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Renal-Urology > AKI & Acute Kidney Failure > Flashcards

AKI & Acute Kidney Failure Flashcards

1
Q

Urea is naturally produced when the liver breaks down protein or amino acids, and ammonia. The kidneys then transfer the urea from the blood to the urine.

(protein meal = high urea but normal creatinine in blood )

What is the name given to when there is rising blood urea& creatinine in response to low gfr?

A

AZOTAEMIA

= rising blood urea & creatinine in response to low GFR

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2
Q

What are the ssx uraemia in the CNS?

A
  • encephalopathy
  • fits
  • twitch or tremor
  • tiredness
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3
Q

What other neurological signs do you get from uraemia e.g. not in CNS?

A

you get peripheral neuropathy

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4
Q

What are the GI symptoms of uraemia?

A

anorexia (loss of appetite & weight)

N&V

colitis

metallic taste

alitosis

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5
Q

What lung/heart conditions can uraemia cause?

A
  • Lung:
    • Pleuritis
    • pleural effusion
  • Heart:
    • pericarditis
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6
Q

What endocrine symptoms can uraemia cause?

A

growth retardation,

sexual dysfunction

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7
Q

What skin manefestations can uraemia cause?

A

pruritus

half-and-half nails (found in CKD)

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8
Q

What effects does uraemia have on the blood?

A

it is pro-haemorrhagic

= impaired platelet function

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9
Q

The diagnosis of uraemia requires 2 components, what are these?

A
  1. Azotaemia
    • (rising blood urea & creatinine in response to low GFR)
  2. SSx uraemia
  • (CNS: encephalopathy, fits, twitch or tremor, tiredness
  • Peripheral neuropathy
  • GI: anorexia (loss of appetite & weight), N&V, colitis, metallic taste, halitosis
  • Pleuritis, pleural effusion
  • Pericarditis
  • Endocrine: growth retardation, sexual dysfunction
  • Skin: pruritus, “half-and-half” nails
  • PRO-HAEMORRHAGIC - impaired platelet function)
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10
Q

As uraemia diagnosis requires rising blood urea & creatinine in response to low GFR (azotaemia) and Ssx uraemia…

Causes of uraemia can be pre-prenal, renal and post renal, what are the pre-renal causes of uraemia?

A
  • Increased hepatic production urea
    • (GI haemorrhage “protein meal”, diet, protein catabolism)
  • Increased renal reabsorption
    • (any cause of reduced renal perfusion)
  • Iatrogenic (
    • drug therapy e.g. tetracyclines, corticosteroid)
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11
Q

As uraemia diagnosis requires rising blood urea & creatinine in response to low GFR (azotaemia) and Ssx uraemia…

Causes of uraemia can be pre-prenal, renal and post renal, what are the pre-renal causes of uraemia?

A
  1. Acute/ chronic renal failure
  2. Any cause of urinary outflow obstruction
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12
Q

What is the definition of acute kidney injury?

A
  • TUBULAR CELL INJURY/DEATH means the bits drop into the TUBULAR LUMEN & cause obstruction
  • (renal tubular cells are in the collecing duct)
  • tubular cell injury/death is common as kidneys are vulnerable to hypoxia & toxic injury

Rise in creatinine 1.5x from baseline (or >26.4umol/L in 48h) and/or decreased urine output (<0.5mL/kg for >6hrs)

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13
Q

What scoring system is used to define the level of AKI?

A

RIFLE

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14
Q

RIFLE scoring system is used to define AKI stages. What criteria does it use?

A

creatinine rise and urine output

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15
Q

Pt X’s urine rise is 2-3x from baseline and their GFR has decreased >50%.

Their urine output has been at <0.5mL/kg for >12 hours.

What RIFLE stage is their kidney injury at?

A

Stage 2 = injury

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16
Q

Pt X’s urine rise is 1.5-1.9x from baseline and their GFR has decreased >35%.

Their urine output has been at <0.5mL/kg for >6 hours.

What RIFLE stage is their kidney injury at?

A

Stage 1 = Risk

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17
Q

Pt X’s urine rise is >3x from baseline and their GFR has decreased >75%.

Their urine output has been at <0.3mL/kg for >24 hours / anuric for 12 hours.

What RIFLE stage is their kidney injury at?

A

Stage 3 - failure

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18
Q

When is kidney “loss” described?

A

complete loss of renal function >4wks

–> end stage renal disease (ESRD)

e.g. in ESRD they have stopped working well enough for you to survive without dialysis or a kidney transplant

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19
Q

What are the pre-renal causes of AKI?

