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Medicine Year 3 > Week 14 - Renal > Flashcards

Week 14 - Renal Flashcards

1
Q

List the functions of the kidneys

A
  • Metabolic waste excretion e.g. urea/creatinine
  • Control of solutes and fluid status
    • Regulation of total body water
    • Regulation of body electrolytes
  • Blood pressure control
  • Acid/base
  • Drug metabolism/excretion
  • Endocrine functions
    • Production of renin
    • Production of EPO
  • Mineral metabolism
  • Glucose metabolism
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2
Q

Where are the glomeruli of the kidneys found?

A

Outer 1-2cm - cortex

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3
Q

What is the primary role of the kidneys?

A

Maintain fluid and electrolyte homeostasis in reponse to blood pressure and hormones

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4
Q

How can kidney function be measured?

A

Measure what is going out in the urine or what is left in the blood

  • Metabolic waste excretion - urea, creatinine
  • Control of solutes and fluid status - sodium, potassium, fluid
  • Endocrine functions - vitamin D, EPO, PTH
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5
Q

Describe the role of the glomeruli

A

Glomerular Filtration Barrier:

  • Blood in through afferent arteriole, out through efferent
  • Glomeruli filter plasma
    • Large molecules/cells/protein are retained in the glomerular tuft - pass out of the efferent arteriole without being filtered due to size and negative charge
    • Small molecules pass through the glomerular basement membrane into Bowman’s space
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6
Q

How is glomerular filtration rate controlled?

A
  • Blood flow
    • Angiotensin II - efferent arteriole vasoconstriction
    • Myogenic control
    • SNS - direct vasoconstriction
    • Reduced blood volume sensed by baroreceptor –> SNS/renin –> ADH/Ang II –> increased sodium reabsorption ‘distal sensing’
  • Intraglomerular pressure
  • Transmembrane pressure - filtration barrier
  • Oncotic pressure
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7
Q

Describe the structure of the glomerular basement membrane

A

Glomerular BM made up of podocyte foot processes and capillary fenestrated endothelium

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8
Q

Describe the movement of fluid through the renal tubules

A
  • Tubules adjust filtrate content, with collecting ducts absorbing water
  • 99% filtrate reabsorbed, small amount of secretion by tubules
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9
Q

Why are the kidneys so sensitive to hypoxia?

A

Very perfusion dependent - 20% of blood volume in kidneys at any one time

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10
Q

What measures of kidney function can be tested using dipstick urinalysis?

A

Blood, protein

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11
Q

Describe normal and abnormal proteinuria

A
  • Normal - less than 150mg protein/24 hours
    • Albumin 15%
    • Other proteins e.g. Tamm Horsfall, Immunoglobulin 85%
      • Tamm Horsfall secreted in tubules + minimal amounts of albumin
    • Glomerular filtration barrier prevents proteins being filtered into urine
  • Urinalysis detects albumin
    • Damage to glomerular filtration barrier - 70% of protein in urine is albumin
    • Should be negative in healthy
  • Dependent on concentration of urine
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12
Q

How can urinary protein excretion be measured?

A
  • 24 hours urine collection (grams/24 hours)
    • Inconvenient, inaccurate
  • Protein:creatinine ratio (PCR) on morning spot sample (mg/mmol)
    • Urine PCR 100 = 1g per day
  • Albumin:creatinine ratio (mg/mmol)
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13
Q

Why is quantification of proteinuria important?

A

Amount of protein lost in urine important for prognosis

  • Risk of declining kidney function increased w/ higher levels of proteinuria
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14
Q

Describe the types of haematuria

A
  • Can be blood detectable on dipstick (non-visible haematuria)
  • Visible haematuria
    • Can come from anywhere in the urinary tract (kidneys, stones, infection, malignancy, cysts, inflammation)
    • Unusual to have visible haematuria from glomeruli - usually further down urinary tract
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15
Q

What do U&Es measure?

A
  • Sodium
  • Potassium
  • Chloride
  • Urea
  • Creatinine
  • eGFR
  • +/- bicarbonate

Urea, creatinine and eGFR most important for kidney function

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16
Q

List the qualities of an ideal substance to measure kidney function

A
  • Freely filtered at glomerulus
  • Not secreted
  • Not reabsorbed
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17
Q

What is creatinine?

A

Creatine and phosphocreatine breakdown product - muscle breakdown

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18
Q

What impacts creatinine concentration?

A
  • Affected slightly by diet - red meat, supplements
  • Concentration affected by plasma volume
  • Up to 15% secreted by tubule
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19
Q

What can impact the concentration of urea?

A
  • Raised by
    • Diet - high protein
    • GI bleed
    • Tissue breakdown e.g. corticosteroid
    • Dehydration - passive reabsorption proximal tubule
  • Liver failure lowers urea
  • Up to 40% reabsorption
  • Less reliable marker for kidney function
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20
Q

Define renal clearance

A
  • Renal clearance of a substance = volume of plasma which would by cleared of the substance per unit of time
  • Usually expressed as ml/min
  • Usually described as Glomerular Filtration Rate (GFR)
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21
Q

How is eGFR calculated?

A

MDRD4 (modification of diet in renal disease 4) formula, based on

  • Plasma creatinine concentration
  • Age (adults only)
  • Gender
  • Race

Gives value expressed ml/min per 1.73m2 body surface area

Also CKD-EPI equation for patients with higher levels of eGFR

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22
Q

Why is eGFR sometimes misleading as a measure of kidney function?

A

eGFR dependent on muscle mass - more muscle mass higher serum creatinine

  • E.g. 20 y/o 90kg healthy male vs 80 y/o 50kg female w/ CKD
    • Both have same creatinine - man has much higher muscle mass, woman has low GFR
  • Have to lose 50% of GFR before creatinine increases - kidneys able to compensate
  • Normal for one patient may not be normal for another

eGFR assumes stable renal function

  • Not a valid measurement when kidney function changing rapidly
  • Plasma creatinine concentration could be100micromols/l but if the patient has no kidneys or is making no urine the GFR is actually 0
  • Important for drug dosing
  • eGFR not suitable in AKI
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23
Q

When is eGFR useful?

A

Staging of CKD

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24
Q

Describe the staging of CKD

A
  • Stage 1
    • eGFR >90
    • With another abnormality, otherwise regard as normal
  • Stage 2
    • eGFR 60-89
    • With another abnormality, otherwise regard as normal
  • Stage 3
    • eGFR 30-59
    • Moderate impairment
  • Stage 4
    • eGFR 15-29
    • Severe impairment
  • Stage 5
    • eGFR <15
    • Advanced renal failure

Abnormalities e.g. persistent proteinuria/haematuria, microalbuminuria in diabetes, structural kidney disease such as polycystic kidney disease in adults or reflux nephropathy

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25
Q

Define glomerulonephritis

A

Inflammatory diseases involving the glomerulus

  • Categorised by biopsy findings
  • Rare in the general population
  • Variable natural history and presentation
  • May be primary or secondary
  • Kidneys vulnerable to insult due to other disease (secondary)
  • Few specific treatments
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26
Q

How many patients w/ glomerulonephritis will require renal replacement therapy?

A

20% patients w/ glomerulonephritis reach end-stage renal failure (require transplant or life-long dialysis)

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27
Q

How should glomerulonephritis be approached?

A
  1. Presentation, history
  2. Kidney biopsy findings
  3. Likely cause and specific management
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28
Q

Which cells are the targets for injury in glomerulonephritis?

A
  • Mesangial - control matrix between capillaries
  • Endothelial cells of capillaries esp. in systemic disease
  • Podocytes - outside of glomerular BM, control size/charge selectivity of filtration barrier, damage = lots of protein in urine
  • Parietal epithelial cell - lines Bowman’s capsule
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29
Q

Describe the potential pathological mechanisms of glomerulonephritis

A
  • Antibodies, immune complexes, complement
    • Pre-formed antibodies travel to glomerulus and form complexes, deposited in kidney and cause damage or activate complement
  • Cell-mediated mechanisms e.g. cytokines, GFs, proteinuria
  • Metabolic (e.g. diabetes), genetic (e.g. some podocytopathies), vascular causes (e.g. hypertension)
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30
Q

List the potential secondary causes of glomerulonephritis

A
  • CV
    • Subacute bacterial endocarditis
  • Respiratory
    • Bronchiectasis
    • Lung cancer
    • TB
    • Pulmonary renal syndromes
  • Infectious diseases
    • Hepatitis
    • HIV
    • Chronic infections
    • Antibiotics
    • Malaria
  • Rheumatological
    • RA
    • Lupus
    • Amyloid
    • Connective tissue disease
  • Drugs
    • NSAIDs
    • Bisphosphonates
    • Heroin
  • Gastrointestinal
    • Alcoholic liver disease
    • IBD
    • Coeliac disease
  • Diabetes
  • Haematological
    • Myeloma
    • CLL
    • Polycythemia rubra vera
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31
Q

How should a patient be investigated for glomerulonephritis

A
  • Full medical and drug (including recreational) history
  • Basics - U&Es, dip urine for blood, quantify proteinuria, check albumin, check USS

Glomerulonephritis screen:

  • ANCA
  • Anti-GBM
  • ANA / dsDNA
  • Complement
  • Anti-PLA2R
  • Immunoglobulins
  • Rheumatoid factor
  • Virology – hep B, C, HIV
  • Others: Myeloma screen , HbA1c

Kidney biopsy - confirm diagnosis

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32
Q

How is a kidney biopsy carried out?

A
  • Done as outpatient day case, local anaesthetic
  • Ultrasound used to visualise kidneys
  • Few samples of cortex taken (glomeruli)
    • Only need to take samples from one kidney - glomerulonephritis will be present in both
    • Usually L kidney done - easier to reach
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33
Q

Why is kidney biopsy avoided where possible?

A
  • Main risk = bleeding (1% risk of significant bleed requiring transfusion/embolisation to stop)
    • Only done when other tests will not give diagnosis
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34
Q

How is a kidney biopsy used to give a diagnosis of glomerulonephritis?

A

Biopsy of kidney cortex examined under:

  • Light microscopy (glomerular and tubular structure)
  • Immunofluorescence (looking for Ig and complement)
  • Electron microscopy (glomerular basement membrane and deposits)
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35
Q

Descrive the histological appearance of FSGS

A

Sclerotic lesions, more pink

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36
Q

Describe the histological appearance of membranoproliferative glomerulonephritis

A

More purple (mesangial matrix) and mesangial cells (dark purple dots)

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37
Q

Describe the clinical presentation of glomerulonephritis

A

Disruption of glomerular filtration barrier - urine abnormal (blood, protein or both)

Main Presentations - Spectrum:

  • Incidental finding of urinary abnormalities +/- impaired kidney function
  • Visible haematuria
  • Synpharyngitic
    • Sore throat, urine looks like coke = classic IgA nephropathy
  • Nephritic syndrome
  • Nephrotic syndrome
  • Acutely unwell with rapidly progressive glomerulonephritis
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38
Q

Describe the features of nephrotic syndrome

A
  • 3.5g proteinuria per 24h (urine PCR >300)
  • Serum albumin <30
  • Oedema (retention of salt and water)
  • Hyperlipidaemia (serum cholesterol 15-20)
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39
Q

What are the risks associated with nephrotic syndrome?

A
  • Risk of venous thromboembolism
    • Lose anticoagulant clotting factors through damaged glomerular BM, procoagulant state
  • Increased risk of infection
    • Lose Igs through damaged glomerular BM, risk of infection
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40
Q

Describe the features of nephritic syndrome

A
  • Hypertension
  • Blood and protein in urine
    • Inflammation involving endothelium
    • Cola-coloured urine (haematuria)
  • Declining kidney function
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41
Q

List the causes of nephritic and nephrotic syndrome

A
  • Nephritic
    • Crescentic GN/vasculitis
    • Post-infectious
    • IgA nephropathy (usually nephritic)
  • Nephrotic
    • Minimal change nephropathy
    • Membraneous nephropathy

Other causes

  • Diabetic nephropathy
  • Lupus nephropathy
  • Membranoproliferative
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42
Q

Describe the spectrum of glomerular diseases

A
  • Nephrotic
    • Injury to podocytes
    • Changed architecture - scarring, depostion of matrix or other elements
    • Always proteinuria, sometimes haematuria
  • Nephritis
    • Inflammation
    • Reactive cell proliferation
    • Breaks in GBM
    • Crescent formation
    • Always haematuria, sometimes protein
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43
Q

What is the most common primary glomerular disease?

A

IgA nephropathy - up to 1% of the normal population

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44
Q

Describe the spectrum of disease in IgA nephropathy

A
  • Minor urinary abnormalities
  • Hypertension
  • Renal impairment and heavy proteinuria
  • Rapidly progressive glomerulonephritis
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45
Q

Give examples of secondary causes of IgA nephropathy

A
  • May be precipitated by infection - synpharyngitic
  • Secondary to Henoch-Schonlein Purpura, cirrhosis, coeliac disease
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46
Q

Describe the pathogenesis of IgA nephropathy

A
  • Abnormal/ over-production of IgA1, IgA I/C
  • Mesangial IgA, C3 deposition
  • Mesangial proliferation
  • Leads to
    • Haematuria
    • Hypertension
    • Proteinuria (varies with prognosis)

About 1/3 progress to ESRF

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47
Q

How is IgA nephropathy managed?

