Acute Kidney Injury

Question 1

What is the current definition of acute renal failure stage 1?

Answer 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

Question 2

AKI stage 2?

Answer 2

2-2.9 x baseline

Question 3

AKI stage 3?

Answer 3

3x baseline
OR
Increase to ≥354 μmol/l 
OR
Initiation of renal replacement therapy

Question 4

What is the incidence of AKI in a hospital setting?

Answer 4

1 in 5 (or 7) patients admissions are complicated by AKI affected

Question 5

What is the incidence of AKI in a community setting?

Answer 5

Uncommon - 1.5% per year

Question 6

What is the incidence of AKI in an ITU setting?

Answer 6

More than 50%

Question 7

Immediately Dangerous consequences of AKI?

Answer 7

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

Question 8

Outcomes of AKI?

Answer 8

Shirt term - death, dialysis, increased length of stay

Long term - death, CKD, dialysis, CKD related CV events

Question 9

Subcategories of causes of AKI?

Answer 9

Pre-renal
Intrinsic
Post-renal

Question 10

Pre-renal causes

Answer 10

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

Question 11

Intrinsic renal causes ?

Answer 11

Damage to renal parenchyma

1. Most commonly due to acute tubular necrosis/injury

Also due to:

2. Tubulointerstitial injury
   Glomerulonephritis or other disease affecting the renal artery/arterioles
3. Myeloma
4. Vasculitis

Question 12

What is pyelonephritis

Answer 12

Inflammation of the kidney, typically due to a bacterial infection

Question 13

How can prolonged pre-renal AKI lead to intrinsic AKI?

Answer 13

If prolonged to the point where autoregulation fails - causes ischemic acute tubular necrosis

Question 14

What can cause acute tubular necrosis/injury?

Answer 14

Prolonged renal AKI
Rhabdomyolysis
Nephrotoxins

Question 15

Name some nephrotoxins.

Answer 15

Iodinated contrast
NSAIDs
Gentamicin

Question 16

Post renal AKI causes?

Answer 16

Kidney stones
Prostatic hypertrophy
Tumours
Retroperitoneal fibrosis

Question 17

What is most common cause of AKI?

Answer 17

Poor perfusion leading to established tubule damage (pre-renal) leading to intrinsic acute tubular necrosis

Question 18

Why is the kidney so susceptible to hypoperfusion?

Answer 18

Cortex is richly perfused by medulla is not even though it is metabolically active

Question 19

Course of acute ischaemic tubular necrosis and recovery?

Answer 19

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

Question 20

What happens if GFR recovers faster than the tubule resorptive ability?

Answer 20

= excessive diruresis

Question 21

What is it called when AKI is caused by administration of an iodinated contrast agent?

Answer 21

Radiocontrast nephropathy

Question 22

Explain radiocontrast nephropathy?

Answer 22

A common hospital acquired AKI

Usually transient renal dysfunction and resolved after 72 hours

May lead to permanent loss of function

Question 23

Risk factors for radiocontrast nephropathy?

Answer 23

DM
Renovascular disease
Impaired renal function
Paraprotein
High levels of contrast

Question 24

What is multiple myeloma?

Answer 24

A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains

2nd most common haematological malignancy

Question 25

Renal failure in myeloma looks like...?

Answer 25

Cast nephropathy Light chain nephropathy Amyloidosis Hypercalcamia and hyperuricemia

Question 26

Investigations for AKI - how would post-renal be ruled out?

Answer 26

Clinical examination - feeling a distended bladder Catheter draining large volumes of urine USS detecting obstruction

Question 27

Investigations for AKI - how would pre-renal be ruled out?

Answer 27

Clinical examinations Assessing volume status Pre and intrinsic difficult to differentiate since so closely linked

Question 28

Other investigations?

Answer 28

Blood tests Urine tests Renal biopsys Radiology

Question 29

How to prevent AKI in hospital setting?

Answer 29

Avoid dehydration Avoid nephrotoxic drugs Optimise BP and volume status Treat/watch for sepsis

Question 30

What nephrotoxic drugs are there?

Answer 30

NSAIDs Gentamicin IV iodinated contrast

Question 31

Management of Pre, intrinsic and post?

Answer 31

Pre - do they need fluid? BP support. Treat cause Intrinsic - Remove the precipitant? Post - catheters Treat the cause

Question 32

5 things to consider in management?

Answer 32

``` 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? ```

Question 33

How can we stop it getting worse?

Answer 33

Support BP - vasopressors and stop anti-hypertensives

Question 34

What is a dangerous consequences of AKI?

Answer 34

Hyperkalaemia

Question 35

How do we manage hyperkalaemia?

Answer 35

Stabilize myocardium with calcium gluconate Shift K into cells - salbutamol or insulin-dextrose Remove K using dialysis, diuresis or anion exchange resins

Question 36

Indications for dialysis in AKI?

Answer 36

Using AEIOU ``` A - a reduced Bicarb E - increase in K+ I - blank O - pulmonary odeama U - pericarditis ```