AKI Flashcards

1
Q

how do NSAIDs damage the kidney?

A

pre-renal: cause constriction of the afferent arteriole because they impair renal autoregulation by inhibiting prostaglandin-mediated vasodilatation of the afferent arteriole.
renal: can cause acute interstitial nephritis
post -renal: long term use can lead to renal papillary necrosis causing obstruction.

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2
Q

how do ACEis damage the kidney?

A

cause vasodilation of the efferent arteriole.
this impairs renal autoregulation and reduces eGFR.

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3
Q

what actually is creatinine and why is it good/bad to measure kidney function?

A

produced by muscle cells at constant rate and filtered by kidneys
creatinine is a slight overestimation of eGFR as creatinine is secreted by the renal tubules. Inulin is more accurate but currently only available in research.

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4
Q

what are the diagnostic criteria for AKI?

A

any of:
-A rise in serum creatinine of 26 micromol/L or greater within 48 hours.
-A 50% or greater rise in serum creatinine (more than 1.5 times the baseline) which is known or presumed to have occurred within the past 7 days.
-A fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours, if measurable (for example, if there is a catheter in situ).

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5
Q

what are the bedside tests for AKI?

A

-urine dip
-assessment of fluid status and full exam looking for cause
-ABG/VBG -esp look for hyperkalaemia

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6
Q

what are some risk factors for rhabdo you’d ask about in an AKI history?

A

skeletal muscle injury
crush injury
muscle overexertion
prolonged immobility

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7
Q

what do the results of a urine dip show in AKI?

A

negative urinalysis -probably pre renal or drug cause
positive protein and blood -glomerular disease esp if 2+ on both, could also be UTI or catheter trauma
increased white cells -infection or interstitial nephritis

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8
Q

what are the criteria for the different stages of AKI?

A

stage 1: creatinine rise of 26 or more within 48 hours OR creatinine rise of 1.5-<2x baseline within 7 days or UO <0.5ml/kg/h for >6h
stage 2: creatinine rise of 2-<3x baseline within 7 days or UO <0.5ml/kg/h for >12h
stage 3: creatinine rise 3x baseline or more within 7 days or UO <0.3ml/kg/h for 24h or anuria for 12h or creatinine rise to 354 or more in 7 days with acute rise of 26 within 48 hours

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9
Q

when would you admit someone with AKI?

A

-stage 3 AKI
-underlying cause requiring urgent hospital management
-no identifiable cause
-urinary tract obstruction
-hypovalaemia and need for IV fluids
-suspected complication of AKI requiring hospital management

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10
Q

what are the complications of AKI that require hospital management?

A

pulmonary oedema
uraemic encephlopathy
pericarditis
severe hyperkalaemia (potassium 6.5 or more)

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11
Q

what is the general treatment of AKI?

A

identify and treat cause
stop drugs that might make situation worse: diuretics, aceis/arbs (in most situations), metformin, NSAIDs, iodine based contrast media, some abx
monitor creatinine, vitals, and fluid balance regularly
look out for and treat complications

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12
Q

which antibiotics should you avoid in AKI?

A

aminoglycosides eg gentamycin
tetracycline
trimethoprim -avoid or reduce dose

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13
Q

when should you refer someone to a specialist following AKI?

A

if they have known diagnosis of CKD and have had 1 or more episodes of AKI
if their eGFR is under 30

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14
Q

what monitoring do you need to do with a patient post AKI?

A

monitor for CKD progression for at least 3 years after episode of AKI
check serum potassium and creatinine 1-2 weeks after restarting any medication which has temporarily stopped and think about dose titration

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15
Q

what are the pre renal causes of AKI?

A

-hypovalaemia eg haemorrhage, GI losses (D+V), renal losses, burns, diuretic use, sweating, DKA, dehydration
-reduced cardiac output eg HF, liver failure, sepsis
-too high doses of drugs which reduce BP

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16
Q

what causes pre-renal AKI?

A

reduced perfusion of the kidneys and/or hypotension leading to reduced eGFR

17
Q

what are the renal causes of AKI?

A

-acute tubular necrosis -most common-ischaemic or toxic injury to cells of PCTs causing necrosis
-acute interstitial nephritis -drug induced, infection induced (TB, legionella), or immune mediated (sarcoidosis, SLE, IgG disease)
-glomerular disease -nephrotic syndrome, nephritic syndrome (glomerulonephritis)
-intra-tubular obstruction -multiple myeloma with paraprotein, rhabdomyolysis
-other: scleroderma renal crisis, malignant hypertension

18
Q

what are the post renal causes of AKI?

