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Renal > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What happens to plasma creatinine in AKI when there is a sudden drop in GFR?

A

Graph interpretation:

  • Top line: Patient with sudden 90% drop in GFR. If there is continued reduction the creatinine continues to climb (up to 5 days later).
  • Middle line: This patient has lost 90% GFR but has no further assault.
  • Bottom line: This patient has had the same insult, but has alread started to regain some GFR.
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2
Q

What assumptions are made with respect to GFR?

A
  • GFR assumes a steady state of creatinine production and filtration - creatinine production remains unchanged.
  • Slow rise in creatinine does not mean a continual change in GFR.
  • Urine output can add information about other kidney function such as water and solute excretion.
  • Clear time frame and staging based on outcome data.
  • It takes several days to reach a new steady state.
  • Inverse relationship between serum creatinine and creatinine clearance so relative changes rather than absolute.
  • Kinetic GFR can be helpful.
  • Cystatin C rises early and can be a useful early predictor of AKI.
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3
Q

How can AKI be recognised?

A
  • >50% rise increatinine or fall of >25% in eGFR within 7 days or urine output <0.6mL/kg/hour for 6 hours.
  • Use this table if a reference creatinine is not available from within the last 3 months.
  • If AKI is suspected tests should be repeated within 24 hours.
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4
Q

Describe the mortality rates associated with AKI stages 1-3.

What are the future risks of a patient who has had an AKI?

A
  • 23.9% mortality overall.
  • Increased risk for CKD in future.
  • 15-30% do not fully recover (the glomeruli do not recover).
  • Accounts for 5-10% of patients on RRT.
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5
Q

Describe the prevalence of AKIs.

A
  • Community acquired AKI’s account for 2/3 of all cases.
  • 5% of hospital admissions have a raised creatinine level.
  • In hospital ATN (acute tubular necrosis) mainly secondary to major surgery, bleeding and sepsis: 14% preventable.
  • CKD patients have fewer nephrons that are more likely to be injured, so AKI is more common.
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6
Q

What is a pre-renal cause of AKI?

A
  • Ineffective perfusion in otherwise normal kidneys.
  • Accounts for 50-65% of AKIs.
  • Caused by:
    • Hypovolaemia - reduced ECV.
    • Cardiac failure - reduced CO.
    • Hypotension / sepsis - reduced blood flow.
    • Vasoactivedrugs - NSAIDs and immunosuppressants.
  • All these pre-renal causes of AKI are risk factors for acute tubuar necrosis which is an intrinsic renal disease (renal cause of AKI).
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7
Q

Describe acute tubular necrosis.

A
  • PCT reabsorbs 70% of the glomerular filtrate, so high energy demand from mitochondria for active transport of Na and other solutes.
  • Cellular processes are disrupted by ischaemia through any of the three pre-renal processes so active transport is lost. Also tight junctions allowing cells to attach to each other are broken resulting in cell slough and frank necrosis.
  • Sloughed / necrotic cells block the tubular lumen increasing pressure, stopping glomerular filtration.
  • Swollen tubules block the vasa recta, reducing glomerular perfusion.
  • Reduced sodium reabsorption due to tubular damage increases Na at macula densa, releasing adenosine and causing further vasoconstriction.
  • There is delayed recovery in ATN to secondary ischaemia in the medulla due to cytokinesis release and mononuclear cell infiltrate and clot activation due to impaired vasodilation.
    • ATN usually recovers in 10-14 days.
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8
Q

What is the principal of sick day rules?

A
  • THEORY: dehydration leads to reduced renal perfusion and risk of AKI so stop drugs that are implicated in already affecting renal perfusion.

Diuretics

ACE-I / ARBs

Metformin (stopped due to high risk of metabolic acidosis)

NSAIDs

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9
Q

What are the risk factors for acute tubular necrosis?

A
  • Drugs:
    • ACE-I / ARBs.
    • NSAIDs - inhibit prostaglandin synthesis so causes vasoconstriction, reducing renal blood flow.
    • Diuretics
  • Pre-existing comorbidities:
    • Liver disease
    • CKD
    • Heart failure (poor CO; poor renal perfusion)
    • PVD (strongly associated with renal artery stenosis)
    • DiabetesMellitus
  • Age
  • Sepsis
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10
Q

What is a renal cause of AKI?

Give examples.

A
  • Damage to the renal apparatus - glomerulus / tubules as a direct result of an external toxin / antibody.
  • Accounts for 20-35% of AKIs.
    • Anti - GBM disease.
    • ANCA positive vasculitis (MPO / PR3).
    • Immune complexes (SBE / cryoglobulinaemia).
    • Tubular toxins (drugs / contrast / myoglobulin / light chains [Important because this cannot be picked up in urinalysis.

