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Year 3 - Paediatrics > Paediatric Nephrology > Flashcards

Paediatric Nephrology Flashcards

1
Q

Part 1

A
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2
Q

what is glomerular disease?

A

Glomerular disease is a disorder of the kidneys, in which the normal functioning of the kidneys is disturbed and the chemical balance is not maintained in your blood and urine

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3
Q

what are the 2 main types of glomerular disease?

A

The two basic types of glomerular disease include nephritic and nephrotic, but, with some diseases, the two types can overlap

The key feature of nephritic disease (“glomerulonephritis”) is blood in the urine (hematuria)

People with nephrotic syndrome have protein in the urine (proteinuria) but, often, little to no blood in the urine (hematuria)

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4
Q

what is teh strucutre of the nephron?

A
  • Receives 25% cardiac output/min
  • GFR:
  • neonate 20-30ml/min/1.73m²
  • Age 2yrs equals adult 90-120

(Don’t have normal kidney function at birth)

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5
Q

glomerular disease cn be caused in 2 main way - what are they?

A

congenital

aquired

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6
Q

what are the 5 kidney functions?

A
  1. Waste handling (urea/creatinine)
  2. Water handling
  3. Salt balance (sodium/potassium/calcium/phosphate)
  4. Acid base control (bicarbonate)
  5. Endocrine - red cells/blood pressure/bone health
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7
Q

what makes up the Glomerular Filtration barrier?

A
  • Endothelial cell - Fenestrated, Vulnerable to immune mediated injury
  • GBM - Synthesis from podocytes and endothelial cells, Mesangial cells playing a role in turnover
  • Podocyte - Proteins
  • Mesangial cells - Glomerular structural support, Embedded in GBM, Regulates blood flow of the glomerular capillaries
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8
Q

This barrier has three major components: what are they?

A

the fenestrated endothelial cell, the glomerular basement membrane (GBM), and the podocyte with their “slit diaphragms”

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9
Q

what are the main things patients present with with glomerular disease?

A

Haematuria and Proteinuria

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10
Q

Glomerulopathy:

•Blood and protein in varying amounts dictate:

  • Clinical _________
  • Suggests ______
  • However - Injury to one part of the GFB affects the other ________
  • Take home message - _________ signifies glomerular injury
A

presentation

diagnosis

components

Proteinuria

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11
Q

does haematuria and proteinuria indicate nephrotic or nephritic syndrome?

A
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12
Q

Acquired Glomerulopathy is common

what commonets are affected?

(Acquired more common than congenital in paediatrics)

A
  • Epithelial cell (podocyte) - Minimal Change Disease
  • Basement Membrane - Post Infectious Glomerulonephritis (PIGN)
  • Endothelial cell - PIGN, Haemolytic Uraemic Syndrome (HUS)
  • Mesangial cell - HSP / IgA nephropathy
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13
Q

Congenital Glomerulopathy is rare

what layers may be affected?

A
  • Podocyte cytoskeletal integrity - Congenital nephrotic syndrome
  • Basement membrane proteins - Alport syndrome (XL), Thin basement membrane disease (AD)
  • Endothelial/microvascular integrity - Complement regulatory proteins (MPGN)
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14
Q

Proteinuria - How much is too much?

A

Dipstix - Measures concentration, ≥ 3+ usually abnormal

Protein Creatinine Ratio (practical) - Early morning urine (best), normal: Pr:CR ratio <20mg/mmol, Nephrotic range: >250mg/mmol

24hr urine collection (gold standard) - normal <60mg/m²/24hrs, Nephrotic range>1g/m²/24hrs

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15
Q

What is Nephrotic Syndrome

A

Nephrotic range proteinuria = Hypoalbuminaemia = Oedema increasing 3rd space fluid volume

Nephrotic syndrome is a collection of symptoms due to kidney damage. This includes protein in the urine, low blood albumin levels, high blood lipids, and significant swelling

the low level of protein in the blood reduces the flow of water from body tissues back into the blood vessels, leading to swelling

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16
Q

how does proteinuria cause oedema?

A

Starling’s forces - Oncotic (Osmotic) vs. Hydrostatic - Protein (Osmotic) = “magnet to water”

no solutes or proteins in the vascular compartment to hold the water so the water moves to the interstitium resulting in peripheral oedema e.g. sweeling of feet

also causes decereased volume in circulation meaning decreased venous return to the heart meaning decereased in renal blood flow and then decreased in GFR

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17
Q

Nephrotic syndrome:

Diagnosis easy once you have clinical presentation

what would ou seen on presentation?

A
  • Oedema
  • Proteinuria

50% of children presenting with minimal change disease have microscopic haematuria

low albumin

Urine Na – 10mmol/l - if less then 20 then means your holding onto water

Serum creatinine will be in the normal range in uncomplicated nephrotic syndrome, such as that occurring in minimal-change nephropathy

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18
Q

What type of nephrotic syndrome are common at different age of presentation?

