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RB Y2 Renal > AKI > Flashcards

AKI Flashcards

1
Q

define AKI

A

rapid reduction in kidney function from hours to days, as measured by serum urea and creatinine, and leading to failure to maintain fluid, electrolyte and acid-base balance homeostasis.

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2
Q

time frame

A

<48 hours

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3
Q

diagnosis criteria

A

Diagnosis: abrupt (<48hrs) reduction in kidney function:

  • Rise in serum creatinine >26.4umol/L
  • Rise in creatinine >50% baseline
  • Reduction in urine output

Must follow adequate fluid resuscitation and exclusion of obstruction.

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4
Q

KDIGO staging system

A
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5
Q

patient risk factors

A
  • Older age (≥65)
  • CKD
  • DM
  • Cardiac failure
  • Liver disease
  • PVD
  • Previous AKI
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6
Q

exposure risk factors

A
  • Hypotension, hypovolaemia
  • Sepsis
  • Deteriorating NEWS
  • Recent contrast
  • Exposure to certain medications
  • History of urinary symptoms
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7
Q

what investigation should be carried out within 24 hours of assessment

A
  • US
  • check for obstruction
  • check size of kidneys - can indicate acute or chronic damage
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8
Q

UCR in pre renal AKI

A

Decreased renal perfusion lead to a reduction in GFR – this decreases both urea and creatinine filtration (increases serum concentration) as they accumulate. Urea is also reabsorbed more in the proximal tubule because it is flowing slower à increased urea:creatinine ratio.

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9
Q

UCR in intra renal AKI

A

Ratio becomes closer to 1 as urea is unable to be reabsorbed.

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10
Q

how much of CO do kidneys receive

A

20% even though they are 0.5% of body weight

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11
Q

causes of decreased blood flow to kidneys

A
  • Absolute loss of fluid:
    • Major haemorrhage, vomiting, diarrhoea, severe burns (body fluid evaporates really fast without protective skin)
  • Relative loss of fluid (total stays the same):
    • Distributive shock – fluids moves from vessels into tissues
    • Congestive heart failure – blood pooled in venous side
  • Hypotension
    • Cardiogenic shock
    • Distributive shock (e.g. sepsis, anaphylaxis)
  • Local to renal artery
    • Narrowed in renal artery stenosis
    • Blocked by embolus
  • Renal hypoperfusion:
    • Hepatorenal syndrome
  • Drugs
    • E.g. NSAIDs
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12
Q

how do NSAIDs cause pre renal AKI

A
  • NSAIDs inhibit COX (and PG production) and may precipitate acute renal failure in conditions where renal blood flow is dependent upon vasodilatory PG (no effect on renal function in healthy people), e.g. CHF, cirrhosis, nephrotic syndrome
  • Cause afferent arteriole vasoconstriction.
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13
Q

assessing fluid status

A
  • Mucous membranes, skin turgor, E+S, BP, JVP, (creps in chest), CRP
  • Bloods: urea, haematocrit, osmolarity + urine osmolarity
  • Peripheral oedema indicates fluid in the wrong place, not necessarily intravascular volume status
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14
Q

pre renal AKI

A
  • the kidneys are v sensitive to low blood flow - decrease in GFR
  • oliguria and a rise in UCR (rise in urea (++) and creatinine)
  • increase in salt and water retention
  • decreased blood flow for a prolonged period of time leads to intrinsic renal failure due to acute tubular necrosis
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15
Q

distinguishing pre renal and renal causes of AKI: urine sodium

A

low in pre renal - kidneys are holding on to sodium to preseve volume

high in renal

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16
Q

distinguishing pre renal and renal causes of AKI: urine specific gravity

A
  • a measure of the concentrating ability of the kidneys
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17
Q

distinguishing pre renal and renal causes of AKI: urine osmolality

A
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18
Q

signs of uremia

A
  • yellow tinge
  • uremic frost
  • involuntary muscle twitching
  • bleeding
  • metabolic acidosis - Kussmaul breathing
  • pericardial rub or haemorrhagic pericarial effusion
  • encephalopathic: flapping tremor and confusion
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19
Q

why is there a metabolic acidosis in renal failure

A

kidney normally excretes H+ ions

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20
Q

how does urea cause bleeding

A

uremia acts as an antiplatelet, less clot formation which means patients bleed and bruise more easily

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21
Q

uremic frost

A
  • occurs in those who have had established renal failure for years, trying to excrete/secrete toxins through skin pores – urea concentration increases in sweat. Evaporation of sweat with high urea concentration causes urea to crystallize and deposit on the skin.
  • stale urine smell to skin
  • rarely seen now due to RRT
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22
Q

intra renal causes of AKI

A
  • vascular eg vasculitis
  • GN
  • interstitial nephritis
  • tubular injury
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23
Q

which drugs cause IN

A

(inflammation of the space between renal tubules)

