Acute Kidney Injury Flashcards
What is the current definition of acute renal failure stage 1?
Increase in serum creatinine by ≥26.5 μmol/l within 48 hours
OR
to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days
Urine volume <0.5 ml/kg/h for 6 hours
AKI stage 2?
2-2.9 x baseline
AKI stage 3?
3x baseline OR Increase to ≥354 μmol/l OR Initiation of renal replacement therapy
What is the incidence of AKI in a hospital setting?
1 in 5 (or 7) patients admissions are complicated by AKI affected
What is the incidence of AKI in a community setting?
Uncommon - 1.5% per year
What is the incidence of AKI in an ITU setting?
More than 50%
Immediately Dangerous consequences of AKI?
Body fluid, acid base and electrolyte homeostasis affected
Excretory function at risk
AEIOU good to remember Acidosis Electroylte imbalance Intoxication via TOXINS Overload Uraemic complications
Outcomes of AKI?
Shirt term - death, dialysis, increased length of stay
Long term - death, CKD, dialysis, CKD related CV events
Subcategories of causes of AKI?
Pre-renal
Intrinsic
Post-renal
Pre-renal causes
Hypovolaemia of any cause - dehydration due to diuretics or vomiting, haemorrhage, burns
Hypotension without
hypovolaemia - cirrhosis or septic shock
A low CO - cardiac failure or cardiogenic shock
Intrinsic renal causes ?
Damage to renal parenchyma
- Most commonly due to acute tubular necrosis/injury
Also due to:
- Tubulointerstitial injury
Glomerulonephritis or other disease affecting the renal artery/arterioles - Myeloma
- Vasculitis
What is pyelonephritis
Inflammation of the kidney, typically due to a bacterial infection
How can prolonged pre-renal AKI lead to intrinsic AKI?
If prolonged to the point where autoregulation fails - causes ischemic acute tubular necrosis
What can cause acute tubular necrosis/injury?
Prolonged renal AKI
Rhabdomyolysis
Nephrotoxins
Name some nephrotoxins.
Iodinated contrast
NSAIDs
Gentamicin
Post renal AKI causes?
Kidney stones
Prostatic hypertrophy
Tumours
Retroperitoneal fibrosis
What is most common cause of AKI?
Poor perfusion leading to established tubule damage (pre-renal) leading to intrinsic acute tubular necrosis
Why is the kidney so susceptible to hypoperfusion?
Cortex is richly perfused by medulla is not even though it is metabolically active
Course of acute ischaemic tubular necrosis and recovery?
IMR
Initiation - exposure to toxic/ischaemic insult leading to the parenchymal injury = AKI is still preventable
Maintenance - an established parenchymal injury. Patient will be maximally oliguric now. This can last typically 1-2 weeks but also several months
Recovery - Gradual increase in urine output and fall in serum creatinine
What happens if GFR recovers faster than the tubule resorptive ability?
= excessive diruresis
What is it called when AKI is caused by administration of an iodinated contrast agent?
Radiocontrast nephropathy
Explain radiocontrast nephropathy?
A common hospital acquired AKI
Usually transient renal dysfunction and resolved after 72 hours
May lead to permanent loss of function
Risk factors for radiocontrast nephropathy?
DM Renovascular disease Impaired renal function Paraprotein High levels of contrast
What is multiple myeloma?
A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains
2nd most common haematological malignancy
Renal failure in myeloma looks like…?
Cast nephropathy
Light chain nephropathy
Amyloidosis
Hypercalcamia and hyperuricemia
Investigations for AKI - how would post-renal be ruled out?
Clinical examination - feeling a distended bladder
Catheter draining large volumes of urine
USS detecting obstruction
Investigations for AKI - how would pre-renal be ruled out?
Clinical examinations
Assessing volume status
Pre and intrinsic difficult to differentiate since so closely linked
Other investigations?
Blood tests
Urine tests
Renal biopsys
Radiology
How to prevent AKI in hospital setting?
Avoid dehydration
Avoid nephrotoxic drugs
Optimise BP and volume status
Treat/watch for sepsis
What nephrotoxic drugs are there?
NSAIDs
Gentamicin
IV iodinated contrast
Management of Pre, intrinsic and post?
Pre - do they need fluid? BP support. Treat cause
Intrinsic - Remove the precipitant?
Post - catheters
Treat the cause
5 things to consider in management?
Do they need fluid? Can you remove the precipitant? Can you stop it getting worse? Do they need a catheter? How to make them safe?
How can we stop it getting worse?
Support BP - vasopressors and stop anti-hypertensives
What is a dangerous consequences of AKI?
Hyperkalaemia
How do we manage hyperkalaemia?
Stabilize myocardium with calcium gluconate
Shift K into cells - salbutamol or insulin-dextrose
Remove K using dialysis, diuresis or anion exchange resins
Indications for dialysis in AKI?
Using AEIOU
A - a reduced Bicarb E - increase in K+ I - blank O - pulmonary odeama U - pericarditis