A

Minimal change is steroid sensitive but if steroid resistant then think about FSGS and MCGN

80% of children will have minimal change disease

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19
Q

Nephrotic Syndrome- MCD - what are the typical and atypical features?

A
  • Typical Features - Age 1 - 10 (2-5yrs most common age range), Normal blood pressure, No Frank haematuria, Normal renal function
  • Atypical features - Suggestions of autoimmune disease, Abnormal renal function, Steroid resistance

Only then consider renal biopsy

Clinical diagnosis

Don’t biopsy in MCD

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20
Q

what is Nephrotic syndrome Treatment?

A
  • If typical features
  • Prednisolone 8 weeks
  • Side effects from high dose glucocorticoids
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21
Q

More readily response to steroid, more likely you have ___

A

MCD

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22
Q

what is the outcome of nephrotic syndrome?

A
  • Remission - 95% in 2-4 weeks
  • Relapse - 80%
  • 80% long term remission
  • Don’t do harm before good! - Second line immunosuppression - Steroid dependant and frequent relapses (>4 relapses/year) – on steriods more than they arnt and that’s when you use second line therapies
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23
Q

Steroid Resistant Nephrotic Syndrome - whata re the causes?

A

•Acquired - Focal Segmental Glomeruloscerosis (FSGS) = Podocyte loss and Progressive inflammation and sclerosis

Acquired cause is more common

50% of children with FSGS will need renal replacement therapy in 5 years

•Congenital - Infant presentations, NPHS1 – nephrin , NPHS 2 – podocin, Podocyte loss

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24
Q
A
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25
Q

when do you investigate haematuria?

A
  • Macroscopic /Frank - Investigate
  • Microscopic – Dipstix adequate - Investigate if > trace on 2 occasions
  • Haemaglobinuria - stix positive + microscopy negative - Associated proteinuria = glomerular disease
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26
Q

whata re the cuases of haematuria?

A
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27
Q

what are the signs and symptoms of nephritic syndrome?

A
  • Haematuria and proteinuria
  • Reduced GFR:
  • Oliguria
  • Fluid overload - Raised JVP, oedema
  • Hypertension
  • Worsening renal failure = Rapidly Progressive GN

•Intrarenal cause of Acute kidney injury (AKI)

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28
Q

how is a diagnosis of nephritic syndrome made?

A

•Clinical diagnosis - describes glomerulonephritis

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29
Q

what is Acute Post-Infectious Glomerulonphritis?

A

Acute post streptococcal glomerulonephritis is an immunologic response of the kidney to infection, characterized by the sudden appearance of edema, hematuria, proteinuria and hypertension . It is essentially a disease of childhood that accounts for approximately 90% of renal disorders in children

PSGN is a kidney disease that can develop after infections caused by bacteria called group A Streptococcus (group A strep)

•Age of onset – 3-5 most common

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30
Q

what causes acute post infection glomerulonephritis?

A
  • Usually Group A Strep
  • Beta hemolytic
  • Site - throat 7-10 days, Skin 2-4 weeks
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31
Q

what is the pathogenesis of Acute Post-Infectious Glomerulonphritis?

A

Pathogenesis:

  1. Antigen “Mimicry”
  2. Ab-Ag complexes
32
Q

what is the treamtent of Acute Post-Infectious Glomerulonphritis?

A

Self limiting

Treatment is focused on relieving symptoms

  • Antibiotic (should be used to treat any bacterial infection)
  • Support renal functions - Electrolyte/acid base
  • Overload/hypertension - Diuretics (Blood pressure medications and diuretic medications may be needed to control swelling and high blood pressure)
  • Outcome (usually very good) - Not recurrent
33
Q

what is IgA Nephropathy?

A

a condition that damages the glomeruli inside your kidneys and can cause kidney disease

The immune response is what affects your kidneys

IgA nephropathy occurs when IgA protein gets stuck in kidneys causing inflammation. The inflammation causes your kidneys to leak blood and protein (usually immediately) and over the course of many years, your kidneys can lose function and lead to kidney failure

  • Most common glomerulonephritis
  • 1-2 days after URTI
  • Usually older children and adults
34
Q

what are the signs of IgA nephropathy?

A
  • Recurrent macroscopic haematuria
  • ± Chronic microscopic haematuria (between relapses)
  • Varying degree of proteinuria
35
Q

IgA nephropathy is a _______ diagnosis

A

clinical

  • Negative autoimmune workup
  • Normal compliment
  • Confirmation Biopsy
36
Q

what is the treatment of IgA nephropathy?