  • NSAIDs
  • diuretics
  • sulphonamides
  • rifampicin
  • PPIs
  • allopurinol
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24
Q

infection and immune causes of IN

A
  • infection eg TB
  • immune reactions eg sarcoidosis and SLE
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25
Q

what haematological thing may drug reactions cause

A

peripheral eosinophilia and allergic picture: fever and rash

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26
Q

what will a biopsy of IN show

A

inflammatory cell infiltrate

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27
Q

causes of tubular injury

A
  • ischaemia due to prolonged renal hypoperfusion etc
  • drugs eg gentamicin
  • radio contrast dye
  • massive haemolysis
  • rhabdomyolysis
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28
Q

what damage do aminoglycosides do to the kidneys

A
  • they are nephrotoxic - cause ATN
  • typically presents as a mild non-oliguric AKI 1-2 weeks into therapy
  • there is a high output of watery urine and high creatinine
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29
Q

what factors increase the risk of gentamicin nephrotoxicity

A
  • Risk is increased by old age, renal hypoperfusion, pre-existing CKD, high dosage/prolonged treatment
30
Q

how does massive haemolysis caues tubular injury

A
  • Deposition of iron and hemosiderosis etc causes damage
31
Q

rhabdomyolysis

A
  • Results from skeletal muscle breakdown with release of its contents into the circulation, including myoglobin, potassium, phosphate, urate and creatinine kinase – some of these are toxic to the renal tubules
  • Massive plasma myoglobin levels are filtered by the glomeruli and precipitate, obstructing renal tubules – myoglobin is nephrotoxic and causes tubular cell necrosis. Turns urine red-brown.
32
Q

who does rhabdomyolysis occur in

A

patients with muscle damage who have been lying for a long time

33
Q

clinical features of Rhabdomyolysis

A
  • history
  • pain
  • swelling
  • tenderness
  • red brown urine
34
Q

biochemistry of Rhabdomyolysis

A

raised CK

35
Q

complications of Rhabdomyolysis

A

AKI and hyperkalaemia

36
Q

causes of Rhabdomyolysis

A

burns, crush injury, trauma

37
Q

management of Rhabdomyolysis

A

treat hyperkalaemia, IV fluid dehydration, maintain urine output

38
Q

NSAIDs on the kidney

A
  • NSAIDs inhibit COX (and PG production) and may precipitate acute renal failure in conditions where renal blood flow is dependent upon vasodilatory PG (no effect on renal function in healthy people), e.g. CHF, cirrhosis, nephrotic syndrome. Cause afferent arteriole vasoconstriction.
  • Directly cause acute interstitial nephritis, this is an immunological reaction and occurs after around a week of NSAID exposure
39
Q

NSAIDs and fluid balance

A
  • NSAIDs increase blood pressure in patients treated for hypertension by impairing PG mediated vasodilatation and salt excretion <ins>(COX2 has a natriuretic effect)</ins> They exacerbate salt and water retention in patients with heart failure, partly by this same mechanism.
  • Over a long period of time, this can lead to hypertension
40
Q

what can aggravate the nephrotoxicity of things eg NSAIDs

A

moderate volume depletion eg diarrhoea and vomiting

41
Q

angiontensin mechanism

A
  • Angiotensin II causes efferent (and some afferent) arteriole vasoconstriction and increases reabsorption of salt and water. Therefore, increasing GFR
42
Q

ACEi/ARB mechanism and kidney damage

A
  • ACEi causes a fall in GFR by causing efferent arteriolar vasodilation, also decreases proteinuria
  • those that already had poor renal perfusion eg bilateral renal artery stenosis, can experience a major fall in GFR
43
Q

inital investigations of renal AKI

A
  • U&Es: Marker of renal function, check for high potassium
  • FBC and coagulation screen
    • Abnormal clotting
    • Anaemia
  • Urinalysis: Haematoproteinuria
  • USS: Check for obstruction and kidney size
  • Immunology: ANA, ANCA, GBM
  • Protein electrophoresis & BJP
44
Q

what must be performed before a biopsy is done

A
  • Blood count and coagulation screen (moderate or severe thrombocytopenia, and coagulation defects are contraindications to renal biopsy, unless they can be easily corrected)
  • Renal US – to check that the 2 kidneys are present, and the size and position of the kidneys
  • Control BP if uncontrolled hypertension – ACEi reduce the BP and also reduce protein excretion (reduction of proteinuria slows progression of kidney disease)
45
Q

urgent indications for a renal biopsy

A
  • suspected RPGN
  • positive immunology and AKI
46
Q

semi urgent renal biopsy indications

A
  • Unexplained AKI to gain a diagnosis
  • Rule out obstruction, volume depletion and ATN
47
Q