Patients over 50 admitted with AKI should be tested for myeloma] ).

* Crystals (uric acid / CaPO<sub>4</sub>.
* RPGN (rapidly progressive glomerulonephritis) - capillary wall necrosis and cells accumulating in Bowman space form crescents.
* AIN - 'allergic' reaction to toxin (penicillins / diuretics / PPIs) with neutrophils and eosinophils infiltrating the interstitium of the kidney.
* Gentamycin (levels must be monitored) accumulates in intracellular lysosomes and when toxic causes lysosomal rupture and cell death.
* Contrast injures proximal tubule and causes severe arterial vasoconstriction, reducing eGFR.
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11
Q

What would be found in the urine of any patient who has a renal cause of AKI?

A
  • Any patient with renal cause of AKI has blood AND protein.
  • Most important - what does the urine show?
  • Inflammation? Blood and protein in the urine? Think about renal causes.
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12
Q

What are the post-renal causes of AKI?

A
  • Accounts for 15% of all AKIs.
  • Obstruction to urine outflow.
  • Anuria is 99% of the time due to obstructive AKI.
  • History is important - prostatic symptoms, previous urological surgery?
  • Usually unilateral.
  • Picture = sloughed papilla. Seen in sickle cell anaemia.
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13
Q

What effect does a unilateral outflow obstruction have on creatinine levels compared with a bilateral outflow obstruction?

A
  • Unilateral obstruction effect on creatinine = nothing.
  • Need bilateral obstruction before you see a change in creatinine.
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14
Q

What are the complications of AKI?

A
  • The effects of AKI = uraemia.
  • Symptoms: anorexia, nausea, confusion, fatigue, oedema.
  • Life threatening effects of AKI:
    • Hyperkalaemia
    • Pulmonary oedema
    • Pericarditis - Renal pericarditis strongly associated with cardiac tampanade and is one of the indications for urgent dialysis.
  • Commonest cause of death = INFECTION.
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15
Q

Describe hyerkalaemia.

A
  • Generally, the definition is K+ >5.5mol/L.
  • Increased risk of hyperkalaemia in:
    • Established CKD (reduced GFR).
    • Metabolic acidosis (K+ shift extracellularly).
    • Drug effects.
    • Cardiac arrhythmia.
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16
Q

Describe the ECG changes associated with hyperkalaemia.

A
  • Increased risk when K+ > 6.5.
  • Reduction in resting membrane potential.
  • Increased cardiac depolarisation.
  • Muscle excitability.
    • More prominent in atrial myocardium.
17
Q

Which drugs make an individual predisposed to developing AKI?

A
  • ACE-I/ARB - impairment of aldosterone secretion causes reduced renal perfusion and so decreased K+ excretion in the distal tubule.
  • NSAIDs - inhibit prostaglandin synthesis, reduce renin, decrease aldosterone etc.
  • Spironolactone and Eplenerone - block aldosterone binding to mineralocorticoid receptor.
  • K+-sparing diuretics and Trimethoprim - inhibit activity of epithelial sodium channel.
18
Q

Describe the basic management of mild, moderate and severe AKI.

A
  • Mild - stop drugs.
  • Moderate - stop drugs, ?admit.
  • Severe - ADMIT.
19
Q

Why would calcium be used in the management of a patient with AKI?

A
  • IV calcium - increasing calcium reduces the depolarisation effect of an elevated K+ on cardiac myocytes.
  • Effective in 3 minutes, lasts 30-60 minutes only.
  • Options for administration:
    • CaCl2 - increased concentration of ionised calcium.
    • Ca gluconate - may require more than one dose.
20
Q

How much calcium would you be giving a patient by administering 10mL 10% calcium chloride?

A

10mL 10% calcium chloride = 6.8mmol Ca2+

21
Q

How much calcium would you be giving a patient by administering 10mL 10% calcium gluconate?

A

10mL 10% calcium gluconate = 2.26mmol Ca2+

22
Q

Why would you give insulin dextrose to a patient with kyperkalaemia?

What effect does co-administration of salbutamol have on this?

23
Q

What effect does pulmonary oedema have on the kidneys?

A
  • Potentially life-threatening.
  • If patient is anuric they need dialysis.
  • Give diuretics - but what about a patient with AKI?
    • ​Life and heart trump kidneys so prescribe diuretics anyway.

Renal (10 decks)

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