A
  • No specific therapy
  • Antihypertensive Rx, ACE inhibitors/ARB
    • Aim for BP <125/75
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48
Q

Which age group is usually affected by membraneous GN?

A

Adults

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49
Q

How does membraneous GN present?

A

Nephrotic syndrome – commonest primary cause, often chronic

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50
Q

What causes membraneous GN?

A
  • Usually idiopathic
  • 10% occur secondary to malignancy, CTD, drugs, diabetes, amyloid etc
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51
Q

Describe the pathology of membraneous GN

A
  • Anti-phospholipase A2 receptor antibody in 70% (receptors on podocytes)
  • Immune complexes in basement membrane/sub-epithelial space
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52
Q

Describe the natural history of membraneous GN

A

Variable

  • A third spontaneously remit
  • A third progress to ESRF over 1-2 years
  • A third persistent proteinuria, maintain GFR
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53
Q

What are the symptoms of membraneous GN?

A

Oedema, clots, fatigue

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54
Q

How is membraneous nephropathy treated?

A
  • Treat underlying disease if secondary
  • Supportive non-immunological – ACEi, statin, diuretics, salt restriction
    • Tight BP control v important
    • Diuretics/salt for symptomatic relief of oedema
  • Specific immunotherapy - if not improving
    • Steroids
    • Alkylating agents (cyclophosphamide)
    • Alternative agents – rituximab, anti-CD20 MAb
    • Cyclosporin
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55
Q

What are the potential outcomes of membraneous GN?

A
  • Complete remission
  • Partial remission
  • ESRD
  • Relapse
  • Death
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56
Q

Describe the prevalence of minimal change disease I

A
  • The commonest form of GN in children
  • 90% of GN < 10 years
  • 50% of older children
  • 20% of adults of all ages
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57
Q

How does minimal change disease present?

A
  • Nephrotic syndrome
  • Acute presentation - may follow URTI
  • GFR - normal, or reduced due to intravascular depletion
  • Very rarely causes renal failure
  • Relapsing course - 50% will relapse
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58
Q

What causes minimal change disease?

A

Idiopathic but may be secondary to malignancy

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59
Q

Describe the pathogenesis of minimal change disease

A
  • T cell and cytokine mediated
  • Target - glomerular epithelial cells, GBM change
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60
Q

Describe the appearance of the glomerulus on microscopy in minimal change disease

A

Glomerulus looks normal under light microscopy, can see pathology on electron microscopy

  • Fenestrated epithelium, podocytes w/ fingerlike processes = normal
  • Minimal change - podocytes fuse, can’t see individual spikes
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61
Q

How is minimal change disease treated?

A

High dose steroids - prednisolone 1mg/kg for up to 8 weeks

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62
Q

Describe the aetiology of primary nephrotic syndrome by age

A
  • Children - 90% minimal change
  • <45 - minimal change, membraneous GN, fibrillary
  • 45-65 - membraneous GN, minimal change, fibrillary
  • >65 - membraneous GN, fibrillary, minimal change/MCGN
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63
Q

What is FSGS?

A

FSGS = focal segmental glomerulosclerosis

  • Some glomeruli affected by a scarred lesion on part of the glomerulus
  • Idiopathic or systemic causes
  • Causes nephrotic syndrome
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64
Q

Describe the pathology of crescentic disease

A
  • Crescent shaped expansion of inflammatory cells, necrosis, ECM around glomerulus
  • Active proliferative disease
  • Crescents heal, whole glomerulus scleroses and dies
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65
Q

What is crescentic GN?

A
  • Group of conditions which demonstrate glomerular crescents on kidney biopsy
  • Aggressive disease – progress to ESRF
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66
Q

List the common causes of crescentic GN/rapidly progressive GN

A
  • ANCA vasculitis (MPO / PR3) - other pathological signs e.g. rash, red eyes
  • Goodpasture’s syndrome (anti-GBM - antibody formed to glomerular BM)
  • Lupus nephritis
  • Infection associated - usually staphylococcal or streptococcal
  • HSP nephritis - IgA vasculitis
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67
Q

What systemic complication is seen in ANCA vasculitis and Goodpasture’s syndrome?

A

Pulmonary haemorrhages

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68
Q

How can systemic diseases manifect in the kidneys?

A
  • Inability to clear waste products =
    • Acute kidney injury
    • Chronic kidney disease
    • inflammation
      • Blood - nephritic syndrome
  • Leakage of protein
    • >3g/day, fall in serum albumin = nephrotic syndrome
    • Less protein leakage = proteinuria
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69
Q

How is renal impairment due to systemic disease diagnosed?

A
  • Renal impairment - old or new?
    • Previous U&E
  • Proteinuria?
    • Urinalysis & quantitative proteinuria (uPCR)
  • Which is it?
    • AKI/CKD/nephritis/nephrotic syndrome/proteinuria
  • Clues to systemic disease?
    • History and examination
  • Other tests
    • Special antibodies, complement, eosinophils,
    • Imaging
    • rRenal biopsy
  • Non-invasive tests first
  • Invasive i.e. biopsy only if needed to make Dx and will change management - higher risk
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70
Q

Describe the impact of diabetes and the association with kidney disease

A
  • 3.5 million diabetics in UK - estimated 4-5 million by 2025
  • >270,000 in Scotland
  • UK cost - £1.5 million per hour, 10% of NHS budget
  • 90% type 2 diabetes
  • 30-40% of diabetics develop kidney problems
  • 26% of people starting RRT are diabetic - 28% Glasgow, 15% Inverness
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71
Q

How does diabetic nephropathy progress? How does this impact mortality?

A
  • No nephropathy - 1.4% mortality/year
  • Proteinuria (micro –> macroalbuminuria) - 4.6% mortality/year
  • Renal impairment - 19.2% mortality/year
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72
Q

How does diabetic nephropathy usually present?

A
  • Proteinuria is hallmark
  • Usually associated with retinopathy
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73
Q

Describe the pathogenesis of diabetic nephropathy

A
  1. Hyperglycaemia
  2. Volume expansion
  3. Intra-glomerular hypertension
  4. Hyperfiltration
  5. Proteinuria
  6. Hypertension and renal failure

Progresses over years

Creatinine can go down as develop hyperfiltration - sign kidney function will decline in future

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74
Q

Describe the structure changes which occur in the glomerulus in diabetic nephropathy

A
  • Thickening of the glomerular BM
  • Fusion of podocyte foot processes
  • Loss of podocytes w/ wearing away of the glomerular B<
  • Mesangial matrix expansion
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75
Q

Describe the histology of diabetic nephropathy

A
  • Pathognomic hyaline material containing nodules (excess mesangial matrix) in glomerular capillary loops
  • Pink nodules - Kimmelstiel-Wilson lesion
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76
Q

What kidney complications occur as diabetes progresses?

A

Anaemia, bone and mineral metabolism abnormalities, retinopathy, neuropathy

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77
Q

How can the risk of diabetic nephropathy be reduced?

A
  • Tight glycaemic control
    • Best OHA or insulin regimen
  • Good BP control - ACEi/ARB
    • Targets for diabetics lower than for general population
  • SGLT2 - inhibitors
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78
Q

Describe the mechanism of action of SGLT2 inhibitors

A
  • SGLT2 channel in renal tubules reabsorbs glucose and water
  • SGLT2 inhibitors block reabsorption - more glucose and water excreted - lowers BG
  • Potentially very useful before CKD develops
  • Main side effect is UTIs
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79
Q

Describe the cardiac/renal protection which SGLT2 inhibitors give

A

SGLT2 inhibition =

  • Glycosuria
    • Negative caloric balance –> reduced total body fat mass –> reduced epicardial fat (increased cardiac contractility) - less inflammation and fibrosis
    • Reduced HbA1c –> less inflammation and glucose toxicity + less atherosclerosis
    • Increased uricosuria –> decreased plasma uric acid –> less atherosclerosis
  • Natriuresis
    • Lowers BP –> less arterial stiffness
    • Reduced plasma volume –> less ventricular arrhythmias, less myocardial stretch
    • Tubuloglomerular feedback –> afferent arteriole constriction –> reduced intraglomerular hypertension, reduced hyperfiltration
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80
Q

How is renal artery stenosis diagnosed?

A
  • Clinical diagnosis
  • No angiogram/CT angiogram/MRI
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81
Q

Is angioplasty/stenting used in stenosed renal vessels?

A
  • Unlike narrowed coronary arteries, there is evidence that angioplasty/stenting is rarely effective in renal vessels
    • Causes subsequent problems w/ BP, recurrent renal stenosis
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82
Q

Describe the pathogenesis of renovascular disease

A
  1. Progressive narrowing of renal arteries with atheroma
  2. Perfusion falls by 20% - GFR falls but tissue oxygenation of cortex and medulla maintained
  3. RA stenosis progresses to 70%, cortical hypoxia causes microvascular damage and activation of inflammation and oxidative pathways
  4. Parenchymal inflammation and fibrosis progress and become irreversible, restoration of blood flow provides no benefit
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83
Q

How is renal artery stenosis managed?

A
  • Medical
    • BP control (not ACEi/ARB)
    • Statin
    • If diabetic, good glycaemic control
  • Lifestyle
    • Smoking cessation
    • Exercise
    • (Low sodium diet)
  • Angioplasty
    • Rapidly deteriorating renal failure
    • Uncontrolled ↑BP on multiple agents
    • Flash pulmonary oedema

Treat the underlying condition

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84
Q

What is amyloidosis?

A
  • Deposition of highly stable insoluble proteinous material in extracellular space (felt-like substance made of beta-pleated sheets)
    • Numerous H-bonds through peptide amide groups make them highly stable
  • Kidney, heart, liver, gut
  • Specific ultrastructural features (8-10nm fibrils)
  • High affinity for the constituents of the capillary wall
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85
Q

Describe the appearance of amyloidosis on microscopy

A
  • Light microscopy
    • Congo red stain - apple green birefringence
  • Electron microscopy
    • Amyloid fibrils 9-11nm cause mesangial expansion
  • First deposits in mesangium, anti-GBM and BVs
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86
Q

List the types of amyloidosis

A
  • AA = systemic amyloidosis (inflammation/infection)
    • From previous chronic pyrogenic or granulomatous infections e.g. TB, familial Mediterranean fever
  • AL = immunoglobulin fragments from haematological condition e.g. myeloma
    • Ig LC λ >κ (12:1 if renal impairment) 12ααs
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87
Q

How is amyloid treated?

A
  • AA amyloid - treat the underlying source of inflammation/infection
  • AL amyloid - treat the underlying haematological condition
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88
Q

Describe the pathogenesis of systemic lupus erythematosis

A
  • Auto-immune disease - immune complex mediated glomerular disease
    • Deposition of immune complexes
  • Multiple autoAbs – directed against DNA, histones, snRNPs, transcriptional/translational machinery
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89
Q

Describe the epidemiology of systemic lupus erythematosis

A
  • Epidemiology:
    • Female>>male (2-12:1)
    • African > Asian > Caucasian
    • 1 in 2500 women, 1 in 25000 men in UK
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90
Q

What causes SLE?

A

Genetic predisposition (12+ genes identified) and environmental trigger

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91
Q

Describe the pathophysiology of lupus nephritis

A
  1. Auto-antibodies produced against dsDNA or nucleosomes (anti-dsDNA, anti-histone)
  2. Form intravascular immune complexes or attach to GBM
  3. Activate complement (low C4)
  4. Renal damage
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92
Q

How is the diagnosis of lupus nephritis confirmed?

A

Renal biopsy - confirm diagnosis and stage disease

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93
Q

How is lupus nephritis treated?

A

Immunosuppression - Steroids, MMF, cyclophosphamide, rituximab

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94
Q

Describe the embryological development of the kidneys

A
  • Pronephros –> mesonephros –> metanephros
  • Nephrogenesis - commences week 10
    • 60% in 3rd Trimester
      • Premature - >30% nephrons may not have developed
    • No new nephrons after 36 weeks
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95
Q

Compare the renal function at birth to that of an adult

A
  • Nephrons
    • At birth: 300 000 to 1.8 million per kidney
    • Mean: 895 000
  • GFR :
    • Adult - 120mls/min/1.73m2
    • At birth: 40-65mls/min/1.73m2
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96
Q

How can paediatric renal function be investigated?

A
  • Antenatal US
  • Ultrasound
  • MCUG – Micturating Cystourethrogram
    • Need to catheterise, only done in children <1y/o
  • Nuclear Medicine
    • DMSA
    • MAG 3
  • CT - requires general anaesthetic in children (avoided)
  • MR
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97
Q

How prevalent are congenital anomalies of the kidney and urinary tract?

A
  • 20-30% of all anomalies in prenatal period
  • Incidence
    • 1 in 500 live births
    • 0.3-1.6 per 1000 live or still births
  • Non-renal anomalies seen in 30%
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98
Q

What percentage of congenital anomalies of the kidneys and urinary tract progress to CKD?

A

30-50% progress to chronic kidney disease needing RRT in children

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99
Q

List the types of congenital anomalies of kidney and urinary tract

A
  • Renal Dysplasia/Hypoplasia
  • Renal Agenesis
  • MCDK
  • Renal Cystic Dysplasia
  • Genetic Cystic Disease
  • Obstructive uropathy
  • Vesico-ureteric Reflux
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100
Q

What is renal agenesis?

