels of cholesterol, triglycerides and low density lipoproteins
High blood pressure
Hyper-coagulability, with an increased tendency to form blood clots
Causes of nephrotic syndrome
The most common cause in children is minimal change disease, causing over 90% of cases in children under 10. In minimal change disease, nephrotic syndrome occurs in isolation, without any clear underlying condition or pathology. There are a number of secondary causes of nephrotic syndrome, where it occurs due to an underlying condition.
It can be secondary to intrinsic kidney disease:
Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis
It can also be secondary to an underlying systemic illness:
Henoch schonlein purpura (HSP)
Diabetes
Infection, such as HIV, hepatitis and malaria
Minimal change disease
Minimal change disease is the most common cause of nephrotic syndrome in children. It can occur in otherwise healthy children, without any clear risk factors or reason for developing the condition. It is not clear why it occurs in most cases.
A renal biopsy and standard microscopy in minimal change disease is usually not able to detect any abnormality. Urinalysis (analysis of the urine) will show small molecular weight proteins and hyaline casts.
Management of minimal change disease is with corticosteroids (i.e. prednisolone). The prognosis is good and most children make a full recovery, however it may reoccur.
TOM TIP: Minimal change disease comes up fairly frequently in exams as the most common cause of nephrotic syndrome in children. If you spot a 2 – 5 year old child with oedema, proteinuria and low albumin, you may be asked about the underling cause. The answer is likely to be nephrotic syndrome.
Managing nephrotic syndrome
Nephrotic syndrome should be managed by experienced paediatricians with input from renal specialists. General management is with:
High dose steroids (i.e. prednisolone)
Low salt diet
Diuretics may be used to treat oedema
Albumin infusions may be required in severe hypoalbuminaemia
Antibiotic prophylaxis may be given in severe cases
High dose steroids are given for 4 weeks and then gradually weaned over the next 8 weeks:
80% of children will respond to steroids, and are referred to as steroid sensitive
80% of steroid sensitive patients will relapse at some point and need further steroids
Patients that struggle to wean steroids due to relapses are referred to as steroid dependant
Patients that do not respond to steroids are referred to as steroid resistant
In steroid resistant children, ACE inhibitors and immunosuppressants such as cyclosporine, tacrolimus or rituximab may be used.
Complications of nephrotic syndrome
Hypovolaemia occurs as fluid leaks from the intravascular space into the interstitial space causing oedema and low blood pressure.
Thrombosis can occur because proteins that normally prevent blood clotting are lost in the kidneys, and because the liver responds to the low albumin by producing pro-thrombotic proteins.
Infection occurs as the kidneys leak immunoglobulins, weakening the capacity of the immune system to respond. This is exacerbated by treatment with medications that suppress the immune system, such as steroids.
Acute or chronic renal failure
Relapse
Nephritis
Nephritis refers to inflammation within the nephrons of the kidneys. It causes:
Reduction in kidney function
Haematuria: invisible or visible amounts of blood in the urine
Proteinuria: although less than in nephrotic syndrome
The two most common causes of nephritis in children are post-streptococcal glomerulonephritis and IgA nephropathy (Berger’s disease).
Post-Streptococcal Glomerulonephritis
Post-streptococcal glomerulonephritis occurs 1 – 3 weeks after a β-haemolytic streptococcus infection, such as tonsillitis caused by Streptococcus pyogenes. Immune complexes made up of streptococcal antigens, antibodies and complement proteins get stuck in the glomeruli of the kidney and cause inflammation. This inflammation leads to an acute deterioration in renal function, causing an acute kidney injury.
Consider a diagnosis of post-streptococcal glomerulonephritis where there is evidence of recent tonsillitis caused by streptococcus. This could be a history of tonsillitis, positive throat swab results and anti-streptolysin antibody titres found on a blood test.
Management is supportive and around 80% of patients will make a full recovery. In some cases patients can develop a progressive worsening of their renal function. They may need treatment with antihypertensive medications and diuretics if they develop complications such as hypertension and oedema.
IgA nephropathy
IgA nephropathy is also known as Berger’s disease. This condition is related to Henoch-Schonlein Purpura, which is an IgA vasculitis. IgA deposits in the nephrons of the kidney causes inflammation (nephritis). When a renal biopsy is taken the histology will show “IgA deposits and glomerular mesangial proliferation”.
It usually presents in teenagers or young adults.
Management involves supportive treatment of the renal failure and immunosuppressant medications such as steroids and cyclophosphamide to slow the progression of the disease.
Haemolytic uraemic syndrome
Haemolytic uraemic syndrome (HUS) involves thrombosis in small blood vessels throughout the body, usually triggered by Shiga toxins from either E. coli O157 or Shigella.
It most often affects children following an episode of gastroenteritis. Antibiotics and anti-motility medication (e.g., loperamide) used to treat gastroenteritis caused by E. coli O157 or Shigella increase the risk of HUS.
HUS leads to the classic triad of:
Microangiopathic haemolytic anaemia
Acute kidney injury
Thrombocytopenia (low platelets)
The formation of blood clots consumes platelets, leading to thrombocytopenia. The blood flow through the kidney is affected by thrombi and damaged red blood cells, leading to acute kidney injury.
Microangiopathic haemolytic anaemia (MAHA) involves the destruction of red blood cells (haemolysis) due to pathology in the small vessels (microangiopathy). Tiny blood clots (thrombi) partially obstruct the small blood vessels and churn the red blood cells as they pass through, causing them to rupture.