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Flashcards in Acute Kidney Injury Deck (23)
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What happens to plasma creatinine in AKI when there is a sudden drop in GFR?

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.


What assumptions are made with respect to GFR?

  • 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. 


How can AKI be recognised?

  • >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. 


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

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

  • 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. 


Describe the prevalence of AKIs.

  • 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. 


What is a pre-renal cause of AKI?

  • 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). 


Describe acute tubular necrosis.

  • 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. 


What is the principal of sick day rules?

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



Metformin (stopped due to high risk of metabolic acidosis)



What are the risk factors for acute tubular necrosis?

  • 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


What is a renal cause of AKI?

Give examples.

  • 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 / CaPO4.
    • 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. 


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

  • 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.


What are the post-renal causes of AKI?

  • 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. 


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

  • Unilateral obstruction effect on creatinine = nothing. 

  • Need bilateral obstruction before you see a change in creatinine.


What are the complications of AKI?

  • 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. 


Describe hyerkalaemia.

  • 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. 


Describe the ECG changes associated with hyperkalaemia.

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


Which drugs make an individual predisposed to developing AKI?

  • 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. 


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

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


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

  • 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. 


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

10mL 10% calcium chloride = 6.8mmol Ca2+


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

10mL 10% calcium gluconate = 2.26mmol Ca2+


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

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


What effect does pulmonary oedema have on the kidneys?

  • 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.