A
  • Congenital absence of renal parenchymal tissue: metanephric stage
  • Associated with increased risk of other anomalies - structural, chromosomal
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101
Q

Compare unilateral and bilateral renal agenesis

A
  • Bilateral mostly sporadic, not compatible with life
  • Unilateral - 5% renal anomalies, prognosis - excellent
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102
Q

Are males or females more commonly affected by renal agenesis?

A

Male:female = 1.7:1

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103
Q

Define renal hypodysplasia

A
  • Renal Hypoplasia - reduction in number of nephrons but normal architecture
  • Renal Dysplasia - malformed renal tissue
  • Renal Hypodysplasia - congenitally small kidneys with dysplastic features
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104
Q

Describe the presentation of renal hypodysplasia

A
  • Antenatal - US growth
  • Neonate - lung issues, IUGR, acidosis, raised Cr
  • Children - FTT, anorexia, vomiting, proteinuria
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105
Q

How is renal hypodysplasia managed?

A

Supportive management

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106
Q

Describe the histological appearance of a hypodysplastic kidney

A

Large glomeruli with interstital fibrosis and foci of atrophic tubules

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107
Q

How is a multicystic dysplastic kidney detected?

A
  • Antenatal - US
  • Neonatal - abdominal mass
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108
Q

What percentage of multicystic dysplastic kidneys spontaneously involute?

A

35-65%

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109
Q

What risks are associated with a multicystic dysplastic kidney?

A
  • Hypertension
  • Malignancy - risk now same as general population
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110
Q

List the types of genetic cystic disease

A
  • Autosomal recessive polycystic kidney disease
  • Autosomal dominant polycystic kidney disease
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111
Q

Describe the clinical presentation of autosomal recessive polycystic kidney disease

A
  • Antenatal:
    • Antenatal US
    • Oligohydramnios
  • Infancy:
    • Large palpable renal mass
    • Respiratory distress
    • Renal failure - HT
    • Hyponatremia - urinary concentrating defect
  • Childhood:
    • Renal failure
    • HT
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112
Q

Describe the histopathology of autosomal recessive polycystic kidney disease

A

Cystic dilatations of the collecting tubules w/ flattening of the epithelium that runs perpendicular to the renal capsule

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113
Q

What anomalies are associated with autosomal recessive polycystic kidney disease?

A
  • Congenital Hepatic Fibrosis - subclinical to liver disease
    • Portal HT
    • Ascending cholangitis
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114
Q

Describe the prognosis of autosomal recessive polycystic kidney disease

A
  • 20-30% mortality in neonatal period
  • 5yr survival: 70-88%
  • Progression to ESRF over 50%, often >15yrs
  • 30-50% in 10yrs
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115
Q

Describe the incidence of autosomal dominant polycystic kidney disease

A

1 in 500-1000

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116
Q

Describe the genetic causes of autosomal dominant polycystic kidney disease

A
  • PKD1 mutation – cc 16: 85%, polycystin 1
  • PKD2 mutation – cc 4: 10-15%, polycystin 2
  • 5-10% new mutation
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117
Q

What is seen on ultrasound in autosomal dominant polycystic kidney disease?

A
  • Large echogenic kidneys
  • Macrocysts
    • Infancy - occasional
    • Older chold - multiple
  • Pathology
    • Cysts originating from tubules
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118
Q

Describe the clinical presentation of autosomal dominant polycystic kidney disease

A
  • Antenatal:
    • Antenatal US
  • Childhood:
    • Haematuria
    • HT
    • Flank pain
    • UTIs
    • Renal US - may be unilateral
  • Adult:
    • Majority of presentations
    • Renal US: often 2nd-3rd decade
    • HT
    • Haematuria
  • Family History
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119
Q

List the anomalies associated with autosomal dominant polycystic kidney disease

A
  • Mitral valve prolapse
  • Cerebral Aneurysm
  • AV malformation
  • Hepatic/pancreatic cysts
  • Colonic diverticula/hernia
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120
Q

How autosomal dominant polycystic kidney disease managed?

A
  • Supportive
  • Directed - Tolvaptan
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121
Q

Describe the prognosis of autosomal dominant polycystic kidney disease

A
  • Progression to ESRF in adulthood
  • 50% by 60 yrs
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122
Q

Are males or females more commonly affected by hydronephrosis?

A

Males:females = 2:1

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123
Q

What percentage of hydronephrosis is bilateral?

A

20-40%

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124
Q

What are the consequences of hydronephrosis?

A

Associated with renal injury and impairment

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125
Q

How can hydronephrosis be diagnosed antenatally/postnatally?

A
  • Antental - AP diameter, can be transient
  • Postnatal ultrasound - renal pelvic diameter >10mm
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126
Q

What can cause hydronephrosis?

A

Vesico-ureteric reflux

Obstruction of the urinary tract

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127
Q

Describe the levels of obstruction of the urinary tract

A
  • Pelvis/ureter - pelvic-ureteric junction
  • Ureter
  • Ureter/bladder - vesico-ureteric junction
  • Bladder
  • Urethra
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128
Q

Define urinary obstruction

A

Impedance to urinary flow which causes gradual/progressive change

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129
Q

How common is PUJ obstruction?

A

1 in 500 births

Males > females

Bilateral 10%

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130
Q

Define PUJ obstruction

A

Partial/total blockage of urine at ureter junction with kidney

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131
Q

How does PUJ obstruction present?

A
  • Antenatal diagnosis
  • Abdominal mass
  • UTI
  • Failure to thrive
  • Abdominal/flank pain
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132
Q

Define VUJ obstruction?

A
  • Functional/anatomical abnormality at vesico-ureteric junction
  • –> megaureter
    • Primary - reflux/obstruction
    • Secondary - bladder issues
  • Ureteric dilatation >7mm
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133
Q

Describe the prevalence of primary VUJ obstruction

A
  • 2nd most common neonatal hydronephrosis - 20%
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134
Q

Describe the incidence of obstruction of the posterior urethral valves

A
  • Most common obstructive uropathy
  • 1 in 4-8000 births
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135
Q

How does posterior urethral valve obstruction present?

A
  • Antenatal detection
  • Bilateral hydronephrosis
  • UTI
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136
Q

What investigations are done to diagnose posterior urethral valve obstruction?

A

US, MCUG

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137
Q

What are the complications associated with posterior urethral valve obstruction?

A

Risk of CKD, bladder dysfunction

Continence problems - catheterisation

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138
Q

Define vesico-ureteric reflux

A

Retrograde passage of urine from bladder into upper urinary tract

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139
Q

What are the complications associated with vesico-ureteric reflux?

A
  • UTIs leading to scarring
  • Hypertension
  • ESRF
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140
Q

How prevalent is vesico-ureteric reflux?

A

1% births

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141
Q

How is vesico-ureteric reflux diagnosed?

A

MCUG

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142
Q

How is vesico-ureteric reflux classified?

A
  • Grades I-V
  • V - into calyx, dilating ureter
  • Grades 1-3 usually resolve spontaneously
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143
Q

Describe the prevelance of UTIs in children

A
  • Prevalence <1-16% in under 2 yrs, 8% in older children
  • Girls> Boys – unless <3 months
  • Variable - age, gender, race, circumcision status
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144
Q

Define significant bacteriuria

A
  • >10^5 colony forming units/ml
  • Single pathogenic bacteria
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145
Q

How is urine collected from children?

A
  • Difficult in young children
    • Clean catch urine sample
    • Mid-stream sample of urine
    • Catheter specimen
    • Supra-pubic aspirate
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146
Q

What is the most common causative agents of UTIs in children?

A
  • E Coli (>80%)
  • Other organisms: Klebsiella/Pseudomonas
    • Associated w/ abnormalities in urinary tract
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147
Q

List the risk factors for UTIs in children

A
  • Age
  • Circumcision - unlikely to get UTIs
  • Urinary Obstruction
  • Vesico-ureteric Reflux
  • Bladder/bowel dysfunction
  • Catheterisation
  • Sexual activity
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148
Q

Describe the clinical presentation of UTIs in children

A
  • Upper Tract
    • Pyrexia (Rigors)
    • Vomiting
    • Systemic upset
    • Abdominal pain
  • Lower Tract
    • Dysuria
    • Frequency
    • Haematuria
    • Wetting
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149
Q

What investigations should be done to diagnose UTIs in children?

A
  • Urine dip + culture
  • Associated w/ underlying anomalies and can lead to scarring/HT/ESRF
    • Ultrasound
    • MCUG
    • Nuclear medicine
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150
Q

Define Von Hippel Lindau

A
  • Rare
  • Autosomal dominant
  • Multisystem - kidneys, pancreas and genital tract
  • Multiple cysts - benign w/ potential for malignant transformation (clear cell carcinoma)
  • Tumours tend to appear in early adulthood
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151
Q

Define tuberous sclerosis

A
  • Autosominal dominant
  • Multisystem, benign tumours - brain, kidneys, heart, eyes, skin
    • Kidneys - tumours called angiomyolipomas
  • Seizures, developmental delay
  • Risk of haemorrhage
  • Rarely progress to ESRD
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152
Q

Define medullary cystic disease

A
  • Autosomal dominant
  • Cystic in medulla not cortex
  • Tubulo-interstitial fibrosis
  • Small to normal sized kidneys
  • Usually results in ESRD
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153
Q

Compare the PKD1 and PKD2 mutations in adults polycystic kidney disease

A
  • PKD 1 gene mutation (chromosome 16) = 85% (1270 mutations). Typical rapid progression with ESRD < 50yrs
  • PKD 2 gene mutation (chromosome 4) = 15% (200 mutations). Slower progression, may never reach ESRD
  • 10-25% - no family history (new mutations)
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154
Q

How prevalent is adult polycystic kidney disease?

A
  • 10% RRT patients in UK
  • Prevalence 1/1000
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155
Q

How do the polycystin gene mutations cause adult polycystic kidney disease?

A
  • Genes code for polycystin 1 and 2
  • Polycystins are located in renal tubular epithelia
    • Membrane proteins - kidneys, brain, heart, bone, muscles, liver and pancreas ducts
  • Overexpressed in cyst cells
  • Membrane proteins involved in intracellular calcium regulation
  • Mechanism of cyst formation poorly understood
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156
Q

Describe the presentation of adult polycystic kidney disease

A
  • Presentation variable – incidental finding on USS, HTN, impaired renal function, loin pain, haematuria, mass on examination
  • Cysts gradually enlarge, normal kidney tissue replaced. Kidney volumes increased and eGFR falls
    • ESDR within 5-10 years
  • Cyst infection, cyst rupture, haematuria, pain
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157
Q

Describe the extra-renal manifestations of adult polycystic kidney disease

A
  • Intracranial aneurysms, arachnoid cysts
    • If FH - screened for aneurysm
  • Cardiac - HTN, LVH, valvular abnormalities
  • Hepatic and pancreatic cysts
  • Bronchiectasis
  • Diverticular disease, abdominal hernias
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158
Q

How is adult polycystic kidney disease diagnosed?

A
  • Ultrasound
  • Differentiate between ‘simple renal cysts’
    • Over 70y, 10% of patients will have cysts in both kidneys and 22% will have at least one kidney cyst
  • Family history – ultrasound at age 21 (if negative, should be repeated age 30 or will miss 14%)
    • Age 15-30 : 2 unilateral or bilateral cysts
    • Age 30-59: 2 cysts in each kidney
    • Over age 60: 4 cysts in each kidney
  • No family history: 10 or more cysts in both kidneys, renal enlargement, liver cysts
  • CT or MRI more sensitive
  • Genetic testing - only identifies 70% mutations
  • Not for screening, useful in abnormalities on US or in potential kidney donors
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159
Q

How is adult polycystic kidney disease managed?

A
  • Management is supportive
  • Early detection and management of blood pressure
    • High BP - renal function more likely to deteriorate faster
  • Treat complications
  • Manage extra-renal associations
  • Prepare for renal replacement therapy
  • Recent development
    • Tolvaptan - used for hypernatraemia
    • Suppresses effects of vasopressin - key in kidney cyst formation
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160
Q

Describe the use of tolvaptan in practice

A
  • Delay onset of RRT by around 4-5 years
  • Intensive monitoring – monthly LFTs for 18 months
  • Side effects of hepatotoxicity, hypernatraemia
  • Polyuric - 6-8L of urine per day, have to drink that amount
  • High rate of discontinuation in a 3 year trial (23% vs. 14%)
  • Expensive
  • Recommended for use by Scottish medicines consortium (SMC) for CKD3 and declining renal function
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161
Q

Describe the inheritance of Alport’s syndrome

A

Usually X-linked if inherited - affected or carrier

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162
Q

Describe the prevalence of Alport’s syndrome

A

Second most common inherited kidney disease (1/5000 prevalence)

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163
Q

Describe the mutation which causes Alport’s syndrome

A

Collagen 4 abnormalities- alpha 3 gene mutation, alpha 4 gene (COL3A4) mutation or alpha 5 (COL3A5) gene mutation

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164
Q

Describe the presentation of Alport’s syndrome

A
  • Deafness
    • Hearing normal at birth but develop high tone hearing loss
  • Renal failure
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165
Q

Describe the histological appearance of Alport’s syndrome

A
  • Collagen 4 deposition at basement membranes
  • Basement membrane thinning and thickening - abnormally split and laminated = basket weave appearance
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166
Q

Describe the clinical consequences of Alport’s syndrome

A
  • Microscopic haematuria, proteinuria and end stage renal failure (ESRF)
  • 90% on dialysis or transplant by age 40y, 50% by age 25y
  • Sensorineural hearing loss late childhood
  • Female Alport’s carriers – 12% ESRF by age 40y
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167
Q

Define Fabry’s disease

A
  • X-linked storage disorder
  • Alpha galactosidase A deficiency resulting in accumulation of globotriaosylceramide (Gb3)
168
Q

Describe the prevalence of Fabry’s disease

A

Rare 1/40,000

169
Q

Describe the pathogenesis of Fabry’s disease

A
  • Gb3 accumulates in glomeruli, particularly podocytes causing proteinuria and ESRF – average age of onset 34y
  • Also causes neuropathy, cardiac and skin features
170
Q

How is Fabry’s disease diagnosed?

