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Urinary System > Acute And Chronic Kidney Disease > Flashcards

Acute And Chronic Kidney Disease Flashcards

1
Q

What is AKI?

A

Clinical syndrome
Abrupt decline in actual GFR (days to weeks)
Upset of ECF volume, electrolytes and acid-base balance
Accumulation of nitrogenous waste products

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2
Q

Why is AKI difficult to diagnose?

A

Doesn’t present with a specific identifiable symptom

Measurements are not massively accurate either

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3
Q

What happens to serum creatinine as kidneys decline?

A

Kidney decline leads to increased serum creatinine

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4
Q

How do we define AKI through measurements?

A

Increased serum creatine > 26.5 micromoles/L within 48 hrs
Increased serum creatinine > 1.5 x their baseline in 7 days
Urine volume <0.5 ml/kg/h for 6 hours

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5
Q

Describe the staging of AKI

A

1 - 3 in increasing severity
1 = 1.5 - 2 times their baseline
2 = 2 - 3 times their baseline
3 = > 3 times their baseline

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6
Q

What are the types of AKI?

A

Pre-renal
Intrinsic renal
Post-renal

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7
Q

What are the causes of pre-renal AKI?

A

Blood supply compromised
Volume depletion
Heart failure
Cirrhosis

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8
Q

Give some renal causes of AKI

A 
Renal artery/vein occlusion 
Glomerulonephritis 
Intrarenal vascular 
Ischaemic ATN
Toxic ATN 
Interstitial disease
Intrarenal disease 
Intrarenal obstruction
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9
Q

What does ATN stand for?

A

Acute tubular necrosis

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10
Q

What type of AKI are the vast majority?

A

Pre-renal

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11
Q

90% of intrinsic renal causes of AKI are due to …

A

ATN

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12
Q

Give some general causes of AKI

A 
Infective
Diarrhoea 
Obstetric illness
Venoms
Malaria 
Dyes
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13
Q

Describe how pre-renal problems cause AKI

A

Actual GFR reduced due to decreased renal blood flow
No cell drainage
Kidney works hard to restore blood flow
Increased reabsorption of salt and water (lots of aldosterone and ADH)
RAAS activated
Responds to fluid resuscitation

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14
Q

Describe autoregulation of the kidneys

A

Keeps the kidneys between a minimum and maximum BP over which they can maintain a normal perfusion pressure
When hypertensive, these values shift to higher BPs (reset)

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15
Q

What is the SM response to decreased renal perfusion?

A

Vasodilation of afferent

Vasoconstriction of efferent

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16
Q

Why do NSAIDs make AKI worse?

A

Inhibition of production of prostaglandins
Cannot vasodilate in the arterioles of kidneys when required
Cannot regulate perfusion pressure

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17
Q

Why can ACEi make AKI worse?

A

Cannot vasoconstrict when need to

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18
Q

Give some causes of reduced ECF volume

A 
Hypovolaemia 
Blood loss
Fluid loss
Sepsis 
Cirrhosis 
Anaphylaxis 
LV dysfunction 
Valve disease
Tamponade
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19
Q

Give some causes of impaired renal autoregulation

A 
Sepsis 
Hypercalcaemia 
Hepatorenal syndrome 
NSAIDs
ACEi
AngII antagonists
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20
Q

What are the causes of ATN?

A

Ischaemia
Nephrotoxins
Sepsis

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21
Q

Why is ATN a misnomer?

A

As there is generally no tubular necrosis

But cells are damaged

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22
Q

Describe ATN

A

Damaged cells cannot reabsorbed salt and water efficiently
Or expel excess water
Aggressive fluid resuscitation risks fluid overload
Lost the ability to concentrate urine therefore urine comes out at the same rate no matter the volume of ECF

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23
Q

If dialysis is required, does the mortality of AKI increased or decreased?

A

Mortality increases

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24
Q

Which parts of the nephron are most susceptible to hypoxia?

A

S3 of PCT

Thick ascending limb LOH

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25
Q

Describe damage in the kidneys due to nephrotoxins

A

Damage the epithelial cells lining the tubules and cause cell death and shedding into the lumen
Can be endogenous or exogenous
ATN more likely if reduced perfusion and a nephrotoxin

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26
Q

Give examples of endogenous nephrotoxins

A

Myoglobin
Urate
Bilirubin

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27
Q

In which treatment does urate build up?

