Paeds - Nephrology Flashcards
UTIs in Children
Risk Factors
Clinical Features
Urine Dipstick
Management
1.) Risk Factors
- age <1yr, female (boys if <3mth), caucasian race
- previous UTI, voiding dysfunction, VUR
- constipation, immunosuppres…, spinal abnormalities
- sexual abuse (urinary sx but infection is uncommon),
2.) Clinical Features
- fever may be the only symptom in a child w/ a UTI
- other sx in babies: vomiting, poor feeding, failure to thrive, lethargy, irritability,
- other general UTI sx: polyuria (more wet nappies), dysuria, suprapubic tenderness, urgency/incontinence, cloudy urine, smelly urine, haematuria
- acute pyelonephritis: temp >38°C OR loin/flank pain
3.) Urine Dipstick - clean catch sample
- positive nitrites +/- positive leucocytes: treat as UTI and send MSU sample for MC+S w/in 24hrs
- if only +ve leucocytes, does not need treating but can send MSU sample for MC+S w/in 24hrs
4.) Management
- fever in a child <3mths is managed as suspected meningitis (full septic screen, IV ceftriaxone, ?LP)
- cystitis in >3mths: PO Abx for 3 days (trimethoprim OR nitrofurantoin OR cefalexin OR amoxicillin)
- upper UTI in >3mths: consider referral OR treat w/
PO Abx for 7-10 days (ciprofloxacin or co-amoxiclav)
- asymptomatic bacteriuria should not be treated
- safety netting if not better after 48hrs or septic sx
- adequate fluid intake, pain relief, address constipation
Investigating Recurrent/Atypical UTIs
Abdominal Ultrasound Scans
DMSA (Dimercaptosuccinic Acid) Scan
Vesico-Ureteric Reflux (VUR)
Micturating Cystourethrogram (MCUG)
1.) Abdominal Ultrasound Scans - criteria
- children <6mths with their first UTI within 6 weeks
- children with recurrent UTIs or an atypical UTI should have the abdominal US during the illness
- recurrent UTI: 1 upper UTI + 1 lower UTI, 2+ episodes of an upper UTI, 3+ episodes of a lower UTI
- atypical UTI: doesn’t respond to Abx within 48hrs, non-E.coli organism, sepsis, raised creatinine, poor urine flow, abdominal or bladder mass, seriously ill
2.) DMSA (Dimercaptosuccinic Acid) Scan - used 4-6 months after the illness in recurrent or atypical UTIs
- injecting a radioactive material (DMSA) and using a gamma camera to assess kidney uptake
- patches of reduced uptake indicates scarring
3.) Vesico-Ureteric Reflux (VUR) - urine flows from the bladder back into the ureters, grades 1-5
- very common (33% infants/kids with a UTI)
- increases risk of upper UTIs and renal scarring
- diagnosed using a micturating cystourethrogram
- Mx: avoid constipation or an excessively full bladder, prophylactic Abx, surgical input from paediatric urology
4.) Micturating Cystourethrogram (MCUG) - used to diagnose VUR in kids w/ recurrent or atypical UTIs
- used in all children < 6mths, family history of VUR, ureteric dilatation on US or poor urinary flow
- inject contrast into the bladder and take X-ray films to determine if the contrast is refluxing into the ureters
- children given prophylactic Abx for 3 days
Vulvovaginitis
Pathophysiology
Clinical Features
Management
1.) Pathophysiology - vulvovaginal inflammation/irritation
- common in girls 3-10yrs due to sensitive and thin skin, improves with puberty due to oestrogen
- RF: wet nappies, constipation, tight clothing trapping moisture/sweat, poor toilet hygiene, threadworms
- chemicals/soap for cleaning, chlorinated pools
- pressure on the area, for example horse riding
2.) Clinical Features
- soreness, itching, dysuria, constipation
- erythema around the labia, vaginal discharge
- urine dip may show +ve WBCs but -ve nitrites
3.) Management
- often already treated for UTI or thrush (unusual before puberty) without improvement in symptoms
- no medical treatment, simple measures improve sx:
- avoid washing w/ soap/chemicals, avoid perfumed or antiseptic products, keep the area dry, loose clothing
- good toilet hygiene, wipe from front to back
- emollients, such as sudacrem can sooth the area
- treating constipation and worms where applicable
- can refer to paediatrician for oestrogen cream
Nephrotic Syndrome
Aetiology
Clinical Triad
Investigations
Management
1.) Aetiology - podocyte damage leading to glomerular charge-barrier disruption causing protein leakage
- most common cause is minimal change disease
2.) Clinical Triad
- proteinuria: >3g/24h in urine OR urine PCR >300, urine dipstick +++, frothy urine
- hypoalbuminaemia: <30 serum albumin
- oedema: periorbital and bilateral pitting leg swelling
- other features: hypertension, hypercoagulability, deranged lipid profile (↑cholesterol, TGs, LDLs)
3.) Investigations
- bloods: FBC, U+Es, albumin, HbA1c
- urinalysis, 24hr urine collection or urinary PCR
- USS guided renal biopsy to confirm the type: only performed
4.) Management
- steroids: high dose PO prednisolone for 4wks then gradually weaned over the next 8wks, 80% are steroid-sensitive
- renal biopsy: only performed if no response to steroids
- steroid-resistant: ACEi and DMARDs (1°cyclophosphamide)