A
  • Measure alpha-Gal A activity in leukocytes
  • Renal biopsy – inclusion bodies of G3b
171
Q

How is Fabry’s disease managed?

A

Enzyme replacement therapy

172
Q

Describe the appearance of IgA nephropathy on immunofluorescence

A

IgA deposits in mesangium

173
Q

Define Henoch-Scholein purpura

A
  • Often paediatric condition
  • Multisystemic vasculitis
  • Purpuric rash on buttocks and backs of legs
  • Immune reaction mediated by IgA causing deposition in blood vessels systemically
174
Q

What does a positive cANCA and high PR3 antibody level suggest?

A

ANCA associated vasculitis

= Granulomatosis with polyangiitis

175
Q

What can be seen on CXR in ANCA associated vasculitis?

A

Acute pulmonary haemorrhage

176
Q

What does a positive MPO suggest?

A

Eosinophilic granulomatosis with polyangiitis (Goodpasture’s syndrome)

177
Q

Describe the systemic effects of granulomatosis with polyangiitis

A
  • Oral cavity - ulcerations throughout oral mucosa
  • Lungs - cavities, bleeds, lung infiltrates
  • Skin - nodules on the elbow, purpura
  • Granulomas and patchy necrosis in blood vessels
  • Eye - pseudotumours, conjunctivities
  • Nose - stuffiness, noseblees, saddle nose
  • Heart - pericarditis
  • Kidneys - glomerulonephritis
  • Positive anti-neutrophil cytoplasm test
178
Q

Describe the mortality associated with AKI

A
  • Overall mortality for patients with AKI requiring dialysis is 20-30%
  • Additional mortality due to sepsis, bleeding, respiratory failure etc.
179
Q

Define AKI

A

UKRA guidelines - decline of renal excretory function over hours or days, recognised by the rise in serum urea and creatinine

180
Q
A
181
Q

How is the severity of AKI graded?

A

KDIGO

  • Stage 1: Serum creatinine ≥1.5 and < 2.0 times AKI baseline or >=26.0 µmol/l increase above AKI baseline
  • Stage 2: Serum creatinine >=2.0 and < 3.0 times AKI baseline
  • Stage 3: Serum creatinine 3.0 times AKI baseline or >=354 µmol/l increase above AKI baseline
182
Q

Define oliguric vs non-oliguric AKI

A
  • Oliguria -urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL or 500 mL per 24h in adults
  • Gives some clues with diagnosis
  • Non-oliguric easier to manage, both serious
183
Q

Describe AKI e-Alerts

A

Highlight AKI using lab algorithm - widely used

  • Calculated - not required knowledge
  • Serum creatinine >1.5 times higher than the median of all creatinine values 8-365 days ago
  • Serum creatinine >1.5 times higher than the lowest creatinine within 7 days
  • Serum creatinine >26 umol/L higher than the lowest creatinine within 48 hours
184
Q

How is AKI classified diagnostically?

A
  • Pre-renal - circulatory failure ‘shock’
  • Renal - cells of the kidney
  • Post-renal - obstruction
185
Q

List the pre-renal causes of AKI

A

Anything that impairs renal perfusion

  • Hypotension
  • Hypovolaemia (burns, diarrhoea, haemorrhage etc)
  • Hypoperfusion
  • hypoxia
  • Sepsis (vasodilation so effective perfusion ↓)
  • Drugs, toxins
186
Q

List the post-renal causes of AKI

A

Obstructive causes - anything between renal pelvis and urethral meatus which obstructs flow of urine

  • Calculi
  • Tumours (ureter, bladder, prostate, cervix, ovarian, can be extrinsic)
  • Lymph nodes (compression)
  • Prostate
187
Q

What are the most common post-renal causes of AKI in women and men?

A

Men - prostate

Women - gynaecological tumours

188
Q

List the most common causes of AKI

A
  • Acute tubular necrosis 80%
  • Obstructive 10%
  • Glomerulonephritis (primary and secondary) - 3%
  • Acute tubulointerstitial nephritis 2%
  • Vasculitis 1.5%
  • Atheroembolic 1%
  • Other 2.5%
189
Q

List the renal causes of AKI

A
  • Glomeruli (vasculitis) - glomerulonephritis, drugs (e.g. gentamicin)
  • Tubules - tubulo-interstitial nephritis, rhabdomyolysis
190
Q

Describe the impact of acute tubular necrosis on renal function

A
  • Usually reversible
  • 10-15% never recover renal function
  • Further 10-15% have chronic renal impairment
191
Q

What causes acute tubular necrosis?

A

Under perfusion of tubules and/or direct toxicity

  • Hypotension
  • Sepsis
  • Toxins

Or often, all three

192
Q

List the exogenous and endogenous toxins which can cause acute tubular necrosis

A
  • Exogenous
    • Drugs e.g. NSAIDs, gentamicin, ACE inhibitors
    • Contrast
    • Poisons e.g. metals, antifreeze
  • Endogenous
    • Myoglobin
    • Haemoglobin
    • Immunoglobulins
    • Calcium
    • Urate
193
Q

Describe the physiological response in glomerular filtration to decreased pressure

A

Prostaglandins dilate afferent arteriole to increase flow as MAP falls towards 80mmHg

194
Q

Describe the immediate assessment of AKI

A
  • Acute or chronic
  • Bloods - both urea and creatinine high
  • Potassium
  • Urine output (usually <400ml/day)
  • Clinical assessment of fluid status (BP, JVP, oedema, heart sounds)
  • Underlying diagnosis - history, examination, medications
195
Q

Describe the immediate treatment of AKI

A
  • Immediate
  • Airway and Breathing
  • Circulation – shock - restore renal perfusion
    • Hyperkalaemia
    • Pulmonary oedema
  • Remove causes
    • Drugs
    • Sepsis
  • Exclude obstruction & consider ‘renal’ causes
    • Are the pre-renal causes sufficient to account for AKI?
  • Ask for help: ICU or renal unit
196
Q

Describe the diagnostic process in AKI

A

Need for urgent action may take precedence over making final diagnosis

  • AKI or CKD?
  • History and exam e.g. septic, rashes, haemoptysis, rhabdomyolysis etc.
  • Drugs - prescribed, OTC, supplements, radio-contrast and abuse
  • Urinalysis
  • GN screen - ANCA, ANA, immunoglobulins + EP, complement, aGBM, urine Bence Jones protein
  • Others blood film, LDH, CK etc.
197
Q

How can obstruction be excluded in AKI?

A
  • Renal US
  • Also gives info on size (small in CKD)
  • Loss of corticomedullary differentiation suggests CKD
198
Q

What levels of serum potassium are considered clinically relevant?

A

K <6.0 - abnormal but no immediate concern

K 6.0-6.4 - risk of arrhythmia, needs treatment esp. if ECG changes

K >6.5 - medical emergency

199
Q

Describe the treatment of hyperkalaemia in AKI

A
  • Reduce absorption from gut – Calcium Resonium 15g 4x day orally (or enema), new drugs coming
  • Insulin 10-15units actrapid + 50ml 50% dextrose moves potassium into cells (watch BM)
  • Calcium gluconate 10ml 10% as cardiac membrane stabiliser
200
Q

How is acidosis treated in AKI?

A
  • If raised potassium and HCO3 <16 also worth bicarb supplementation
  • IV NaBicarb 1.26%
201
Q

What are the indications (absolute and relative) for dialysis in AKI?

A

Absolute Indications for Dialysis:

  • Refractory potassium >6.5 mmol/l
  • Refractory pulmonary oedema

Relative indications for Dialysis:

  • Acidosis (pH <7.1)
  • Uraemia (esp if urea >40)
  • Pericarditis, encephalopathy
  • Toxins (lithium, ethylene glycol etc.)
202
Q

Describe the outcomes in AKI

A
  • Dialysed for AKI- mortality 20-30% (often in ITU)
  • 85% return to baseline kidney function
  • 10% are left with some renal impairment
  • 5% do not recover kidney function i.e. need long term dialysis or transplant
203
Q

Describe the recovery of the kidneys from ATN

A
  • Often a polyureic phase for 48-72hr
  • May be up to 6l urine/day
  • Often subsequent low K, Ca, Mg as ‘low quality’ urine
  • Tubules fail to concentrate urine
204
Q

Define chronic kidney disease

A

CKD = kidney damage or GFR <60 ml/min per 1.73m2 for 3 months or more

205
Q

What are the problems with using serum creatinine to calculate eGFR?

A

Exponential relationship leads to:

  • Slow recognition of loss of the first 70% of renal function i.e. LAG TIME
  • Surprise at the sudden rise in creatinine with late renal referral

Effect of muscle mass leads to:

  • Overestimation of function in women
  • Overestimation of function in the elderly
  • Overestimation in other low muscle mass groups e.g. amputees, para/quadriplegics, rheumatoid arthritis
206
Q

List the problems with using eGFR as a measurement of kidney function

A
  • Only validated in whites and African-Americans
  • Mean age 50 - not validated in elderly
  • Values above 60ml/min not distinguishable so reported as eGFR >59ml/min
  • Drug dosing - doesn’t take weight into account
  • AKI - not valid
  • Pregnancy
207
Q

When can proteinuria be seen in a healthy patient?

A

After exercise, fever

208
Q

Describe normal ACR, PCR and albuminuria

A
  • Normal ACR <2.5
  • Normal PCR <20
  • Albuminuria ACR >30
  • ACR is about 2/3 of equivalent PCR result
    • E.g. ACR 70 = PCR 100 = 24h urine protein 1g
  • Nephrotic range proteinuria: PCR >300 (3g/24 hour)
  • If heavy albuminuria use PCR to follow progress
209
Q

List the signs and symptoms of advanced CKD

A
  • Symptoms:
    • Pruritus
    • Nausea, anorexia, weight loss
    • Fatigue
    • Leg swelling
    • Breathlessness
    • Nocturia
    • Joint/bone pain
    • Confusion
  • Signs:
    • Peripheral and pulmonary oedema
    • Pericardial rub
    • Rash/excoriation
    • Hypertension
    • Tachypnoea
    • Cachexia
    • Pallor &/or lemon yellow tinge
210
Q

Describe the general principles of CKD

A
  • Targeted screening for CKD
  • Interventions to slow the rate of progression of CKD and reduce cardiovascular risk
  • Medicines to replace impaired individual functions of the kidney
  • Advanced planning for future renal replacement therapy (RRT)
  • Renal replacement therapy
211
Q

How can you slow the rate of progression of CKD?

A
  • Aggressive BP control
  • Good diabetic control
  • Diet
  • Smoking cessation
  • Lowering cholesterol
  • Treat acidosis
212
Q

Which drugs should be used for BP control in CKD?

A
  • ACEI/ARB drugs of choice for hypertension in CKD if
    • All BP lowering will reduce rate of progression
  • Reduction in eGFR of up to 25% in first few weeks is good
  • Will get more of a reduction if critical reduced renal perfusion (volume depletion, sepsis, RAS)
213
Q

How is anaemia managed in CKD?

A
  • Replace iron, B12, folate first if low
  • ESA e.g. Darbepoetin alfa 30microg every 2 weeks
  • Trigger usually Hb <100g/l
  • Target Hb 100-120g/l.
  • Higher associated with adverse CV events
214
Q

Describe the pathophysiology of secondary hyperparathyroidism in CKD

A
  • CKD - low activated vitamin D, phosphate not excreted properly so high serum phosphate
  • Insoluble calcium phosphate forms and removes calcium from circulation
  • Leads to hypocalcaemia –> secondary hyperparathyroidism
  • Secondary hyperparathyroidism - muscle aching/weakness, bone pain
215
Q

How is metabolic bone disease in CKD treated?

A
  • Activated vitamin D - Alfacalcidol, start 0.25mcg
  • Occasionally Mg supplements
  • Phosphate binder - target phosphate 0.9-1.5 mmol/l
    • Calcium based - calcium carbonate/acetate
    • Non-calcium - sevelamer, lanthanum, aluminium
  • Calcimimetic - cinacalcet
  • Parathyroidectomy
216
Q

When should dialysis be started in CKD?

A
  • Individual approach based on symptoms
  • Most start with eGFR 6-8ml/min
  • No benefit to early start
  • Weight loss and persistent nausea
  • Persistent hyperkalaemia, acidosis, severe hyper-phosphataemia or pruritis
  • Problematic fluid overload
  • Best to have permanent access
217
Q

What are the indications to commence RRT?