A

Chemotherapy

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28
Q

Give some examples of exogenous nephrotoxins

A

Bacteria endotoxins
Xray contrast
Drugs (ACEi, aminoglycosides, NSAIDs)
Poisons (weedkillers, antifreeze)

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29
Q

How does rhabdomylosis cause ATN?

A

Muscular necrosis releases myoglobin ‘crush injury’
In wars and natural disasters
Can occur in drug users and elderly when cannot move
Myoglobin is toxic to tubule cells and can also cause obstruction

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30
Q

Describe acute glomerulonephritis

A

Immune disease affecting the glomeruli

Can be primary or secondary

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31
Q

Give 2 types of rapidly progressing glomerulonephritis

A

Granulomatosis with polyangiitis

Crescenteric necrotising glomerulonephritis

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32
Q

Describe acute tubulo-interstitial nephritis

A

Caused by infection or toxins

Massive inflammatory infiltrate (lymphocytes)

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33
Q

What percentage of AKIs are post-renal causes?

A

5-10%

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34
Q

What is the general mechanism for post-renal AKI?

A

Obstruction most block both kidneys or a single functioning kidney
Rise in intraluminal pressure
Dilation of renal pelvis
Decrease in renal function

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35
Q

Give some causes of post-renal AKI

A

Within lumen - stones, clots
Within wall - strictures (eg. Post-TB)
Pressure from outside - BPH, tumour, aortic aneurysm

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36
Q

Describe the serum changes common to all AKIs

A

Increased urea

Increased creatinine

37
Q

What are the ECG changes of hyperkalaemia?

A 
Tall T waves
Small/absent P waves
Increased P-R interval 
Wide QRS 
Sine wave pattern 
Asystole
38
Q

What do we check to see if the patient is volume depleted?

A 
Cool peripheries 
Increased pulse
Decreased BP 
Postural hypotension 
Low JVP 
Reduced skin turgor
39
Q

What do we assess when looking for fluid overload?

A 
Gallop rhythm 
Increased BP 
Raised JVP 
Pulmonary oedema 
Peripheral oedema
40
Q

Describe the Hx of a patient will post-renal AKI

A 
Anuria 
A single functioning kidney 
Loin/supra-pubic pain 
Hx of stones
Hx of prostration or previous pelvic/abdo surgery
41
Q

What should we examine for in post-renal AKI?

A

Palpable bladder
Pelvic/abdo masses
Enlarged prostate
(Blocked catheter)

42
Q

What is essential to do for every patient with AKI?

A

Urinanalysis

Blood, protein, leukocytes

43
Q

What features of a urinanalysis of AKI when suggest intrinsic renal disease?

A

Blood and/or protein

44
Q

How do we image AKI?

A

Ultrasound scan - obstruction

CXR - fluid overload, infection

45
Q

Name some preventative methods for AKI

A 
Identify risk factors 
Monitor at risk patients 
Ensure adequately hydrated 
Avoid nephrotoxins
Detect early and identify cause
46
Q

Give some of the susceptibilities for AKI

A 
Increased age 
CKD
Heart disease
Liver disease 
Diabetes mellitus 
Neurological impairment 
Cancer
Previous AKI
47
Q

Give some exposure risk factors for AKI

A 
Dehydration/volume depletion
Sepsis 
Critical illness 
Burns/trauma 
Cardiac surgery 
Emergency surgery 
Nephrotoxins 
Contrast
48
Q

What is the management for AKI?

A

Treat fluid overload - restrict Na+ and water
Treat hyperkalaemia with calcium gluconate, restriction of dietary K+, stop K+ sparing diuretics, ACEi etc, give dextrose and insulin, sodium bicarbonate
Treat acidosis - protein restrict, sodium bicarbonate

49
Q

What are the indications that an AKI patient needs dialysis?

A 
Increased K+
Metabolic acidosis 
Fluid overload 
(All not responding to normal treatment) 
Presence of dialysable nephrotoxin 
Signs of uraemia
50
Q

What is the prognosis for uncomplicated ATN?

A

Recovery in 2-3 weeks if no extra insults

51
Q

What is the overall AKI mortality?

A

24%

52
Q

What is the normal GFR range?

A

90 - 120 ml/min

53
Q

How many nephrons do we have and how many do we need to survive?

A

2 million

Need 40,000 approx (2%) to survive

54
Q

What is chronic kidney disease?