- proteinuria: ACEi or ARBs, also control BP
- fluid overload: diuretics, salt and water restriction
- hypoalbuminaemia: albumin infusions if severe
- treat potential complications
Causes of Nephrotic Syndrome
Minimal Change Disease
Focal Segmental Glomerulosclerosis (FSGS)
Membranous Nephropathy
Secondary to Systemic Illness
1.) Minimal Change Disease - commonly ages 2-5yrs
- reversible so usually no progression to renal failure
- without any clear underlying condition or pathology
- diagnosis: urinalysis (small molecular weight proteins and hyaline casts), renal biopsy is not useful
- Mx: can be fully treated w/ high dose prednisolone
- if no improvement w/ steroids, consider FSGS
- can advance to FSGS
2.) Focal Segmental Glomerulosclerosis - can affect children and adults
- scarring of small sections of each glomeruli
- circulating factor damaging podocytes
- HIV infections can be a cause of FSGS
- can progress to renal failure
3.) Membranous Nephropathy - affects mainly adults
- can be primary (autoimmune) or secondary (caused by other diseases e.g. lymphoma)
4.) Secondary to Systemic Illness
- Henoch schonlein purpura (HSP), diabetes
- infection: HIV, hepatitis and malaria
Complications of Nephrotic Syndrome
Hypovolaemia
Infection
Thromboembolism
Hyperlipidaemia
Hypocalcaemia
AKI/Worsening CKD
1.) Hypovolaemia - fluid leaks from intravascular space into interstitial space causing oedema and low BP
- must assess their hydration status
- albumin infusions can be given if severe
2.) Infection - due to leakage of immunoglobulins
- antibiotic prophylaxis may be given in severe cases
3.) Thromboembolism - loss of ATIII, plasminogen
- stroke, DVT, renal vein thrombosis, mesenteric ischaemia
- prophylactic dalteparin if albumin <20
4.) Hyperlipidaemia - altered lipoprotein metabolism
- can start patients on a statin
5.) Hypocalcemia - loss of vitamin D
6.) AKI/Worsening CKD
- may require renal replacement therapy if severe
Nephritic Syndrome
Aetiology
Clinical Features
Investigations
Management
1.) Aetiology - disruption of endothelium results in inflammatory response causing damage to the GBM
2.) Clinical Features
- haematuria +/- proteinuria +/- mild-moderate oedema
- proteinuria <3g/24hrs or urine PCR <300
- AKI (↓GFR): rapidly progressive GN
- hypertension
3.) Investigations
- bloods: FBC, U+Es, clotting, PSA
- urinalysis, 24hr urine collection or urine PCR
- exclude infection and malignancy for haematuria
- renal biopsy to confirm diagnosis/type
4.) Management
- fluid overload: diuretics, salt and water restriction
- proteinuria: ACEi or ARBs, also control BP
- immunosuppressive therapy depending on specific cause of GN, is decided by renal +/- resp + rheum
- plasma exchange for anti-GM or ANCA vasculitis
- dialysis in severe AKI due to RPGN
Causes of Nephritic Syndrome in Children
Post Streptococcal/Infectious
IgA Nephropathy/Henoch-Schonlein Purpura
1.) Post-Streptococcal GN (Post-Infectious)
- occurs 1-3wks after a group A ß-haemolytic strep (pyogenes), tonsillitis/pharyngitis, impetigo/cellulitis
- acute deterioration in renal function –> AKI
- low serum C3, + anti-streptococcal antibodies
- biopsy: immune complex deposition (IgG, IgM, C3)
- Mx: self-limiting, ACEi/ARB, low sodium diet
2.) IgA Nephropathy (Berger’s Disease) - usually presents in teenagers and young adults
- related to Henoch-Schonlein Purpura (IgA vasculitis)
- IgA deposits in the nephrons causes inflammation
- x: visible haematuria associated with a URTI or GI infection, purpuric rashes (bleeding underneath skin), can also have joint pain and abdominal pain
- Mx: supportive treatment of renal failure and immunosuppressants to slow progression
Haemolytic Uraemic Syndrome
Pathophysiology
Clinical Features
Investigations
Management
1.) Pathophysiology - occurs when there is thrombosis within small blood vessels throughout the body which produces a classical triad of:
- MAHA (↓Hb) + thrombocytopenia + AKI
- usually triggered by Shiga toxin (E.coli 0157) (90% in kids), increased risk when using Abx and anti-motility medication to treat E.coli gastroenteritis
- mainly seen in young children
- other causes: pneumococcal infection, HIV, SLE, drugs, cancer
2.) Clinical Features
- brief gastroenteritis, often with bloody diarrhoea
- HUS sx often starts 5 days after onset of diarrhoea:
- reduced urine output, haematuria, bruising
- abdominal pain, oedema, hypertension
- lethargy and irritability, confusion
3.) Investigations
- bloods: FBC (↓Hb), clotting (↓plts), U+Es (AKI)
- blood film: schistocytes
- MAHA: confirmed if Hb <80 w/ a negative Coombs test
- stool culture: looking for STEC infection (PCR for Shiga toxins)
4.) Management - medical emergency (10% mortality)
- urgent referral to the paediatric renal unit
- self-limiting but supportive management is vital
- careful maintenance of fluid balance
- if required: dialysis, antihypertensive, transfusions
- 70 to 80% of patients make a full recovery