A
  1. Medically resistant hyperkalaemia
  2. Medically resistant pulmonary oedema
  3. Medially resistant acidosis
  4. Uraemic pericarditis
  5. Uraemic encephalopathy

& specific drug overdoses

218
Q

Describe the symptoms of clinical uraemia

A
  • Anorexia
  • Vomiting
  • Itch
  • Restless legs
  • Weight loss
  • Metallic taste
219
Q

At what level of GFR should RRT be commenced?

A
  • No absolute rule
  • Generally eGFR between 5-10ml/min/1.73m2
  • Assessed on individual patient basis
220
Q

What are the options for RRT?

A
  • Haemodialysis
    • Hospital vs home
    • Daily vs nocturnal
  • Peritoneal dialysis
    • CAPD vs APD
    • Daily vs nocturnal
  • Renal transplant
    • Cadaveric vs living
    • Other - SPK, pre-emptive, altruistic
221
Q

Describe the aims of haemodialysis

A
  • Removal of solutes e.g. potassium, urea = diffusion
  • Removal of fluid ‘ultrafiltration’ - pressure = hydrostatic filtration
222
Q

Describe the process of haemodialysis

A
  • Blood out
  • Diffusion removes solutes
  • Filtration removes fluid
  • Dialysate discarded
  • Blood in
223
Q

Describe the options for haemodialysis

A
  • Tunnelled central venous catheter –> superior vena cava –> right atrium of heart
  • Arteriovenous fistula - graft between vein and artery
224
Q

How is haemodialysis carried out in practice?

A
  • Hospital or home based - hospital much more common
  • Standard - 4h, 3x per week
  • Multiple other options - mainly home based
    • 6h 3x per week
    • Short daily dialysis
    • Daily overnight
  • Home based treatment gives greater flexibility and empowerment but need carer, space and capital investment
225
Q

What are the complications of haemodialysis?

A
  • ‘Crash’ (acute hypotension)
  • Access problems
  • Cramps
  • Fatigue
  • Hypokalaemia
  • Blood loss
  • Dialysis disequilibrium
  • Air embolism
226
Q

Describe the process of peritoneal dialysis

A
  • 2-3L of dialysis fluid into abdomen
  • Waste products (urea, creatinine) diffuse across peritoneum from underlying blood vessels
  • 4-6 hours later fluid removed and replaced with fresh fluid
    • Fluid contains sodium chloride, lactate or bicarbonate and a high percentage of glucose to ensure hyperosmolarity - drives filtration of fluid by osmosis from peritoneal capillaries to peritoneal cavity (glucose into peritoneal capillaries)
227
Q

How is peritoneal dialysis carried out in practice?

A
  • Home-based therapy
  • Better with some residual renal function
  • Different glucose concentrations of dialysate to provide more or less ultrafiltration
  • Dialysate contains other electrolytes like in HD
  • Gradual treatment - no good for AKI
  • Simple procedure once taught
  • Maintain independence
228
Q

What are the complications of peritoneal dialysis?

A
  • Infection - peritonitis
  • Glucose load – development or worsening control of diabetes
  • Mechanical – hernia, diaphragmatic leak, dislodged catheter
  • Peritoneal membrane failure
  • Hypoalbuminaemia
  • Encapsulating peritoneal sclerosis
229
Q

Which patients are not suitable for peritoneal dialysis?

A
  • Grossly obese
  • Intra-abdominal adhesions
  • Frail
  • Home not suitable
230
Q

What are the options other than RRT in CKD?

A
  • Conservative care
    • Increasingly frail and elderly population
    • Survival may be better on RRT but quality of life may not
    • Symptom based management
231
Q

What considerations should be made when choosing the modality of RRT?

A
  • Lifestyle
  • Frailty
  • Vascular access
  • Time – travel to and from hospital
  • Carer
  • Physical – concurrent medical problems e.g. disseminated malignancy, severe dementia, severe psychiatric disease
232
Q

What problems in CKD are not helped by dialysis?

A
  • Anaemia
    • Need erythropoesis supplementing agents and iron
  • Renal bone disease
    • Need phosphate binders and vitamin D
  • Neuropathy
  • Endocrine disturbances

Dialysis only gives around 10ml/min eGFR - not as good as transplant

233
Q

How long do patients have to wait for cadaveric kidney transplants?

A
  • Cadaveric waiting list
    • Kidney after brainstem death
    • Kidney after cardiac death
  • Average wait 3 years
234
Q

Describe the pros and cons of kidney transplantation

A
  • Pros
    • No dialysis
    • Better level of renal function
    • Can live much more independently
    • Better life expectancy
    • Fertility better
  • Cons
    • Immunosuppressive medication for duration of transplant
    • Increased cardiovascular risk
    • Increased infection
    • Post transplant diabetes
    • Skin malignancies and others
235
Q

Define bacteriuria

A

Bacteria in urine

236
Q

Give examples of lower urinary tract infections

A

Cystitis

237
Q

Give examples of upper urinary tract infections

A

Pyelonephritis, renal abscess

238
Q

What is an uncomplicated vs complicated UTI?

A
  • Uncomplicated UTI
    • Lower UTI, normal structure & neurology
  • Complicated UTI
    • UUTI +/- systemic signs and symptoms
    • CAUTI - catheter associated urinary tract infection
239
Q

What is a relapsed UTI vs recurrent UTI

A

Relapse = infection w/ same organism

Recurrent = infection w/ same or different organism

240
Q

Define urosepsis

A

Complicated UTI

  • Temp >38
  • HR >90
  • RR >20
  • WBC >15.0 or <4.0
241
Q

Describe the prevalence of bacteruria and groups at high risk

A
  • Preschool age, girls > boys
  • Adults
    • Non-pregnant females, 1-3%
    • Males 0.1%
  • Other at risk groups
    • Hospitalised
    • Catheterised
    • Diabetics
    • Anatomical abnormalities
    • Pregnant
242
Q

How is bacteriuria managed?

A
  • Treat asymptomatic bacteriuria only in
    • Preschool children
    • Pregnancy
    • (Renal transplant)
    • (Immunocompromised)
  • Treatment in other asymptomatic not indicated
243
Q

Describe the types of urinary tract infections

A
  • Ascending
    • Urethral colonisation
    • F>M
    • Multiplication in bladder –> ureteric involvement
  • Descending/haematogenous
    • Blood-borne infections
    • Involvement of renal parenchyma
244
Q

Are urinary tract infections usually caused by a single organism or multiple?

A
  • >95% caused by single organism
  • Multiple organisms in
    • Long term catheters
    • Recurrent infection
    • Structural/ neurological abnormalities
245
Q

In which cases are multi-drug resistant organisms seen in UTIs?

A
  • Anatomical/neurological abnormalities
  • Frequent infections
  • Multiple antibiotic courses
  • Prophylactic antibiotic use

Increasing prevalence of carbapenem resistant organisms - ESBL, Amp C

246
Q

List the clinical features of urinary tract infections

A
  • Suprapubic discomfort
  • Dysuria
  • Urgency
  • Frequency
  • Cloudy, blood stained, smelly urine
  • Low-grade fever
  • Sepsis
  • Failure to thrive, jaundice in neonates
  • Abdominal pain and vomiting in children
  • Nocturia, incontinence, confusion in the elderly
247
Q

List the common organisms which cause urinary tract infections

A
  • Gram -ve bacilli
    • E coli
    • Klebsiella sp.
    • Proteus sp.
    • Pseudomonas sp.
  • Gram +ve bacteria
    • Streptococcus sp.
      • S agalactiae (group B strep)
    • Enterococcus sp.
    • Staphylococcus sp. - S saphrophyticus, S. aureus
  • Anaerobes
  • (Candida sp.)
248
Q

What investigations/treatment should be done in non-pregnant women with uncomplicated UTIs?

A
  • 1st presentation - culture not mandatory
    • Dipstick, high false positive rate
    • Check previous culture results
    • Antibiotic 3-7/7
  • No response to treatment
    • Urine culture
    • Change antibiotic
249
Q

How should children/men with uncomplicated UTIs be investigated/managed?

A
  • Send urine for culture every presentation
  • Treat appropriately
250
Q

How should an uncomplicated UTI in pregnancy be investigated/managed?

A
  • Common
  • Send urine sample w/ every presentation
  • Treat for 7-10 days
    • Amoxicillin and cefalexin relatively safe
    • Avoid trimethoprim in 1st trimester
    • Avoid nitrofurantoin near term
  • May need hospital admission for IV if severe
  • Can develop into pyelonephritis (30%)
251
Q

Define recurrent UTIs

A
  • >2 episodes in 6 months
  • >3 episodes/year
  • Mostly women
252
Q

How are recurrent UTIs investigated/managed?

A
  • Send urine sample w/ each episode
  • Urology investigation
  • Encourage hydration, urge initiated + post coital voiding
  • Intravaginal/oral oestrogen
  • Self administered single dose/short course therapy
  • Single dose post coital abx
  • Prophylactic antibiotics
    • If simple measures fail
    • Ideally 6 months
      • Trimethoprim
      • Nitrofurantoin
        • Associated risk w/ long term use
    • Development of antimicrobial resistance
253
Q

Describe catheter associated UTIs

A
  • Colonisation of catheters common - treatment not required
  • Hospital associated infection, 35%
    • Disturbance of flushing system
    • Colonisation of urinary catheter
    • Biofilm production by bacteria
  • Likely organisms
    • Patient’s flora
    • Healthcare environment
254
Q

What complications are associated with catheters?

A
  • CAUTI
  • Obstruction-hydronephrosis
  • Chronic renal inflammation
  • Urinary tract stones
  • Long term risk of bladder cancer
255
Q

How can catheter infections be prevented?

A
  • Catheterise only if necessary
  • Remove when no longer needed - ‘forgotten catheter’
  • Remove/replace if causing infection
  • Catheter care (bundles)
  • Hand hygiene
256
Q

How is CAUTI treated?

A
  • Check recent/previous microbiology
  • Start empirical antibiotics
  • Remove catheter if not needed
  • Replace catheter under antibiotic cover
    • Historically Gentamicin/Ciprofloxacin
      • Poor gram -ve cover
      • Increase in resistant GNB - treatment failure
  • May need broad spectrum
257
Q

What is acute pyelonephritis?

A
  • Upper UTI
  • Moderate –> severe
  • Ascending infection involving renal pelvis
  • Enlarged kidney w/ abscesses on surface
258
Q

How is acute pyelonephritis treated?

A
  • Check previous/recent microbiology results
  • Send urine +/- blood culture +/- imaging
  • Community - co-amoxiclav/ciprofloxacin/trimethoprim (NICE)
  • Options may be limited
    • Allergy
    • Drug interaction
    • Antimicrobial resistance
  • Hospital - often broad spectrum abx
  • May remain symptomatic for few days
  • No response warrants further investigation
  • Uncomplicated pyelonephritis, 7-14/7 antibiotic
  • Complicated pyelonephritis, >14/7 therapy
  • +/- radiological/surgical intervention
259
Q

What is the long term complication of acute pyelonephritis?

A

Renal abscess

260
Q

What is a renal abscess?

A
  • Complication of pyelonephritis
  • Similar symptoms to pyelonephritis
  • Usually positive urine and blood culture
261
Q

What is the likely causative organism in renal abscesses?

A

Gram negative bacilli

262
Q

What is the life threatening complication of a renal abscess?

A

Emphysematous pyelonephritis - need urgent urology review, high mortality rate

263
Q

What are the risk factors for a perinephric abscess?

A
  • Untreated LUTI, anatomical abnormalities
  • Renal calculi
  • Bacteraemia, haematogenous spread
264
Q

What are the common causative organisms of a perinephric abscess?

A
  • Gram negative bacilli - E. Coli, Proteus sp.
  • Gram positive cocci, S. Aureus, streptococci
  • Candida sp.
265
Q

What are the symptoms of a perinephric abscess?

A
  • Similar to pyelonephritis
  • Localised signs/symptoms
  • Usually positive blood cultures
  • Pyuria +/- bacterial growth
266
Q

How are perinephric abscesses managed?

A
  • Treat empirically as complicated UTI
  • Poor response to antibiotic therapy
  • Surgical management
267
Q

How should all patients be investigated in complicated UTIs?

A
  • FBC, U+Es, CRP
  • Urine sample
    • Urethral, CSU, Suprapubic, Nephrostomy
  • Blood culture if pyrexia or hypothermic
  • Renal ultrasound
  • CT KUB
  • Antibiotic therapy 14/7 or more
268
Q

How are urine microscopy results interpreted?

