Nephrology Flashcards
Features of bed wetting - Enuresis
Day and night time continence usually achieved by 3 or 4.
Enuresis = involuntary discharge of urine by day or night or both, in a child aged 5 years or older, in absence of congenital or acquired defects or nervous system or urinary tract.
Primary - child never achieved continence
Secondary - Child been dry for at least 6 months before
Often occurs at night due to deep sleep = nocturnal enuresis.
Day time = diurnal enuresis.
More common in girls.
Causes of bed wetting?
Primary - normal variation on development, small bladder, failure to wake up to sensation of needing to urinate, psychological distress, secondary to another condition.
Secondary - UTI, constipation, diabetes, new psychosocial problems such as stress in family or school life/abuse.
Management of enuresis?
Look for possible underlying cause/triggers to treat.
Advise on fluid intake, diet and toileting behaviour.
Reward systems.
Enuresis alarm first-line for children under age of 7 - need to be used for at least 3 months.
Desmopressin used first-line in children >7 years of age, particularly if short-term control needed or enuresis alarm ineffective.
Oxybutinin (anticholinergic), reduces contractility of bladder, and helpful with urge incontinence with children who have diurnal enuresis.
Causes of haematuria?
Idiopathic Trauma UTI Bleeding disorders - ITP, HSP Nephritic syndrome Kidney stones Wilms tumour Hydronephritis Renal vein thrombosis Haemolytic uraemic syndrome (bloody diarrhoea)
Investigations of haematuria?
Microscopic haematuria with normal BP and kidney function -> check urine over several months. If continues -
- Renal USS
- Urinalysis for protein, calcium, creatinine
- Blood (U&Es)
Microscopic haematuria, with proteinuria/HTN/abnormal bloods/FMH of kidney disease -
- Kidney biopsy.
Management of haematuria?
Surveillance if child is otherwise healthy.
Manage underlying cause.
What is haemolytic uraemic syndrome?
Similar condition of TTP
- arteriolar thrombi are predominantly formed in kidneys.
Causes and features of haemolytic uraemic syndrome?
Toxin produced by E. coli causes acute renal failure Ciclosporin SLE HIV Pregnancy Tumours The pill
Triad of: haemolytic anaemia, thrombocytopenia, AKI.
E. coli can cause brief gastroenteritis with bloody diarrhoea. After 5 days of diarrhoea: - Reduced urine output - Haematuria Abdominal pain - Lethargy and irritability - Confusion
Investigations of haemolytic uraemic syndrome?
FBC - anaemia, thrombocytopenia, fragmented blood film
U&E (AKI)
Stool culture
Management of haemolytic uraemic syndrome?
Urgent referral to paediatric renal unit for renal dialysis if required.
Supportive treatment - fluids, blood transfusion, dialysis.
Self-limiting and 80% make full recovery.
Does not respond to plasma exchange as it is not brought about by the deficiency in VWF-cleaving protease.
Causes of nephritic syndrome?
Reduction in kidney function
Haematuria
Proteinuria
Features of nephritic syndrome?
Haematuria
HTN
Azotemia (increased blood urea nitrogen and creatinine) - reduced kidney function
Proteinuria
Blurred vision
Oliguria
Oedema
Causes of nephritic syndrome in children?
Often post-strep glomerulonephritis
IgA nephropathy
Haemolytic uraemic syndrome (GI infection produces toxins causing haemoylsis of RBCs).
Henoch-Shonlein purpura (purple spots on skin, joint pain, GI problems, glomerulonephritis).
Features and management of post-streptococcal glomerulonephritis?
Occurs 1-3 weeks post beta-haemolytic strep infection (eg tonsillitis).
Immune complexes from strep antigens along with ab’s and complement proteins from person’s immune system get stuck in glomeruli causing inflammation.
Management is supportive and patients usually make full recovery (80%). Some can have progressive worsening renal function.
Features and management of IgA nephropathy?
Related to HSP (IgA vasculitis)
IgA deposits in nephrons causes inflammation and nephritic syndrome.
Histology shows IgA deposits and glomerular mesangial proliferation.
Often presents with haematuria a few days after URTI.
Management - supportive treatment (antihypertensives, etc)
Investigations of nephritic syndrome?
Blood pressure (high) Urine dip - protein and blood Urinalysis Blood U&Es Complement levels are low Test for streptococcus (ASOT) Kidney biopsy
Management of nephritic syndrome?
Bed rest Low potassium/salt/fluid diet (due to fluid overload) Strict fluid input/output chart Regular weight checks (twice daily) Consider antihypertensives Consider anti-inflammatory medication Consider antibiotic for streptococcus
What is Henoch-Schonlein Purpura?
IgA mediated small vessel vasculitis.
Usually seen in children following an infection.
Features of Henoch-Schonlein Purpura?
Palpable purpuric rash over buttocks and extensor surfaces
Abdominal pain
Polyarthritis
Features of IgA nephropathy - GN, haematuria, renal failure
Investigations, treatment and prognosis of Henoch-Schonlein Purpura?
ANCA?
Analgesia for arthralgia
Supportive treatment for nephropathy.
Usually self-limiting - especially if have no renal involvement
Around 1/3 have relapse.
Causes of nephrotic syndrome?
Minimal change
Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis
Systemic illness - HSP, DM, Infectious diseases (eg HIV, hepatitis, malaria)
Features of nephrotic syndrome?
Triad - Proteinuria, hypoalbuminaemia, oedema.
Oliguria, weight gain, hyperlipidaemia/hypercholesterolaemia, hyper coagulable state due to antithrombin III, predisposition to infection due to loss of Ig.
What features of nephrotic syndrome prompt renal biopsy?
Age <1 year or >12 years HTN Impaired renal function Frank haematuria Steroid resistant nephrotic syndrome
Features of minimal change disease and management?