A
  • Mild disease - proteinuria with ACEi (These are blood pressure medications used to reduce protein loss and control blood pressure)
  • Moderate to Severe disease - immunosuppresion (KDIGO) (These medications are used to calm your immune system (your body’s defense system) and stop it from attacking your glomeruli)
37
Q

what is Henoch Schonlein Purpura IgA related vasculitis?

A
  • Age of onset : 5-15yrs
  • Clinical diagnosis
  • Mandatory palpable purpura
  • one of 4
  1. Abdominal pain
  2. Renal involvement
  3. Arthritis or arthralgia
  4. Biopsy - IgA depostition
38
Q

IgA Vasculitis- what causes it and how long does it last?

A
  • 1-3 days post trigger - Viral URTI in 70%, Streptococcus, drugs can trigger IgA
  • Duration of symptoms - 4-6 weeks, 1/3rd relapse
  • Nephritis - Mesangial cell injury
39
Q

what is the treatment of IgA Vasculitis?

A
  • Symptomatic - Joints, gut
  • Glucocorticoid therapy
  • Immmunosuppresion

The disease usually goes away on its own. However, your health care professional may suggest certain medicines to relieve symptoms such as abdominal pain, joint pain, and swelling. If your kidneys are involved, the treatment goal will be to prevent CKD

40
Q
A
41
Q

part 3

A
42
Q

what is Acute Kidney Injury (AKI)?

A
  • “abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes”
  • Anuria/oliguria (<0.5ml/kg/hr)
  • Hypertension with fluid overload
  • Rapid rise in plasma creatinine
43
Q

what is calssified as a AKI?

A
  • Serum creatinine: > 1.5x age specific reference creatinine (or previous baseline if known)
  • Urine output <0.5 ml/kg for > 8hours
  • Interpretation of AKI warning score:
  • AKI 1: Measured creatinine >1.5-2x reference creatinine/ULRI
  • AKI 2: Measured creatinine 2-3x reference creatinine/ULRI
  • AKI 3: Serum creatinine >3x reference creatinine/ULRI
44
Q

what is AKI management?

A
  • Prevention
  • 3 Ms
  • Monitor - Paediatric Early Warning Scores(BP) (Resp rate, Saturations, Heart rate, BP, Temperature), Urine Output, weight
  • Maintain - good hydration/electrolytes/acid - base
  • Minimise - Drugs (can cause further kidney injury)
45
Q

what are the 3 different classifications of causes of AKI?

A

Pre-renal, renal and post renal

46
Q

Causes of Acute Kidney injury - What are pre-renal causes?

A

•Perfusion problem

Volume depletion

Oedematous states

Hypotension

Renal hypoperfusion - Drugs, renal artery stenosis or occlusion, Hepato-renal syndrome

47
Q

Causes of Acute Kidney injury - what are intrinsic renal problems?

A
  • Glomerular disease - HUS, Glomerulonephritis
  • Tubular injury - acute tubular necrosis (ATN) due to Consequence of hypoperfusion andDrugs
  • Interstitial nephritis - NSAID, autoimmune
48
Q

Causes of Acute Kidney injury - what are post renal causes?

A

obstructive uropathies

49
Q

what is the defnition of Haemolytic Uraemic Syndrome?

A
50
Q

Haemolytic-Uraemic Syndrome - when does it occur?

A

•Typical HUS:

post diarrhoea - Entero-Haemorrhagic E.coli (EHEC)

  • Other causes - pneumococcal infection, drugs
  • Atypical HUS – pattern of haemolysis, thrombocytopenia and AKI and in absence of obvious cause then think of this, genetic system resulting in over activation of the alternative complement pathway
51
Q

how does HUS present?

A
  • E coli O157:H7 serotype
  • Period of risk of HUS:
  • Up to 14 days after onset of diarrhoea
  • 15% develop HUS

•Bloody diarrhoea is a medical emergency in children

52
Q

what is the triad seen in Haemolytic-Uraemic Syndrome?

A
  • Microangiopathic haemolytic anaemia
  • Thrombocytopenia
  • Acute Kidney Injury / Acute Renal Failure
53
Q

Management of bloody diarrhoea and HUS:

Prevention of oliguric HUS = ???

A

Prevention of oliguric HUS = intravascular volume expansion

54
Q

Once you have HUS, management is the same as all AKI

Haemolytic-Uraemic Syndrome - what are the 3 Ms

A

Monitor:

  • 5 kidney functions - Fluid balance - hypertension, Electrolytes, Acidosis, Waste, Hormones - hypertension
  • Aware of other organs

Maintain:

  • IV normal saline and fluid
  • Renal replacement therapy

Minimise:

•No antibiotics/NSAIDS

55
Q

what are the long term consequences of AKI?

(Applies for all causes of AKI)

A
  • Blood pressure
  • Proteinuria monitoring
  • Evolution to CKD
56
Q

Part 4

A
57
Q

what is CKD?

A
58
Q

Chronic Kidney Disease - what are the main causes?