A
  • Epithelial cells, contamination
  • Bacteria with no WBC, contamination
  • Bacteria with WBC and no catheter, infection
  • Bacteria with WBC + catheter, assess clinically
  • Pyuria with no bacteria
    • Previous/recent antibiotic
    • Tumour
    • Calculi
    • Urethritis (check for Chlamydia)
    • Tuberculosis
269
Q

Describe the antibiotic guidelines for UTIs

A
  • Empirical cover
  • Check previous/recent microbiology
  • Check drug interaction and allergies
270
Q

Describe antibiotic treatment of an uncomplicated UTI

A

PO amoxicillin, trimethoprim, nitrofurantoin, pivmecillinam, fosfomycin (co-amoxiclav, ciprofloxacin, cefalexin)

271
Q

Describe antibiotic treatment of a complicated UTI

A
  • Usually IV
    • Amoxicillin/vancomycin
    • Gentamicin/Aztreonam/Temocillin
  • Many not be suitable for all patients
    • Resistant organisms, ESBL, Amp C producers
    • Contraindications e.g. renal failure
  • Drug monitoring may be needed e.g. Gentamicin
  • Different antibiotics have different activities
  • Do not omit an antibiotic without finding an alternative
272
Q

What are the problems caused by multi-drug resistant bacteria in UTIs?

A
  • Selection pressure of antibiotic use - development of resistant bacteria
  • Simple UTIs unmanageable in community
  • Out-Patient Parenteral Antimicrobial Therapy (OPAT)
  • For some patients, very little left
  • Hospital admission and risk of HAIs
  • Morbidity/mortality
  • Bed occupancy
  • Cost
273
Q

What causes acute bacterial prostatitis?

A
  • Usually spontaneous
  • May follow urethral instrumentation
274
Q

List the symptoms of acute bacterial prostatitis

A
  • Fever
  • Perineal/back pain
  • UTI
  • Urinary retention
  • Diffuse oedema
  • Microabscesses
275
Q

What are the likely causative organisms in acute bacterial peritonitis?

A
  • Gram negative bacilli, e.g. E.coli, Proteus sp.
  • S aureus (MSSA, MRSA)
  • N gonorrhoea (less common)
276
Q

What investigations should be done in acute bacterial prostatitis?

A
  • Urine culture, usually positive
  • Blood culture
  • Trans-rectal U/S
  • CT/ MRI
  • Obtaining prostatic secretions NOT advisable
277
Q

What are the complications of acute bacterial prostatitis?

A
  • Prostatic abscess
  • Spontaneous rupture
    • Urethra, rectum
  • Epididymitis
  • Pyelonephritis
  • Systemic sepsis
278
Q

Describe antibiotic management of acute bacterial prostatitis

A
  • Check recent/previous microbiology
  • Ciprofloxacin/ofloxacin (no streptococcus cover)
  • D/W microbiology in systemic infections
279
Q

What causes chronic prostatitis?

A
  • Rarely associated w/ acute prostatitis
  • May follow chlamydia urethritis
  • Recurrent UTIs
280
Q

List the symptoms of chronic prostatitis

A
  • Most asymptomatic
  • Perineal discomfort/back pain
  • +/- low grade fever
  • UTI symptoms
281
Q

What are the common causative organisms in chronic prostatitis?

A
  • Gram negative bacilli, e.g. E.coli, Proteus sp.
  • Enterococcus sp.
  • S aureus (MSAA, MRSA)
282
Q

What is epididymitis?

A

Inflammatory reaction of the epididymis

Relatively common

283
Q

Describe the aetiology of epididymitis

A
  • Ascending infection from urethra
  • Urethral instrumentation
284
Q

List the symptoms of epididimytis

A
  • Pain, fever, swelling, penile discharge
  • Symptoms of UTI/urethritis
285
Q

List the common causative organisms of epididimytis

A
  • GNB, enterococci, staphylococci
  • TB in high risk areas and individuals
  • In sexually active men
    • Rule out chlamydia and N gonorrhoea (urethritis)
286
Q

What is orchitis?

A

Inflammation of one or both testicles

287
Q

List the symptoms of orchitis

A
  • Testicular pain and swelling
  • Dysuria
  • Fever
  • Penile discharge
288
Q

Describe the aetiology of orchitis

A
  • Usually viral
    • Mumps
  • Bacterial
289
Q

What causes bacterial orchitis?

A
  • Complication of epididimytis
  • Rule out sexually transmitted bacteria
290
Q

How does bacterial orchitis present?

A

Acutely unwell

291
Q

How is bacterial orchitis managed?

A
  • IV antibiotics
    • As per complicated UTI
  • Urgent urological review
292
Q

What are the complications of bacterial orchitis?

A
  • Testicular infarction
  • Abscess formation
293
Q

What is Fournier’s gangrene?

A
  • Form of necrotising fasciitis affecting the genitals/perineal area
  • Rapid onset and spreading infection
  • Systemic sepsis
294
Q

What age group are most often affected by Fournier’s gangrene?

A

Usually >50 y/o

295
Q

List the risk factors for Fournier’s gangrene

A
  • UTI
  • Complications of IBD
  • Trauma
  • Recent surgery
296
Q

What pathogens commonly cause Fournier’s gangrene?

A

Mixed infections, mainly gram -ve bacteria and anaerobes

297
Q

What investigations should be done in Fournier’s gangrene?

A
  • Blood cultures
  • Urine
  • Tissue/pus - culture
298
Q

How is Fournier’s gangrene managed?

A
  • Surgical debridement 1st line
  • D/W microbiology
  • Broad spectrum/combination antibiotics initially
    • E.g. Pip-tazobactam + Gentamicin + Metronidazole +/- Clindamycin
299
Q

Describe the gross anatomy of the kidneys

A
  • Paired retroperitoneal organs
  • Located T12-L3
  • Right lower than L
  • Normally 10-12cm length, 5-7cm wide, 3cm thick
  • Gerota’s fascia covers - deficient inferiorly
  • Upper pole more posterior + medial, medial surface more anterior
300
Q

Describe the anatomy of the ureters

A
  • 25-30cm long, 4-5mm calibre
  • 3 segments
    • Proximal: PUJ-pelvic brim
    • Mid: segment over sacral bone
    • Distal: lower sacral border to UO
  • 4 layers – vary depending on site
    • Urothelial mucosa
    • Lamina propria
    • Muscular layer
    • Adventitial layer
301
Q

Where do the ureters narrow physiologically? Why is this clinically relevant?

A
  • Physiological narrowing
    • Pelvic ureteric junction (PUJ)
    • Crossing iliac at pelvic brim
    • Vesico-ureteric junction (VUJ)
  • Where calculi likely to obstruct - may limit flexi-regid ureteroscopies
302
Q

Describe the prevalence of kidney stones

A
  • 10% Caucasian men develop stone by 70 years
  • Prevalence increasing
  • Once a stone has formed 50% will form another within 10 years
303
Q

List the risk factors for kidney stones

A
  • Intrinsic factors
    • Sex - M:F 2:1 (closing)
      • M - higher oxalate production, F - higher urinary citrate
    • Age - peak 20-50 years
    • Family history
    • Comorbid conditions
  • Extrinsic factors
    • Fluid intake - <1200ml/day
    • Diet
    • Lifestyle - sedentary
    • Climate
    • Country of residence (USA highest - but we are catching up)
      • General high incidence in hot climates
304
Q

Describe the genetic risks for kidney stones

A
  • Uncommon in Blacks
  • More common in Caucasian, Asian
  • 25% family history
  • Familial renal tubular acidosis
  • Cystinuria
305
Q

What kind of diet predisposes to kidney stones?

A
  • High animal protein (high oxalate, low pH, low citrate)
  • High salt (hypercalciuria)
  • Low calcium diets
306
Q

Why is the composition of kidney stones clinically relevant?

A
  • If presenting in emergency doesn’t matter
  • Different types can be v hard or soft - may influence management
  • Most commonly calcium oxalate
    • If other type something more may need to be done e.g. cysteine likely to be genetic, urate can be managed w/ medication
  • ESWL unlikely to be successful for calcium oxalate dihydrate - v hard
  • Some types are radio-opaque and some aren’t
307
Q

List the most common types of kidney stones by composition

A
  • Calcium oxalte - 80-85%
  • Uric acid - 5-10%
  • Calcium phosphate and calcium oxalate - 10%
  • Pure calcium phosphate - rare
  • Struvite (infection stones), Mg, ammonium, phosphate - 2-20%
  • Cysteine - 1%
308
Q

Which kidney stones are radio-opaque?

A
  • Calcium oxalate, calcium phosphate, calcium oxalate - radio-opaque
  • Struvite, cysteine - relatively radiolucent
  • Uric acid - radiolucent
309
Q

Why do calcium oxalate kidney stones form?

A
  • Excess oxalate
  • Commonly found in some fruit, vegetables, nuts and chocolate
310
Q

What causes a struvite stone to form?

A
  • Caused by infection of urinary tract
  • Can grow quickly and become quite large
311
Q

Why do uric acid stones form?

A
  • Chronic dehydration
  • Risk increases in those with gout, a genetic tendency or a diet too high in protein
312
Q

Why do cysteine stones form?

A
  • Genetic condition - cysturia
    • Causes kidneys to excrete an excess of certain amino acids e.g. cysteine
313
Q

Why do xanthine stones form?

A
  • Enzyme deficiency - xanthine oxidase deficiency
  • Causes build up of xanthine deposits
314
Q

Why do silica stones form?

A
  • Rare, caused by certain medications or herbal supplements
315
Q

How do kidney stones form?

A
  • Under-saturated
  • Supersaturated but stable – metastable
  • Supersaturated with spontaneous precipitation – unstable
  • Saturation product – level at which no more solute will dissolve in a solution without change in pH, temp
  • Formation product – level at which spontaneous formation occurs
316
Q

List the factors that affect kidney stone formation

A
  • Low volume
  • Low pH (acidic)
  • Low citrate
  • Low magnesium
  • High uric acid
  • High calcium
  • High oxalate
317
Q

How do kidney stones present?

A
  • Incidental
    • Imaging for another reason
  • Pain
    • Colic, radiates from loin to groin, cannot settle, unable to stay still
  • Haematuria
    • Visible or non visible
  • Sepsis/infection
    • Unknown source until imaged
318
Q

What initial investigations should be done in kidney stones?

A
  • History and examination
  • Bloods
    • U&E, CRP, FBC
  • Urine
    • Non visible haematuria = 85%
  • Imaging
    • Gold standard = CT KUB (non contrast)
319
Q

Describe the biochemical tests which should be done following a patients first kidney stone

A
  • U&E
  • Calcium
  • Urate
  • Urine dip
  • MSSU
  • (Sodium nitroprusside – Cystine)
  • Stone analysis
320
Q

What biochemical tests should be done in recurrent kidney stones?

A
  • U&Es
  • Calcium
  • Urate
  • Venous bicarbonate
  • 24 hour urine analysis
321
Q

Why is CT KUB the gold standard for kidney stone imaging?

A
  • 94-100% sensitivity
  • 92-100% specificity
  • Other benefits
    • Stone diameter
    • Skin to stone distance
    • Hounsfield units
    • No contrast
    • Lower radiation dose
322
Q

How effective is ultrasound in imaging kidney stones?

A
  • 45% sensitivity
  • 88-94% specificity
323
Q

How effective is X-ray KUB for imaging kidney stones?

A
  • 44-77% sensitivity
  • 80-87% specificity
  • Better for follow up of known stone
324
Q

Describe the risk of radiation exposure in imaging

A
  • Annual background radiation 2-3mSV
  • Annual occupational limit 50mSV
  • Lifetime risk of fatal cancer 20%
  • Radiation dose 10mSV increases risk by 0.05% (1in 2000)
    • CXR - 0.02
    • XRAY KUB - 0.5
    • CT KUB - 4.7
325
Q

How are kidney stones managed medically?

A
  • Analgesia
  • NSAIDs or opiates?
    • NSAIDs reduce pain due to reduced glomerular filtration, renal pressure and ureteric peristalsis
  • Medical Expulsive Therapy
  • Lancet 2015 – multicentre, randomised, placebo controlled trial - no benefit from tamsulosin
326
Q

What are the surgical options for management of kidney stones?

A
  • Various options depending on location and size
  • Ureteroscopy and basket
  • Ureteroscopy and fragmentation
  • FURS – flexible ureteroscopy
  • ESWL – extracorporeal shockwave lithotripsy
  • PCNL – percutaneous nephrolithotomy
  • Emergency stent or nephrostomy
327
Q

When is admission required in kidney stones?

A
  • Uncontrollable pain
  • Fever or signs of sepsis
  • Solitary kidney with a ureteric stone
  • Bilateral ureteric stones
  • Renal failure caused by an obstructing stone
  • If discharging a patient be sure to give them clear worsening advice and when to come back to hospital
328
Q

Describe the emergency presentation of kidney stones with pain, what are the differential diagnoses for this pain?

A
  • Worst pain ever
    • Worse than labour
  • Typical loin pain which radiates to groin
    • Beware in male it can be testicular or penile pain
  • BEWARE AAA
  • Other differentials
    • Appendicitis
    • Gyn pathology
329
Q

What do we worry about in an emergency presentation of kidney stones?

A

Infected obstructed systems:

A patient with sepsis and obstructing stone is a urological emergency and must be seen and assessed urgently

330
Q

How should a patient with infected obstructed systems be managed?

A
  • Take full history and examine the patient
  • Is there any evidence of sepsis?
    • Implement “sepsis 6” protocol
    • Cultures and antibiotics
  • Check bloods for renal function and inflammatory markers
  • Urgent imaging – USS or CT
  • The patient may need urgent decompression of an obstructed infected collecting system by nephrostomy or ureteric stenting
331
Q

Describe the sepsis 6

A
  1. Give O2 to keep sats above 94%
  2. Take blood cultures
  3. Give IV antibiotics
  4. Give a fluid challenge
  5. Measure lactate
  6. Measure urine output
332
Q

Describe the presentation of elective stones

A
  • Pain
  • Recurrent urinary tract infections
  • Haematuria
  • Incidental finding on scan
  • AKI/CKD
333
Q

How can elective kidney stones be managed?