A

obstruction -kidney stone, BPH, prostate cancer, bladder cancer, blocked catheter, pelvic mass

19
Q

what are the common potentially nephrotoxic drugs and via which mechanisms?

A

GFR alteration: ACEis, ARBs, cyclosporin, tacrolimus, NSAIDs
tubular cell toxicity: aminoglycosides (gentamycin, vancomycin), amphotericin B, cisplatin
interstitial nephritis: NSAIDs, rifampicin
crystal nephropathy: acyclovir, ampicillin
also: bisphosphonates, diuretics, lithium, mesalazine

20
Q

what are some specific history points to ask in AKI that you might not ask in a normal history?

A

reason for admission to hospital -looking for cause
recent imaging investigations using iodinated contrast, esp if delivered arterially (eg CT with contrast, angio)
whether they have both their kidneys

21
Q

what is goodpasture syndrome?

A

also known as anti–glomerular basement membrane disease.
rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs, glomerulonephritis, and kidney failure

22
Q

what is multiple myeloma and how does it damage the kidneys?

A

cancer that causes excess plasma cell production
the loads of plasma cells produce even more antibodies and they can build up in the kidneys blocking flow through the tubules.

23
Q

what are some typical findings to look for on examination of AKI?

A

-hypovalaemia signs -dry mucous membranes, reduced skin turgor, tachycardia, hypotension
-volume overload signs -HTN, pulmonary oedema, peripheral oedema, elevated JVP
-uraemia signs -ecchymosis due to platelet dysfunction, uraemic encephelopathy (flap, confusion, seizures)
-signs of post renal obstruction -palpable or distended bladder

24
Q

what is ecchymosis?

A

bruise

25
Q

what are the indications for emergency renal replacement therapy for a AKI?

A

AEIOU:
acidosis (ph <7.15)
electrolyte abnormalities -K+ >6.5
ingested toxins (toxic alcohols, aspirin, lithium)
overloaded with fluid -diuretic resistant pulmonary oedema
uraemia -encephelopathy or pericarditis

26
Q

what are the potential causes of low albumin in someone unwell in hospital?

A

-protein enteropathies -bowel causing you to lose too much protein
-kidneys
-malnutrition
-liver

27
Q

what is post obstructive diuresis (POD)?

A

polyuric state in which copious amounts of salt and water are eliminated after the relief of a urinary tract obstruction.

28
Q

what is pulmonary renal syndrome?

A

the occurrence of renal failure in association with respiratory failure, characterised by autoimmune-mediated rapidly progressive glomerulonephritis (RPGN) and diffuse alveolar haemorrhage (DAH), respectively

29
Q

which recreational drug can cause haemoptysis?

A

crack cocaine

30
Q

what causes pulmonary renal syndrome?

A

almost always an autoimmune disorder: most common ones =goodpasture syndrome, SLE, GPA, microscopic polyangitis

31
Q

what are the basic diagnosis and treatment strategies for pulmonary renal syndrome?

A

diagnosis: blood tests, sometimes lung and renal biopsy
treatment: typically immunosuppression with corticosteroids and cytotoxic drugs

32
Q

what are the antibodies for goodpasture’s disease?

A

anti-GBM

33
Q

what actually is goodpastures disease/anti-GBM disease?

A

rare form of small vessel vasculitis, affects capillary beds and basement membranes of kidneys and lungs, autoimmune

34
Q

what is the treatment for goodpastures/anti-GBM?

A

plasma exchange to remove anti-GBM antibodies
prednisolone
cyclophosphamide

35
Q

what does pee look like in rhabdomylosis?

A

coca cola urine

36
Q

what is the management for rhabdo AKI?

A

admission
regular monitoring of U+E and CK
fluid resuscitation with 0.9% NaCl at rate of 10-15 ml/kg/h to achieve high urinary flow rates (>100ml/hour)
cautious addition of sodium bicarbonate 1.4% to maintain urinary pH >6.51.

37
Q

what leaks into the blood in rhabdomyolysis?

A

contents of muscle cells: potassium, phosphate, cK, urate, myoglobin

38
Q
A