A
  1. If there is Decreased renal blood flow & impaired renal tissue oxygenation
  2. → afferent arteriole vasodilation (PGs) & efferent vasoconstriction (ang II) [to keep blood in the kidney to filter it–> bloodstream]
  3. → Na & water retention

The decreased renal BF & impaired renal tissue oxygenation is caused by:

  1. Hypovolaemia
  2. Decreased effective volume
  3. RAS
  4. Altered intrarenal haemodynamics - NSAIDs/ACEI/ARB interference
    • nsaids affect the afferent arteriole
    • ACEi and ARB affect the efferent arteriole - ACEi blocks the enzyme making ang2 and ARB blocks ang2 effects in the body via the receptor
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20
Q

What are the renal causes of AKI?

A

Nephrotoxins

→ drugs e.g. NSAIDs, aminoglycosides, chemo agents, radiocontrast agents

→ haemolysis or rhabdomyolysis

→allergic reaction to drugs e.g. ampicillin, rifampicin

  1. Acute tubular necrosis (ATN)
  2. Acute interstitial nephritis (inflam of ecm&fluid around tubules - used in f&e exchang. & kidney endocrine)
  3. Acute glomerulonephritis (inflam and prolif of glomeruli)
  4. Vascular (small & large vessel diseases)
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21
Q

What are the post-renal causes of AKI?

A
  • obstructuve uropathy ~10% - important to rule out as obstruction can be relieved easily once dx made.
  1. Ureteric obstruction
    • Luminal e.g. stones, clots
    • Mural (attached/limited to a wall) e.g. malignancy, strictures, BPH
    • Extra-mural e.g. pelvic malignancy, retroperitoneal fibrosis
  2. Urinary bladder outflow tract obstruction
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22
Q

What do ischaemia, sepsis, nephrotoxins & prostate disease all have in common?

A

*ischaemia, sepsis, nephrotoxins (& prostate disease) all cause AKI

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23
Q

What are the RFs for AKI?

A
  • Age: >75yrs,
  • Medical conditions: CKD, HF, PVD, chronic liver disease, DM, newly started drugs, sepsis,
  • Other: poor fluid intake/increased losses,
  • hx urinary symptoms
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24
Q

In AKI the general symptoms are variable and non-specific e.g. N&V, tiredness, lethargy –

a hx of decreased urine output is useful… it is important though to make note if pt is volume depleted or volume overloaded…

How can you check if a patient is volume depleted or volume voerloaded?

A

do a lying standing BP

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25
Q

What symptoms may you get in pre-renal inury?

NB: pre renal causes maybe:

  • Hypovolaemia
  • Decreased effective volume
  • RAS
  • Altered intrarenal haemodynamics - NSAIDs/ACEI/ARB interference
A
  • (volume depletion & hypotension);
    • D&V,
    • dizziness,
    • weakness
  • hx bleeding
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26
Q

What symptoms may you get in drug induced-renal inury?

A
  • hx for
    • ACEIs,
    • ARBs,
    • chemo,
    • aminoglycosides,
    • penicillin’s,
    • other antibiotics;
  • joint pains & erythematous skin rash (allergic interstitial nephritis)
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27
Q

What symptoms relating to AKI would you get in vasculitis e.g. an autoimmune/vascuitis cause of AKI?

A
  • skin rash,
  • palpable purpura,
  • joint pains,
  • haematuria/smoky urine
28
Q

What symptoms relating to AKI would you get in lupus nephritis e.g. an autoimmune/vascuitis cause of AKI?

A
  • oral ulcers,
  • loss of scalp hair,
  • facial rash
29
Q

What symptoms relating to AKI would you get in rhabdomyolysis e.g. an autoimmune/vascuitis cause of AKI?

A
  • hx muscle injury,
  • dark urine
30
Q

What symptoms relating to AKI would you get in sepsis e.g. an autoimmune/vascuitis cause of AKI?

A
  • fever
  • rigors
  • chills
31
Q

What symptoms relating to AKI would you get in obstructive uropathy?

A
  • poor urine flow
  • hesitancy
32
Q

What vasculitis/autoimmune causes of AKI are there?

A
  • Vasculitis
  • lupus nephritis
  • rhabdomyolysis
  • sepsis
33
Q
  • What do these symptoms indicate in AKI?
    • D&V,
    • dizziness,
    • weakness
  • hx bleeding
A

Pre - renal causes of AKI

34
Q
  • What does the following indicate for AKI?
  • hx for
    • ACEIs,
    • ARBs,
    • chemo,
    • aminoglycosides,
    • penicillin’s,
    • other antibiotics;
  • Drugs + joint pains & erythematous skin rash
A

all those drugs –> ?drug induced-renal inury

drugs + Joint pains & erythematous skin rash = allergic interstitial nephritis

35
Q

What does this hx in AKI indicate?