A

Various options depending on patient factors, patient choice, location and size, symptoms

  • Observation
  • Ureteroscopy and basket
  • Ureteroscopy and fragmentation
  • FURS – flexible ureteroscopy
  • ESWL – extracorporeal shockwave lithotripsy
  • PCNL – percutaneous nephrolithotomy
  • Emergency stent or nephrostomy
334
Q

What is ESWL? How is it used in the management of kidney stones?

A
  • Produces a shockwave
    • Electrohydraulic
    • Electromagnetic
    • Piezoelectric
  • Direct effect
    • Shearing
    • Spalling
  • Cavitation effect
    • Shockwave in fluid causes a microbubble
    • Dissolved gas in fluid around bubble expands into bubble
    • Bubble collapses
    • Microjets
    • Pit stone surface
335
Q

What are staghorn calculi? How are they treated?

A
  • Staghorn calculi refer to branched stones that fill all or part of the renal pelvis and branch into several or all of the calyces
  • They are most often composed of struvite (magnesium ammonium phosphate)
  • Percutaneous Nephrolithotomy (PCNL)
336
Q

How common are tumours of the urinary tract

A
  • Prostate, kidney, bladder - 3 of top 8 cancers
  • Prostate and renal cancer on the rise
  • Prostate cancer is most common cancer death in men
337
Q

What is the prostate cancer iceberg?

A
  • Symptomatic cases only a small proportion of the histological prevalence
    • Autopsy studies
    • Live long enough all will get - myth?
338
Q

Describe the epidemiology of prostate cancer

A
  • Commonest urological malignancy
  • 2nd commonest cause of male cancer death
    • Cancer specific 10 year survival is 84%
339
Q

Describe the incidence of prostate cancer

A
  • 1 in 6 UK males will be diagnosed with prostate cancer in their lifetime
  • 1 in 8 in 80 years probably over estimated, based on autopsy studies
340
Q

What are the risk factors for prostate cancer?

A
  • Age - 85% diagnosed in over 65 y/o
    • Microscopic foci 30% 50 y/o and 70% >80 y/o
  • Familial and genetic factors
    • 2x risk if 1st degree relative <60 y/o
    • 4x risk if two 1st degree relatives (any age)
    • BRCA2 gene mutations reported
    • PTEN and TP53 - TSGs
  • Environmental/occupation
    • Industrial chemicals e.g. cadmium
    • Working in nuclear power industry or exposed to high levels of UV light
  • Hormones
    • Normal function regulated by testosterone and DHT
    • Men castrated before puberty/those deficient in 5 alpha reductase (converts T –> DHT) almost never develop prostate cancer
  • Sexual behaviour - increased risk if sexually active at early age or history of STDs
  • Diet
    • Link between total fat consumption and prostate cancer deaths
    • High serum levels of alpha linolenic, palmitoleic and palmitic acid
  • Racial factors
    • African American 1.6x risk of white American
  • Geographic variations
    • Highest incidence in Westernised nations, least in Asia and Far East
    • US migrants from Japan and Asia 20x increase
341
Q

List the signs and symptoms of prostate cancer

A
  • Local (66%) and locally advanced (27%)
    • OFTEN ASYMPTOMATIC
    • Painful or slow micturition, Urinary retention (may cause anuria, uraemia), Urinary tract infection
    • Haematuria - blood in urine
    • Lymphoedema
  • Metastatic (7%)
    • Bone pain - most common symptom of metastases
    • Renal failure- ureteric obstruction
    • Weight loss, lethargy

Raised PSA level - on suspicion or screening

342
Q

List the methods of diagnosis/screening for prostate cancer

A
  • DRE - digital rectal examination
  • PSA - prostate-specific antigen
  • PIRADS - Prostate MRI
  • TRUS - guided needle biopsy
343
Q

Describe the pathology of prostate cancer

A
  • Adenocarcinoma
  • Usually arises in peripheral zone of prostate
  • Enlargement of prostate often due to BPH not cancer
344
Q

Describe the grading system for prostate cancer

A

Gleason grading stem - based on extent to which tumour cells are arranged into recognisable glandular structures, a spectrum of histological malignancies. Tumours given a score (Gleason Score)

  • Gleason score = sum of two most prominent Gleason grades seen histologically in a sample
    • <4 - well differentiated, 25% 10-year likelihood of local progression
    • 5-7 - moderately differentiated, 50% 10-year likelihood of local progression
    • >7 - poorly differentiated, 75% 10-year likelihood of local progression
345
Q

Describe the clinical use of prostate specific antigen

A
  • Serine protease (33kD) secreted into seminal fluid
  • Responsible for liquefaction of seminal coagulation
  • Small proportion leaks into circulation
  • Tissue not Tumour specific
    • Great tumour marker
    • Poor diagnostic test
  • Tends to rise with age
  • Depends on prostate size
  • Other influences e.g. inflammation, infection
346
Q

How is PSA measurement used clinically?

A
  • PSA measurements can provide information about prostate cancer from the initial screening and early detection through to the staging of the disease
  • Can also be used to monitor progression
347
Q

How is localised prostate cancer managed?

A
  • Watchful waiting
  • Active Surveillance
  • Radiotherapy (with or without LHRH analogue)
    • External beam
    • Brachytherapy
  • Radical prostatectomy
  • Cryotherapy/HIFU
  • TURP if symptomatic
348
Q

Why aren’t all patients with localised prostate cancer given treatment?

A
  • Need life expectancy of 10 years to benefit from treatment for localised prostate cancer
    • Many will die of other causes before prostate cancer kills them
349
Q

Describe the metastatic complications of prostate cancer. How are they managed?

A
  • Spinal cord compression
    • Urological emergency
    • Severe pain
    • Off legs
    • Retention
    • Constipation
    • Urgent MRI
    • Radiotherapy vs spinal decompression surgery
  • Ureteric obstruction
    • Anorexia, weight loss, raised creatinine
    • To nephrostomise or not and then to stent or not
    • Temporary measure will not improve cancer progression
350
Q

How is advanced prostate cancer treated?

A
  • Androgen ablation therapy - medical castration (LHRH analogue) or surgical castration (orchidectomy)
    • Good response in 70-80%, long term outcome less favourable as remission not usually maintained
    • Lowers testosterone by 95% (testicular), adrenal remains
    • LHRH analogues have largely replaced surgical castration
  • Chemotherapy
  • TURP for relief of symptoms
  • Radiotherapy
351
Q

Describe the hypothalamic-pituitary-testicular axis

A
  • LHRH secreted from hypothalamus, stimulates the pituitary to produce LH and FSH, stimulate the testes to secrete testosterone
  • ACTH released from pituitary gland after stimulation by CRH from hypothalamus, ACTH regulates secretion of adrenal androgens, some of which are converted to testosterone
352
Q

List the risk factors for bladder cancer

A
  • Age – rare <50yrs, most common 80th decade
  • Male > Female
  • Race- more common in Caucasians
  • Chronic inflammation- stones, infection (schistosomiasis), long term catheters
  • Drugs - cyclophosphamide, pioglitazone
  • Pelvic radiotherapy
  • Occupation
  • Smoking - accounts for 30-50% of bladder cancers, risk only returns to normal after smoking cessation of 20 years
353
Q

Which drugs increase the risk of bladder cancer?

A
  • Aromatic hydrocarbons - anilines
  • 25-45 year latency
  • 2-naphythlamine, 4-aminobiphenyl (4-ABP)
    • Liver metabolism but excreted in urine
  • E.g. pioglitazone, cyclophosphamide
354
Q

Describe the presentation of bladder cancer

A
  • Classically painless frank haematuria
  • 25% serious cause for this in over 65s
  • All should have cystoscopy and upper tract imaging
  • Some present with microscopic haematuria (5% serious causes)
355
Q

Describe the pathology of bladder cancer

A
  • Transitional cell carcinoma 90%
    • (Superficial 75% and invasive 25%)
  • Squamous carcinoma – 5%
  • Adenocarcinoma – 2%
  • Other secondaries
356
Q

Describe the staging of bladder cancer

A
  • Carcinoma in situ
  • Ta - mucosa
  • T1 - into lamina propria
  • T2 - into inner muscle layer
  • T3a - into outer muscle layer
  • T3b - through outer muscle layer
  • T4a - into prostate gland
  • T4b - into bony pelvis

Non-muscle invasive bladder cancer vs muscle invasive bladder cancer

357
Q

Describe the initial treatment of bladder cancer

A
  • Diagnosed at flexible cystoscopy
  • Urgent TURBT (trans-urethral resection of bladder tumour)
  • CT IVU (5% chance upper tract involvement)
  • Bimanual examination carried out at TURBT
358
Q

How is localised bladder cancer treated?

A
  • Cytoscopy and resection (TURBT) - to confirm presence of bladder cancer and see its location, number and extent
  • Non-muscle invasive
    • Tis - intravesical chemotherapy
    • Ta - intravesical chemotherapy or observation
    • T1
      • Low grade - intravesical chemotherapy
      • High grade - cystectomy
  • Muscle invasive
    • T2a/T2b
      • For cystectomy candidates - cystectomy +/- chemotherapy
      • For non-cystectomy candidates - radiotherapy +/- chemotherapy
359
Q

What chemotherapy is used in bladder cancer?

A
  • Mitomycin C
  • Once off or 6 week course
  • DNA synthesis
360
Q

Describe the immunotherapy used in bladder cancer

A
  • Immunotherapy
  • Induction and maintenance
  • Cell mediated immune response
361
Q

How is a radical cystectomy carried out?

A
  • Bladder and prostate/uterus removed
  • Urine diverted
  • Mortality 2%
  • Sometimes required after radiotherapy failure ‘salvage cystectomy’
362
Q

List the most common types of renal cancer

A
  • 85% renal cell carcinoma
  • Others
    • Transitional cell carcinoma
    • Sarcoma
    • Metastases
363
Q

Describe the epidemiology of renal cancer

A
  • Age peak 40-70 y/o
  • Male > females 2:1
364
Q

List the risk factors for renal cancer

A
  • Smoking (RR 1.4-3.0)
    • Causes chronic hypoxia and DNA damage secondary to benzo (alpha) pyrene diolepoxide (BPDE)
  • Obesity (RR 1.5-3.0)
  • Hypertension
  • Acquired renal cystic disease (RR 4)
  • Haemodialysis
  • Genetics- VHL (vhl), HPRCC (Met), HLRCC (FH), Birt-Hogg-Dube (FLNC), Tuberous sclerosis (TS)
    • VHL 3p penetrance 1 in 36000 - phaeochromocytoma, renal and pancreatic cysts, RCC, cerebellar hemangioblastoma
365
Q

How does renal cancer present?

A
  • 80% incidental
  • <25% systemic symptoms-
    • Night sweats, fever, fatigue, weight loss
  • 10% classic triad- mass, pain, haematuria
  • Varicocele
  • Lower limb oedema
  • Paraneoplastic syndromes
366
Q

Which paraneoplastic syndromes could renal cancer present with?

A
  • Polycythaemia (3-10%)
  • Hypercalcaemia (3-13%) - either from a PTH-like substance, or from osteolytic hypercalcaemia
  • Hypertension (up to 40%) renin secretion
  • Deranged LFT’s - Stauffer’s syndrome, from hepatotoxic tumour products
  • Rare:
    • ACTH (Cushing’s syndrome)
    • Enteroglucagon (protein enteropathy)
    • Prolactin (galactorrhoea)
    • Insulin (hypoglycaemia)
367
Q

How is renal cancer diagnosed?

A
  • Initial diagnosis:
    • Usually on USS
    • CT kidneys +/- MRI RV
    • Renal Biopsy
    • CT Chest
  • Histology:
    • Conventional or clear cell (80%)- vascular, granular and clear (lipids)
    • Papillary (10%)
    • Chromophobe (5%)- large polygonal

Collecting duct- rare

Medullary cell- rare

368
Q

Describe the staging of renal cancer

A
  • T1a <4cm
  • T1b 4-7cm
  • T2 >7cm
  • T3a into renal vein
  • T3b IVC below diaphragm
  • T3c IVC above diaphragm
  • T4 beyond Gerota’s and/or adrenal gland

Perioperative mortality 3% in I, 9% in II/IV

Downstaging of great surgical importance e.g. IV to III

369
Q

Describe the treatment of metastatic renal cancer

A

Tyrosine kinase inhibitors

370
Q

Describe the epidemiology of testicular cancer

A
  • Most Common solid cancer in men 20-45
  • Most curable cancer
  • Increasing Incidence
371
Q

List the risk factors for testicular cancer

A
  • Age 20-45y/o
  • Cryptorchidism
  • HIV
  • Caucasian population
372
Q

What investigations should be done in testicular cancer?

