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Flashcards in Acute And Chronic Kidney Disease Deck (88):
1

What is AKI?

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

2

Why is AKI difficult to diagnose?

Doesn't present with a specific identifiable symptom
Measurements are not massively accurate either

3

What happens to serum creatinine as kidneys decline?

Kidney decline leads to increased serum creatinine

4

How do we define AKI through measurements?

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

5

Describe the staging of AKI

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

6

What are the types of AKI?

Pre-renal
Intrinsic renal
Post-renal

7

What are the causes of pre-renal AKI?

Blood supply compromised
Volume depletion
Heart failure
Cirrhosis

8

Give some renal causes of AKI

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

9

What does ATN stand for?

Acute tubular necrosis

10

What type of AKI are the vast majority?

Pre-renal

11

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

ATN

12

Give some general causes of AKI

Infective
Diarrhoea
Obstetric illness
Venoms
Malaria
Dyes

13

Describe how pre-renal problems cause AKI

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

14

Describe autoregulation of the kidneys

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)

15

What is the SM response to decreased renal perfusion?

Vasodilation of afferent
Vasoconstriction of efferent

16

Why do NSAIDs make AKI worse?

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

17

Why can ACEi make AKI worse?

Cannot vasoconstrict when need to

18

Give some causes of reduced ECF volume

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

19

Give some causes of impaired renal autoregulation

Sepsis
Hypercalcaemia
Hepatorenal syndrome
NSAIDs
ACEi
AngII antagonists

20

What are the causes of ATN?

Ischaemia
Nephrotoxins
Sepsis

21

Why is ATN a misnomer?

As there is generally no tubular necrosis
But cells are damaged

22

Describe ATN

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

23

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

Mortality increases

24

Which parts of the nephron are most susceptible to hypoxia?

S3 of PCT
Thick ascending limb LOH

25

Describe damage in the kidneys due to nephrotoxins

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

26

Give examples of endogenous nephrotoxins

Myoglobin
Urate
Bilirubin

27

In which treatment does urate build up?

Chemotherapy

28

Give some examples of exogenous nephrotoxins

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

29

How does rhabdomylosis cause ATN?

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

30

Describe acute glomerulonephritis

Immune disease affecting the glomeruli
Can be primary or secondary

31

Give 2 types of rapidly progressing glomerulonephritis

Granulomatosis with polyangiitis
Crescenteric necrotising glomerulonephritis

32

Describe acute tubulo-interstitial nephritis

Caused by infection or toxins
Massive inflammatory infiltrate (lymphocytes)

33

What percentage of AKIs are post-renal causes?

5-10%

34

What is the general mechanism for post-renal AKI?

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

35

Give some causes of post-renal AKI

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

36

Describe the serum changes common to all AKIs

Increased urea
Increased creatinine

37

What are the ECG changes of hyperkalaemia?

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

38

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

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

39

What do we assess when looking for fluid overload?

Gallop rhythm
Increased BP
Raised JVP
Pulmonary oedema
Peripheral oedema

40

Describe the Hx of a patient will post-renal AKI

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

41

What should we examine for in post-renal AKI?

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

42

What is essential to do for every patient with AKI?

Urinanalysis
Blood, protein, leukocytes

43

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

Blood and/or protein

44

How do we image AKI?

Ultrasound scan - obstruction
CXR - fluid overload, infection

45

Name some preventative methods for AKI

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

46

Give some of the susceptibilities for AKI

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

47

Give some exposure risk factors for AKI

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

48

What is the management for AKI?

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

What are the indications that an AKI patient needs dialysis?

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

50

What is the prognosis for uncomplicated ATN?

Recovery in 2-3 weeks if no extra insults

51

What is the overall AKI mortality?

24%

52

What is the normal GFR range?

90 - 120 ml/min

53

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

2 million
Need 40,000 approx (2%) to survive

54

What is chronic kidney disease?

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

What is the commonest cause of CKD?

Unknown

56

Name some causes of CKD

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

57

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

Small, shrunken kidney
With irregular outline
Lots of fibrous scarring

58

Who should be screened by CKD?

Diabetes
Hypertension
Ischaemic heart disease

59

Who is CKD more common in?

Elderly
Ethnic minorities
Multi-morbid people
Socially disadvantaged

60

What is CKD classification based on?

GFR

61

Describe the stages of CKD

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

62

Which measures of GFR are not very accurate?

> 60 GFR

63

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

ACR
Albumin:creatinine ratio
Higher it gets = worsened condition

64

What are the stages of ACR?

A1 < 3
A2 3 - 30
A3 > 30

65

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

Approx 7%

66

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

25%
Even though no symptoms

67

What indicators what make us check kidney function?

High BP
Proteinuria
Haematuria

68

Proteinuria and CKD together increase the risk of ...

Death by cardiovascular disease
More likely to need dialysis

69

What is the normal serum creatinine?

80 - 120 micromoles/L

70

What clearance markers can we use to represent eGFR?

Creatinine
Inulin
Cr EDTA
Iohexol

71

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

Expensive
Require hospital stays
Collecting urine has bad compliance

72

Is the relationship between serum creatinine and GFR linear?

No

73

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

~ 60%

74

Creatinine concentration in serum is determined by:

Renal function
Muscle mass (age, sex, race, exercise)

75

Why can't we use eGFR in AKI?

Can only use the eGFR formula if GFR is relatively stable

76

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

Autoantibody screen
Complement
Immunoglobulin
ANCA
CRP
SPEP/UPEP

77

Describe polycystic kidneys

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

Acidosis can affect which organs?

Muscles
Bones
Renal function decline further

79

Acidosis is not a problem until GFR is ...

< 25

80

How does CKD lead to anaemia?

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

81

How do we treat anaemia from CKD?

Give EPO subcutaneous injections

82

How can CKD cause mineral and bone disorders?

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

83

What types of renal osteodystrophy can occur?

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

84

What are vertebral end plates?

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

85

What other non-bone calcification can occur in CKD?

Aorta
Shoulder joint
Small vessels in skin

86

What can we do to help prevent/delay CKD?

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

87

When is renal replacement therapy usually needed? (GFR)

GFR = 8 - 10 ml/min

88

What are the indications in CKD for dialysis?

Uraemic symptoms
Acidosis
Pericarditis
Fluid overload
Hyperkalaemia