A

Long term condition
Abnormal kidney function and/or structure
The irreversible and sometimes progressive loss of renal function over a period of months to years

55
Q

What is the commonest cause of CKD?

A

Unknown

56
Q

Name some causes of CKD

A 
Unknown 
Immunological - glomerulonephritis 
Infection - pyelonephritis 
Genetic - PCK, Alport
Obstruction and reflux nephropathy 
Hypertension 
Vascular 
Systemic disease - diabetes, myeloma
57
Q

What is the common end point for the kidneys of many CKDs?

A

Small, shrunken kidney
With irregular outline
Lots of fibrous scarring

58
Q

Who should be screened by CKD?

A

Diabetes
Hypertension
Ischaemic heart disease

59
Q

Who is CKD more common in?

A

Elderly
Ethnic minorities
Multi-morbid people
Socially disadvantaged

60
Q

What is CKD classification based on?

A

GFR

61
Q

Describe the stages of CKD

A 
G1  >90
G2  60-89
G3a 45-59
G3b 30-44
G4  15-29 
G4  < 15
62
Q

Which measures of GFR are not very accurate?

A

> 60 GFR

63
Q

Other than GFR, what other measurement can we look at?

A

ACR
Albumin:creatinine ratio
Higher it gets = worsened condition

64
Q

What are the stages of ACR?

A

A1 < 3
A2 3 - 30
A3 > 30

65
Q

What percentage of the adult population have CKD 3 or worse?

A

Approx 7%

66
Q

Risk of death starts to increase when kidney function has declined by what percentage?

A

25%

Even though no symptoms

67
Q

What indicators what make us check kidney function?

A

High BP
Proteinuria
Haematuria

68
Q

Proteinuria and CKD together increase the risk of …

A

Death by cardiovascular disease

More likely to need dialysis

69
Q

What is the normal serum creatinine?

A

80 - 120 micromoles/L

70
Q

What clearance markers can we use to represent eGFR?

A

Creatinine
Inulin
Cr EDTA
Iohexol

71
Q

What are the problems with using clearance markers to estimate GFR?

A

Expensive
Require hospital stays
Collecting urine has bad compliance

72
Q

Is the relationship between serum creatinine and GFR linear?

A

No

73
Q

How much of your renal function can you lose before serum creatinine will change?

A

~ 60%

74
Q

Creatinine concentration in serum is determined by:

A 
Renal function 
Muscle mass (age, sex, race, exercise)
75
Q

Why can’t we use eGFR in AKI?

A

Can only use the eGFR formula if GFR is relatively stable

76
Q

What can we look for in blood to indicate the cause of CKD?

A 
Autoantibody screen
Complement 
Immunoglobulin
ANCA
CRP 
SPEP/UPEP
77
Q

Describe polycystic kidneys

A

Autosomal dominant
Can become very large
Have CKD from the day they are born by definition but usually an issue until later in life

78
Q

Acidosis can affect which organs?

A

Muscles
Bones
Renal function decline further

79
Q

Acidosis is not a problem until GFR is …

A

< 25

80
Q

How does CKD lead to anaemia?

A

Decreased production of EPO
Increased resistance to EPO (uraemic environment)
Reduced RBC lifespan

81
Q

How do we treat anaemia from CKD?

A

Give EPO subcutaneous injections

82
Q

How can CKD cause mineral and bone disorders?

A

Decreased GFR leads to increased serum phosphate and decreased serum calcium
Increased production of PTH
Decreased active vitamin D - decreased Ca2+ gut absorption

83
Q

What types of renal osteodystrophy can occur?

A

Rugger jersey spine - sclerosis of end plates
Erosion to terminal phalanges
Bone cysts

84
Q

What are vertebral end plates?

A

The top and bottom portions of vertebral bodies that interface with vertebral discs

85
Q

What other non-bone calcification can occur in CKD?

A

Aorta
Shoulder joint
Small vessels in skin

86
Q

What can we do to help prevent/delay CKD?

A 
Stop smoking
Increased exercise 
Lose weight 
Treat diabetes 
Treat BP 
Treat proteinuria (ACEi)
Lipid lowering
87
Q

When is renal replacement therapy usually needed? (GFR)

A

GFR = 8 - 10 ml/min

88
Q

What are the indications in CKD for dialysis?

A 
Uraemic symptoms 
Acidosis 
Pericarditis
Fluid overload
Hyperkalaemia

Urinary System (14 decks)

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