A
  • Scrotal ultrasound
  • Tumour markers:
    • Alpha-fetoprotein (50-70% Teratoms and Yolk Sac Tumours)
    • Beta hCG (40% Teratoma, 15% Seminoma)
    • LDH (10-20% Seminoma)
  • CT staging if advanced
373
Q

Describe the classification of testicular cancer

A
  • Germ cell tumours (most common)
    • Seminoma
    • Teratoma
    • Mixed
    • Yolk sac
  • Stromal tumours (10% malignant)
    • Leydig
    • Sertioli
  • Other
    • Lymphoma
    • Metastasis
374
Q

How is testicular cancer treated?

A
  • Radical Orchidectomy
  • Chemotherapy
  • Para-aortic nodal radiotherapy
  • Retroperitoneal Lymph Node Dissection
375
Q

Describe the prevalence of penile cancer

A
  • Rare (0.2% male cancers in the west)
  • Associated with HPV infection (16,18,21); smoking
  • Premalignant lesions: chronic changes
  • Even rarer in males circumcised at birth
376
Q

How is penile cancer treated?

A
  • Circumcision
  • Topical treatment CO2/5FU
  • Penectomy +/- reconstruction
  • Lymphadenectomy
  • Chemo-radiotherapy
377
Q

Where does a transplant kidney go?

A
  • Old kidneys left in the body
  • Donor kidney usually placed in the groin and attached to blood vessels and the bladder
  • Ureter carries urine from new kidney to the bladder
378
Q

How is kidney failure defined? What are the options in kidney failure?

A

When your kidneys have failed (eGFR 7-10ml/min) what are your options?

  • Dialysis
  • Transplantation
  • Conservative care
379
Q

What do patients dislike most about dialysis?

A
  • Always exhausted
  • Fluid restriction
  • Restricted diet - K+, PO4-
  • Women are infertile
  • Reduced life expectancy - I’m going to die soon
380
Q

What are the benefits of kidney transplant vs dialysis?

A
  • Increase life expectancy
  • Increase quality of life
    • Less time in hospital etc.
381
Q

Which patients are unsuitable for kidney transplant?

A
  • Reduced life expectancy
    • Older age
    • Co-morbidity
    • Unlikely to survive 5 yrs
  • Surgical contraindications
    • No bladder
    • Calcified BVs
  • Medical contraindications
    • Hypertension
    • Hypotension
    • Diseases that will recur in the transplant
382
Q

Which renal disease are treated in the dialysis clinic vs the transplant clinic?

A
  • Dialysis clinic
    • Renovascular disease
    • T2 diabetic nephropathy
    • Vasculitis
    • Obstructive uropathy
  • Transplant clinic
    • APKD
    • Glomerulonephritis
    • Reflux nephropathy
    • T1 diabetic nephropathy
383
Q

Where do transplant kidneys come from?

A
  • Deceased donors:
    • Brain stem death – heart beating/non-heart beating
    • No malignancy or unidentified/untreated infections
    • Good kidney function – you only get one kidney
    • Kidneys donated in any part of the UK are allocated to most appropriate patient in UK via NHS Blood & Transplant
    • Average waiting time 2-3 years
    • Around the world
  • Living donors:
    • Relative
    • Friend
    • Social media ‘friend’ - directed altruistic
    • Altruistic donor
384
Q

What are the advantages of living vs deceased kidney donation?

A
  • Pre-emptive transplantation
  • Better kidneys
  • Better outcomes - longer kidney survival
385
Q

What are the requirements for living kidney donation?

A
  • Donor
    • Fit and healthy
    • Excellent kidney function
    • Blood group and HLA compatible - or not
386
Q

Describe the financial indications for kidney transplant

A
  • Average costs England 2003 (NHS commissioning board 2013)
  • Transplantation
    • £17,000 for first year
    • £5,000 for every subsequent year
  • Dialysis - £30,800
387
Q

What is the challenge with kidney transplant?

A
  • Immune system
    • Recognised foreign cells and proteins
    • Responds to destroy foreign tissue through complex amplification pathways
    • Evolved to deal w/ infection and malignancy
  • Recognising cell surface proteins as ‘non-self’
  • Blood group incompatibility
  • HLA incompatibility
  • T cell mediated and antibody mediated rejection
388
Q

Describe the pathogenesis of immune rejection in a kidney transplant

A
  • Antigen presenting cell presents foriegn antigenic peptide from graft to T cell
  • Binds to T cell receptor and activates T cell
  • Cascade of events activating
    • T-helper cells
    • NK cells
    • Macrophages
    • B cells
    • Antibody production
  • = death of foriegn cell type
389
Q

How is graft rejection prevented in kidney transpants?

A
  • Immunosuppression
    • Galiximab – chimeric mouse-human monoclonal antibody directed against IL-2 receptor
    • Tacrolimus – calcineurin inhibitor
    • Mycophenolate mofetil - inhibitor of inosine-5’-monophosphate dehydrogenase - depletes guanosine nucleotides in T and B lymphocytes and inhibits proliferation
    • +/- Steroids
390
Q

List the complications of kidney transplantation

A
  1. Rejection
  2. Infection
  3. Malignancy
391
Q

Describe rejection in kidney transplantation

A
  • Cell-mediated rejection – interstitial inflammation and tubulitis
    • Often easily treated with steroids if caught early
  • Antibody-mediated rejection – endothelial swelling, glomerulitis and peri-tubular capillaritis
    • Donor specific antibodies
    • Often difficult to treat

Increase immunosuppression

392
Q

Describe infection in kidney transplant, how is it treated?

A
  • Common organisms in common sites
    • Chest infection Skin/wound infections
    • Urine infection
  • Re-activation infections
    • CMV disease – pneumonitis, colitis, hepatitis, renal disease
    • BK nephropathy
  • Uncommon organisms
    • Pneumocystis jjrovecii
  • Reduce immunosuppression
  • Treat with antibiotic/anti-viral
393
Q

Describe malignancy in kidney transplantation, how is it treated?

A
  • Kaposi sarcoma* (KS; SIR 61 and EAR 15)
  • Skin (nonmelanoma, nonepithelial SIR 13.9 and EAR 22)
  • Non-Hodgkin lymphoma (SIR 7.5 and EAR 168)
  • Lung (SIR 2.0 and EAR 85)
  • Kidney** (SIR 4.7 and EAR 76)
  • Colon and rectum (SIR 1.2 and EAR 15.8)
  • Pancreas (SIR 1.5 and EAR 6.4)
  • Hodgkin lymphoma (SIR 3.6 and EAR 7.9)
  • Melanoma (SIR 2.4 and EAR 29)

Reduce immunosuppression +/- rituximab or chemotherapy

394
Q

Describe the fluid compartments of the body

A
  • 2/3 of body weight fluid
  • 2/3 intracellular - harder to access
    • Potassium
  • 1/3 extracellular - more prone to fluctuation
    • Interstitium (30%) - sodium chloride
    • Plasma (7%)
395
Q

Describe the fluid distribution of a 75kg person

A
  • Intravascular 5L
  • Interstitial 10L
  • Intracellular 30L
396
Q

Describe the normal fluid intake and output

A
  • Normal intake
    • 20-30ml/kg/day water
    • If 75kg = 2L/day
    • 50kg = 1.5L/day
  • Normal output
    • Total losses approx. 2L/day
    • Urine losses 500-1500 mls/day
    • Insensible losses 500mls/day
397
Q

Describe the fluid input and output of a 70kg male

A
  • Input
    • Drinking - 1.5L
    • Food - 0.5L
    • Metabolic - 0.5L
    • Total = 2.5L
  • Output
    • Urine - 1.5L
    • Respiration - 0.4L
    • Sweating - 0.5L
    • Faeces - 0.1L
    • Total = 2.5L
398
Q

What can go wrong w/ fluid/electrolyte balance?

A
  • Imbalance between input and output/losses
    • Not able to eat or drink - drowsy/fasting/obstruction
    • Medicine - laxatives, diuretics
    • Excess losses - diarrhoea, vomiting, polyureic (e.g. diabetes insipidis), pyrexical
  • Redistribution of fluid
  • Osmolar problems
399
Q

How can imbalance between input and output of water occur?

A
  • Altered input
    • Inadequate hydration
    • Overhydration
  • Altered output
    • Excess losses
      • Vomiting
      • Diarrhoea
      • Stoma
      • Drains
      • Fever
      • Polyuria
    • Poor output
      • Oliguria
400
Q

Describe the electrolyte content of body fluids

A
  • Gastric
    • High chloride content - vomiting can result in hypochloraemia
  • Diarrhoea
    • High potassium content - can result in hypokalaemia
401
Q

What can cause redistribution of fluids?

A
  • Nephrotic syndrome
    • Patient hypoalbuminaemic - osmotic pressure in plasma lost, fluid into interstitium (extracellular or 3rd space)
402
Q

Describe the normal osmolarity of serum

A
  • Normal serum osmolarity is 280-300 mOsm/kg
  • This is a measure of the serum concentration of small diffusible ions, mainly Na, K, glucose and urea (sodium is most important)
  • Together these ions exert a ‘pressure’ which causes water to move across cell membranes from weaker to stronger solutions until the concentration of solutes is equal on both sides
403
Q

What is the clinical relevance of the osmolarity of body fluids?

A
  • Risk of cerebral oedema i.e. water from ECF –> ICF
  • In acute hyponatraemia or out of brain if sodium corrected too quickly
404
Q

What are the aims of fluid management?

A
  • Oral route is always best if possible - patient’s drink to thirst and fluid balance achieved naturally
    • If oral not available IV fluids

What are the aims of fluid management?

  • Maintenance –water and electrolytes
    • Daily fluid requirements + insensible loss
  • Replacement
    • To replace ongoing losses (vomit, diarrhoea, fistulae, stoma output etc.)
  • Resuscitation
    • To correct an intravascular or extracellular volume deficit
405
Q

What 5 questions should be asked before prescribing fluid?

A
  1. Is the patient dry, wet or euvolaemic?
  2. Does the patient need IV fluid?
  3. Why does the patient need IV fluid?
  4. How much fluid?
  5. What type of fluid?
406
Q

How can you assess volume status?

A
  • Fluid depletion
    • Relevant history - abnormal losses? Diuretic therapy?
    • Symptoms - thirst, dry mouth, dry skin, dark urine, postural dizziness
    • Signs - reduced skin turgor, dry mouth, dry axillae, CRT >2 secs, postural hypotension, tachycardia, tachypnoea
    • Laboratory tests - UEs (esp high urea)
    • Monitoring - BP + heart rate, response to fluid challenge, urine output, fluid balance, daily weight, CVP
  • Fluid overload
    • Relevant history - heart failure? Renal failure?
    • Symptoms - breathlessness, swollen ankles
    • Signs - hypertension, increased JVP, 3rd heart sound, pulmonary/peripheral oedema
    • Laboratory tests - serum albumin
407
Q

What are the NICE guidelines 5 R’s for fluid management?

A
  • Resuscitation
  • Routine maintenance
  • Replacement
  • Redistribution
  • Reassessment
408
Q

List the types of IV fluid

A
  • Crystalloids
  • Saline (various, 0.9% is standard)
    • Dextrose (various, 5% is standard)
    • “Balanced solutions” (eg Hartmann’s or Ringer’s lactate)
    • (Sodium bicarbonate (1.26%) – expert advice only)
  • Colloids
    • E.g. Gelofusion or starch-based fluid
    • Larger molecules - stay intravascular and restore circulation but studies show poorer outcomes, not used frequently
  • Blood products
    • Packed red cells
    • Platelets or fresh frozen plasma (clotting factors)
    • Human albumin solution
409
Q

Where does IV colloids, saline/Hartmann’s and Dextrose go?

A
  • Collid - stay intravascular
  • Saline/Hartmann’s - equilibriate between intravascular and interstitial compartments
  • Dextrose like giving water - moves intracellularly, not good for resuscitation (lost from interstitium and intravascular space)
410
Q

When is sodium bicarbonate used?

A

In renal failure

411
Q

What are the clinical signs of hypovalaemia (‘shock’)?

A
  • Hypotension (systolic BP <100 mmHg)
  • Tachycardia (HR >90 bpm)
  • Peripherally cool
  • Capillary refill time >2 secs
  • NEWS >5
  • Passive leg raising suggests fluid responsiveness
412
Q

Which IV fluids are used for resuscitation?

A

Fluid bolus, usually saline or Hartmann’s - stay extracellular

413
Q

How can the amount of fluid needed for routine maintenance be calculated?

A
  • Calculate requirements based on
    • Projected losses
    • Any intake e.g. IV drug volumes/NG feed
414
Q

When should you ask for seniour help when prescribing fluid for replacement/redistribution?

A
  • Any time you aren’t sure what to do.
  • Specific situations with complex fluid and electrolyte redistribution issues:
    • Gross oedema
    • Severe sepsis
      • Peripherally vasodilated - no amount of fluid will correct BP
    • Hyponatraemia/hypernatraemia - care not to correct too quickly
    • Renal, liver and/or cardiac impairment
    • Post-operative fluid retention and redistribution
    • Malnourishment/feeding issues
415
Q

Describe reassessment in fluid management

A
  • Daily UEs and fluid balance
  • Remember IV drugs contribute
  • Consider daily bicarbonate/magnesium if abnormal GI or renal losses
  • Review need for IV fluid daily, and adjust rate appropriately
    • Inappropriate IV fluid = IV access for prolonged time (risk of infection), fluid overload and electrolyte imbalances

Medicine Year 3 (15 decks)

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