  • skin rash,
  • palpable purpura,
  • joint pains,
  • haematuria/smoky urine
A

Vasculitis

36
Q

What does this history relating to AKI indicate?

  • oral ulcers,
  • loss of scalp hair,
  • facial rash
A

Lupus nephritis

37
Q

What does this history in relation to AKI indicate?

  • hx muscle injury,
  • dark urine
A

rhabdomyolysis

38
Q

What does this history in relation to AKI indicate?

  • fever
  • rigors
  • chills
A

Sepsis

39
Q

What do these features + AKI indicate?

  • poor urine flow
  • hesitancy
A

obstructive uropathy

40
Q

What bedside Ix is useful for AKI?

A

urine dip! –> proteinuria and haematuria

41
Q

Laboratory urinalysis is used in AKI.

If on urine biochemistry there is low urine Na what type of cause for AKI does this indicate?

A

Low urine Na established pre-renal

(Na being retained to keep volume up??)

42
Q

Laboratory urinalysis is used in AKI. Urine biochemistry is done to look at Na etc. You can also do microscopy on urine.

In glomerulonephritis, vasculitis, malignant hypertension and (rarely) interstitial nephritis what would you see on urine microscopy

A

Red Blood Cell casts –>

They are a yellowish-brown color and are generally cylindrical with sometimes ragged edges; their fragility makes inspection of a fresh sample necessary. They are usually associated with nephritic syndromes or urinary tract injury.

[e.g. glomerulonephritis/nephritic = haematuria, protein urea and RBC casts in urine]

43
Q

Laboratory urinalysis is used in AKI. Urine biochemistry is done to look at Na etc. You can also do microscopy on urine.

In severe pyelonephritis, allograft rejection, leukaemic infiltration & AIN (rarely AGN) what would you see on urine microscopy?

(AIN = interstitial inc ECM and fluid around renal tubules vs AGN = glomeruli inflam and proliferation)

A

WBC casts!

[Urinary casts are tiny tube-shaped particles made up of white blood cells, red blood cells, or kidney cells. They form in kidney structures called tubules. Casts are held together by a protein released by the kidney. The content of a cast can tell your health care provider whether your urine is healthy or abnormal]

44
Q

Laboratory urinalysis is used in AKI. Urine biochemistry is done to look at Na etc. You can also do microscopy on urine.

In allergic AIN, atheroembolic disease what would you see on urine microscopy?

(AIN = interstitial inc ECM and fluid around renal tubules)

A

Eosiophiluria

45
Q

Laboratory urinalysis is used in AKI. Urine biochemistry is done to look at Na etc. You can also do microscopy on urine.

In acute uric acid nephropathy, acyclovir, ethylene oxalate what would you see on urine microscopy?

A

crystalluria

46
Q

Laboratory urinalysis is used in AKI. Urine biochemistry is done to look at Na etc. You can also do microscopy on urine.

What do granular casts look like in acute tubular nephritis?

A

muddy brown casts = ATN

47
Q

What does urinary sodium help differentiate between?

A

differentiates between pre-renal uraemia (<20 Na e.g. low) & acute tubular necrosis (>40 e.g. high)

48
Q

if Urinary sodium helps differentiates between pre-renal uraemia (<20) & acute tubular necrosis (>40)

what else can?

A

usine osmolality helps too

49
Q

What bloods should be done for AKI?

A

Bloods:

  • creatinine,
  • urea,
  • ANA (lupus)
  • ANCA, (granulomatosis, churg-strauss, polyangitis)
  • Complement (lupus),
  • anti-GBM, (goodpastures)
  • Bence jones (myeloma)
  • serum electrophoresis Myeloma)
50
Q

What Ix is done for obstructive uropathy?

A

US kidney and bladder

51
Q

When is a renal biopsy done?

A

if suggestion of glomerular disease

(e.g. for acute glomerulonephritis)

52
Q

What is the main way of AKI prevention in unwell patients?

A

DRUG REVIEWS

Avoid or withold -

  1. Diuretics,
  2. ACEi,
  3. Anti-hypertensives if BP low,
  4. Metformin if creatinine is rising
    • (as there is a risk of lactic acidosis)
  5. NSAIDS
  6. Nephrotoxic antibiotics
    • gentamicin, nitrofurantoin
53
Q

What drugs should be used with caution in unwell patients (due to aki risk)?

A
  • Opiates
  • IV contrast –> keep hydrated
54
Q

one of your patients is oligo/anuric & they have hyperkalaemia

or

your pt is unresponsive to AKI rx, urea >40mmol/L +/- signs of uraemia such as pericarditis

Who do you refer to?