Renal biopsy and standard microscopy not usually able to detect abnormality.
Urinalysis - small molecular weight proteins and hyaline casts.
Good prognosis
Management with corticosteroids (ie prednisolone).
Investigations for nephrotic syndrome?
Urine dip Urine protein:creatinine ratio U&E FBC Serum albumin Varicella Zoster serology Additional tests - complement levels, hepatitis serology, anti-streptolysin O titre (ASOT), ANA, ANCA, anti-dsDNA.
Management and complications of nephrotic syndrome?
High dose oral pred for 4 weeks, followed by smaller dose for another 4 weeks.
Biological agents for steroid resistant nephrotic syndrome - eg levamisole, cyclophosphamide, cyclosporin or tacrolimus.
Low salt diet - avoid worsening oedema
Prophylactic antibiotics - as high risk of infection
Diuretics may reduce fluid build-up.
Albumin infusion may be required if hypoalbuminaemia is severe.
Complications:
- Hypovolaemia
- Thrombosis
- Infections
- Acute or chronic renal failure
- Varicella Zoster (chicken pox) - prophylactic aciclovir or treat with IV acyclovir.
Causes of UTI?
E. coli Proteus mirabilis Pseudomonas Staphylococcus saprophyticus Klebsiella
Predisposing factors to UTI?
Age <1 Female sex (shorter urethral length) White children Uncircumcised boys in first year of life Previous UTI Voiding dysfunction - constipation, foreign body, ineffective posture when voiding Vesicoureteric reflux Sexual activity (adolescents) Poor hygiene - eg not wiping from front to back in girls Incomplete bladder emptying: - Infrequent voiding - Hurried micturition - Obstruction by full rectum due to constipation - Neuropathic bladder
Features of UTI
More common in boys until 3 months of age (due to more congenital abnormalities), and then higher in girls.
Presentation based on age:
Infants - poor feeding, vomiting, irritability
Younger children - abdominal pain, fever, dysuria
Older children - dysuria, frequency, haematuria
Features suggesting upper UTI - temp >38 degrees, loin pain/tenderness.
Cystitis - frequency, urgency, dysuria, suprapubic pain
Acute pyelonephritis - ill-looking, fever, flank pain, irritability, vomiting.
Investigations for UTI?
Urine sample if:
- Any symptoms or signs of UTI
- Unexplained fever of 38 degrees or higher
- With alternative site of infection but who remain unwell.
- Urine collection method - clean catch is preferable, if not then urine collection pads.
Blood cultures - febrile or systemically unwell neonates/infants
USS scan if:
- Within 6 weeks post infection in all infants under 6m, or over 6m old with recurrent UTI
- During acute infection in all infants with atypical UTI, or under 6m old and recurrent UTI
Micturating cystourethrogram if:
- 6 week post infection, in infants under 6m old with atypical or recurrent UTIs (consider if 6m-3y)
- 6 weeks post infection, if UTI abnormal
DMSA scan:
- 4-6 months after illness to assess damage from recurrent or atypical UTIs.
- Shows scarring of kidneys.
Management of UTIs?
<3 months - refer to paediatrics - IV cefriaxone, full septic screen.
> 3 months with upper UTI - consider admission or oral abx co-amoxiclav for 7-10 days.
> 3 months with lower UTI - oral abx for 3 days - trimethoprim, nitrofurantoin, cephalosporin or amoxicillin.
Safety net
Antibiotic prophylaxis if recurrent UTIs
Prevention of UTIs?
Good posture when voiding Good toilet hygiene Good hydration Double toileting Prophylactic low dose trimethoprim for recurrent UTIs
What is vesicoureteric reflux?
Abnormal back flow from bladder into ureters and kidneys.
Predisposes to UTI - found in 30% of children who present with UTI.
Pathophysiology of vesicoureteric reflux?
Ureters laterally displaced, entering bladder in more perpendicular fashion than at an angle. Therefore shortened intramural course of ureter.
VUJ cannot therefore function adequately.
Investigations of vesicoureteric reflux?
VUR diagnosed following micturating cystourethrogram.
DMSA scan to look for renal scarring.
Grades of VUR?
1 - reflux into ureter only, no dilatation
2 - reflux into renal pelvis on micturition, no dilatation
3 - mild-moderate dilatation of ureter, renal pelvis and calyces
4 - dilatation of renal pelvis and calyces with moderate ureteral tortuosity
5 - gross dilatation of ureter, pelvis and calyces with ureteral tortuosity.
Management of VUR?
Surgical correction.
Whats the most common cause of AKI in children?
HSP
Causes of CKD?
Congenital dysplasia
Inherited renal disease - Alport syndrome, autosomal recessive polycystic kidney disease
Reflux nephropathy
Chronic glomerulonephritis (IgA nephropathy)
What is Alport syndrome?
Inherited disease of collagen IV (integral part of basement membrane)
X-linked dominant and autosomal dominant types
Features - ocular defects, SNHL, hereditary nephritis
Renal biopsy for diagnosis.
Features of renal agenesis?
Bilateral = potters syndrome.
No foetal urine production - oligohydramnios, pulmonary hypoplasia, beaked nose, low set ears - death.
Unilateral - likely to have normal kidney function if other kidney is normal.
Features of ectopic kidney?
Abnormalities of ascent and rotation.
Kidney function normal as long as other kidney normal.
Features of duplex kidney?
Two ureters on one kidney, one ureter may be ectopic.
Horseshoe kidney features?
Fusion of two kidneys at lower poles, may also be dysplastic.
Causes of HTN in children?
Renal parenchymal disease Renal vascular disease Coarctation of aorta Essential or primary HTN Pheochromocytoma Congenital adrenal hyperplasia