A

Congenital Anomalies of the Kidney and Urinary Tract (CAKUT):

  • 55% of paediatric CKD
  • Reflux nephropathy
  • Dysplasia
  • Obstructive Uropathy (example - posterior urethral valves)

Hereditary conditions - 17% , Cystic kidney disease, Cystinosis

Glomerulonephritis - 10%

59
Q

Congenital Anomalies of the Kidney and Urinary Tract (CAKUT) may not be isolated, it may be syndromic

what are some examples?

A
  • Turner
  • Trisomy 21
  • Branchio-oto-renal
  • Prune Belly syndrome
60
Q

what ar ethe stages of CKD

A

<60 start to find signs and symptoms

61
Q

Presentation of CKD - the symptoms are variable depending what?

A

Symptoms variable depending which function affected

62
Q

what is the defnition of a UTI?

A
  • Clinical signs PLUS
  • Bacteria culture from midstream urine
  • Any growth on suprapubic aspiration or catheter
63
Q

Clinical Findings
upper vs lower tract

A

Principle:

  • younger the age more systemic symptoms
  • older the age more lower tract symptoms

Upper tract symptoms circled

64
Q

Obtaining Urine Specimen- how should it be done?

A
  • Normal social cleanliness - water
  • Clean catch urine or midstream urine
  • Sick infants - catheter samples or suprapubic aspiration (USS)
  • Acutely unwell - do not delay treatment
65
Q

how is a diagnosis of UTI made?

A
  • Dipstix - unreliable < 2 yrs of age
  • Microscopy - UTIs can be found by analyzing a urine sample. The urine is examined under a microscope for bacteria or white blood cells, which are signs of infection
  • Culture > 10<span>5</span> Colony forming units/ml
66
Q

So why worry about UTIs? :

What is Vescico-Ureteric Reflux?

A

VUR causes urine to flow back up through the urinary tract, often leading to urinary tract infections. VUR can cause urinary tract infections (UTI) and, less commonly, kidney damage

when the flow of urine goes the wrong way. This condition is more common among infants and young children

67
Q

what are the grades of VUR?

A
68
Q

What are we looking for?

A

Principles:

  • Congenital vs. acquired - Screening for children at risk of progressive scaring (Reflux nephropathy), Capture those with renal dysplasia
  • Urological abnormalities
  • Unstable bladder - Voiding dysfunction

Guidelines who to investigate - Upper tract symptoms, Younger, Recurrent

69
Q

what invesitgations can be done?

A
  • Ultrasound- structure
  • DMSA (isotope scan) - Scaring/function
  • Micturating cysto-urethrogram, MAG 3 scan -dynamic
70
Q

how do we treat UTI?

A
  • Lower tract - 3 days oral antibiotic
  • Upper tract/pyelonephritis - antibiotics for 7-10 days (Oral if systemically well), Role of prophylaxis ??
  • Prevention - Fluids, hygiene, constipation
  • Manage voiding dysfunction
71
Q

what are Factors affecting progression of CKD?

A

•Late referral

•Hypertension

•Proteinuria

  • High intake of protein, phosphate and salt
  • Bone health
  • Acidosis
  • Recurrent UTIs
72
Q

how can you measure blood pressure?

A
  • Gold standard - Sphigmanomter
  • Doppler (under age 5)
  • NEVER use cuff too small
  • White coat effect - 24 hour Ambulatory Blood Pressure
73
Q

Blood Pressure Chart:

Factors affecting BP = sex, age, height specific

what is the defnition fo hypertension?

A
  • 3 occasions
  • Hypertension: ≥95th percentile
  • Borderline ≥90 but <95th pc
74
Q

Management of CKD:

Variable depending on what?

A

which function affected

75
Q

Metabolic bone disease is a common complication of chronic kidney disease (CKD)

how is it caused?

A
  • Kidneys wee out phosphate
  • High phosphate = increase PTH

High PTH causes metabolic bone disease and cardiovascular disease

Kidneys activate Vitamin D3

  • Treatment Principles - Low phosphate diet, Phosphate binders, Active Vitamin D
  • If ongoing poor growth - Growth hormone
76
Q

what is the cardiovascular risk?

A
  • Accelerated atherosclerosis
  • Traditional risk factors PLUS Anaemia/metabolic bone disease (PTH)

(Traditional – hypertension, smoking, diabetes, dyslipidaemia, obesity)

77
Q

Take home messages:

  • Acute kidney injury predisposes to CKD
  • Proteinuria and hypertension - Result of and predictor of ongoing kidney injury, Manage 5 renal functions
  • UTI - Reflux nephropathy – reduce recurrent injury, Monitor for Upper tract symptoms/Younger/Recurrent UTIs, Limited place for prophylaxis
A

Year 3 - Paediatrics (40 decks)

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