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.
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.
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.
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.
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.
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).
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.
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
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
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.
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.
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.
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.
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.
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.
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.
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.
22
Q
Why would you give insulin dextrose to a patient with kyperkalaemia?
What effect does co-administration of salbutamol have on this?
A