A

Nephrologist!

55
Q

What is the approach for managing AKI?

A
  1. General measures
  2. treat underlying cause e.g. pre, post or intrinsic renal
  3. manage complications e.g. hyperkalaemia, pulm oedema, uraemia and acidaemia
56
Q

What are the general measures for the management of AKI?

A
  • assess volume status & aim for euvolemic
  • assess nutrition & consider NG early
  • medication review for nephrotoxins
    • (ACEi ARBs, NSAIDS, penicillins, rifampicin, PPIs)
57
Q

How do you treat the underlying cause of AKI if it is pre-renal?

A
  • fluids,
  • abx for sepsis,
  • ICU for inotropic support if signs of shock (get the blood pumping back around the body)
58
Q

How do you treat the underlying cause of AKI if it is post-renal?

A
  • catheterise,
  • CTKUB (CT of kidney, ureter and bladder)
  • & urology referral if obstruction
59
Q

How do you treat the underlying cause of AKI if it is intrinsic?

A

early referral to nephrology

60
Q

Complications of AKI include hyperkalaemia, pulmonary oedema, uraemia and acidaemia.

At what levle is hyperkalaemia life threatening and why?

A

hyperkalaemia >6.5mmol/L is life threatening

–> get ventricular arrhythmias

61
Q

Complications of AKI include hyperkalaemia, pulmonary oedema, uraemia and acidaemia.

How do you Rx hyperkalaemia in the short term?

A

(stop K+ containing drugs)

Give:

  • Calcium gluconate 10mL of 10% IV over a few mins - s_tabilise myocardium_
  • Insulin + dextrose (15U insulin in 50mL 50% dextrose over 10-20mins) - drives K into cells
  • Salbutamol nebulisers 10-20mg work the saw way as insulin/dextrose - high doses required
  • If patient is acidotic, IV sodium bicarbonate 50mL of 8/4% NaHCO3 - can help drive K+ into cells but effect is unpredictable
62
Q

Complications of AKI include hyperkalaemia, pulmonary oedema, uraemia and acidaemia.

How do you Rx hyperkalaemia in the longer term?

A

if Need more permanent fix for hyperkalaemia (>6.5mmol/L is life threatening via ventricular arrhythmias)

  • Establish diuresis
  • OR urgent dialysis
  • OR K-exchange resins e.g. calcium resonium can help in interim (give with laxative)
63
Q

Complications of AKI include hyperkalaemia, pulmonary oedema, uraemia and acidaemia.

How do you treat pulmonary oedema?

(come from na retention? why you get low na in the urine if pre-renal?)

A

ABCDE approach then start –> LMNOP aka

  • Loop diuretic - furosemide 40-80mg (or double their dose) - repeat until SoB stops
  • Morphine 1.25-5mg IV slowly (caution in low BP)
  • (No N)
  • Oxygen
  • Position
  • Urgently consider haemodialysis or haemofiltration
  • CPAP
64
Q

How do you manage these symptoms?

  • CNS: encephalopathy, fits, twitch or tremor, tiredness
  • Peripheral neuropathy
  • GI: anorexia (loss of appetite & weight), N&V, colitis, metallic taste, halitosis
  • Pleuritis, pleural effusion
  • Pericarditis
  • Endocrine: growth retardation, sexual dysfunction
  • Skin: pruritus, “half-and-half” nails
  • PRO-HAEMORRHAGIC - impaired platelet function
A

they are syx of uraemia… so Rx of uraemia–>

may require dialysis if severe or complications e.g. encephalitis, pericarditis;

otherwise symptomatic management

(and fix aki by cause e.g. pre, post or intrinsic renal i guess)

65
Q

How do you manage acidaemia in AKI?

A

may require dialysis,

IV sodium bicarbonate 50mL of 8/4% NaHCO3 (HDU setting) or PO

e.g. so you give bicarb to neutralise (like seen in ABGs but use its as chemical NaHCO3)

66
Q

What are the indications for dialysis (Renal Replacement Therapy)?

A

–> basically = persistent any of the AKI complications we mentioned & then BLAST drug OD e.g…

  1. Refractory pulmonary oedema
  2. Persistent hyperkalaemia (>7) [NB: remember over 6.5 gives risk of life threatening ventricular arrhythmias]
  3. Severe metabolic acidosis (pH<7.2 [norm= 7.35-.45] or base excess <10)
  4. Uremic complications (syx) such as encephalopathy, pericarditis
  5. Drug overdose - BLAST: barbiturates, lithium, alcohol, salicylates, theophylline [so dialyse for BLAST drugs OD!]

Renal-Urology (8 decks)

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