contra indications to renal biopsy

A
  • Small kidneys – increased risk of bleeding, and biopsy would probably be uninformative, showing scarred kidney
    • Kidneys tend to be small because they are scarred
  • Uncontrolled hypertension – increased risk of bleeding
  • Untreated urine infection – risk of secondary haemorrhage – about 10 days after biopsy
    • Also increases the risk of bacteremia
  • Presence of a single kidney is a relative, not absolute, contra-indication – potential risks and benefits of the procedure must be considered (as in all cases)
48
Q

treatment of intra renal AKI

A
  • Establish a good perfusion pressure
    • Fluid resuscitation
    • If they are still not achieving adequate BP consider inotropes or vasopressors
  • Treat underlying cause
  • Stop nephrotoxics
  • Dialysis if remain anuric and uraemia – can be urgent
49
Q

is ATN reversible

A

tubular cells can regenerate rapidly so it can be

50
Q

what happens when patients drink with oliguria

A

hyponatraemia is common

51
Q

how should fluid be given

A
  • crystalloid or colloid
  • give a bolus (250/500?)
  • if >1000mls given an no improvement seek help
  • consider positive inotropes
52
Q

post renal AKI

A
  • AKI due to obstruction of urine outflow at any point from the calcyes to the external urethral orifice, leading to back pressure and thus loss of concentrating ability
  • If the patient previously had normal function, and has 2 kidneys, both must be obstructed to cause ARF. So the obstruction must be at the level of the bladder or urethra, or of both ureters.
53
Q

hydronephrosis

A
  • Hydronephrosis refers to the dilation of the renal pelvis and can be present with/out obstruction
54
Q
A
55
Q

pathology of post renal AKI

A
  • build up of pressure in the kidney decreases the pressure gradient between the glomerulus and tubules, thus reducing GFR
  • oliguria
56
Q

causes of post renal AKI

A
  • stones
  • cancers
  • strictures
  • extrinsic pressure eg intra abdominal tumour or BPH
57
Q

investigations of post renal obstruction

A

USS

or CT KUB

58
Q

assessing volume status

A
  • Mucous membranes, skin turgor, E+S, BP, JVP, (creps in chest), CRP
  • Bloods: urea, haematocrit, osmolarity + urine osmolarity
  • Peripheral oedema indicates fluid in the wrong place, not necessarily intravascular volume status
59
Q

sick day rules: nephrotoxic drugs that must be stopped

A
  • NSAIDs
  • diuretics
  • ACEi/ARB
  • gentamicin
60
Q

drugs that must be stopped in AKI as there is an increased risk of toxicity

A
  • metformin
  • allopurinol
  • lithium
  • digoxin
    • half life is increased due to decreased renal excretion
61
Q

metformin and kidney damage

A
  • stop metformin if creatinine is >150mmol/L
  • there is an increased risk of developing lactic acidosis
62
Q

complete anuria in AKI patient

A

this is unusual - suspect an obsructive cause

63
Q

danger of hyperkalaemia

A

life threatening, there is a danger of ventricular fibrillation and cardiac arrest

64
Q

hyperkalaemai values

A
  • Normal K+: 3.5-5.0, hyperkalaemia >5.5, life-threatening hyperkalaemia: >6.5
65
Q

features of hyperkalaemia

A

ECG changes and muscle weakness

66
Q

outline the ECG changes as serum K increases

A
  • Peaked T waves is the earliest sign
  • P wave widens and flattens, PR lengthens, and P waves eventually disappear
  • Broad QRS complexes and bizarre QRS morphology
  • Cardiac arrest due to asystole or ventricular fibrillation
67
Q

management of hyperkalaemia

A
  • continuous cardiac ECG monitor and IV access
  • Stabilise cardiac membrane: 10ml 10% calcium gluconate IV is cardio-protective against arrhythmias, doesn’t affect K+ levels
    • Can be given repeatedly
  • short term shift in K from EC to IC fluid compartment
  • IV Sodium bicarbonate can be given if venous bicarbonate is low
68
Q

what can be used for a short term shift in K+ from EC to IC fluid compartment

A
  • insulin (actarapid 10 units) and to drive K+ back into cells. Glucose (50ml 50% dextrose) to prevent hypoglycaemia. Monitor blood glucose level
  • Salbutamol works in the same way as ^ but high doses are required, and tachycardia can limit use
    • 2.5mg by nebuliser
    • ß agonists also cause potassium to move into cells
69
Q

how is K removed from the body

A
  • calcium resonium binds K in the gut and prevents its absorption. used in mild cases to reduce K slowly
  • loop diuretics
  • dialysis
70
Q

urgent indications for haemodialysis

A
  • Bloods: severe resistant hyperkalaemia (>7), GFR<5, Ur>45, unresponsive acidosis
  • Refractory fluid overload due to oliguria – pulmonary oedema
  • Uraemic symptoms: nausea, seizure, pericarditis, bleeding
  • Toxins/drugs
  • Symptoms: nausea and vomiting, loss of appetite??

RB Y2 Renal (26 decks)

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