AKI

Question 1

Define AKI

Answer 1

Clinical syndrome

Abrupt decline in actual GFR

Upset of ECF volume, electrolyte and acid-base homeostasis

Accumulation of nitrogenous waste products

Question 2

When is a spike in creatinine seen after kidney insult?

Answer 2

4-7 days

Question 3

What criteria give a diagnosis of AKI?

Answer 3

Increase in serum creatinine by ≥ 26.5 μmol/L within 48 hours

Increase in serum creatinine by ≥1.5 times baseline within 7 days

Urine volume <0.5 ml/kg/h for 6 hours

Question 4

How is kidney function measured in AKI?

Answer 4

Actual GFR

Question 5

What % of hospitalised pts have AKI?

Answer 5

5%

Question 6

Outline the major causes of AKI

Answer 6

Pre-renal failure = blood isn’t getting to kidney

Intrinsic renal failure = damage inside the kidney, acute tubular necrosis, thrombotic microangiopathy

Post-renal failure = blocking urine coming out, blocking renal vein

Question 7

What are the commonest causes of AKI globally?

Answer 7

Hypotension

Dehydration

Question 8

Outline pre-renal AKI

Answer 8

Actual GFR reduced due to decreased renal blood flow

No cell damage so kidneys works hard to restore blood flow

Avidly reabsorption of salt and water (aldosterone and ADH release)

Responds to fluid resuscitation i.e. potentially reversible

Question 9

What are the causes of pre-renal AKI

Answer 9

Hypovolaemia, systemic vasodilation, cardiac failure, pre-glomerular vasoconstriction, post-glomerular vasodilation

Question 10

How do ACEi and NSAIDs affect renal perfusion?

Answer 10

ACEi = inhibit AngII vasoconstriction on EA

NSAIDs = inhibit PG vasodilation of AA

Question 11

What causes acute tubular necrosis?

Answer 11

Ischaemia = proximal tubules, thick ascending loop

Nephrotoxins = damage ep that lines tubules causing death, rhabdomyolysis release of myoglobin toxic to tubule cells

Sepsis

Question 12

What are the causes intrinsic renal failure?

Answer 12

Acute tubular necrosis

Thrombotic microaniopathy

Toxins

Infections

Question 13

What is thrombotic microangiopathy?

Answer 13

Endothelial damage = platelet thrombi = partial obstructions of small arteries = destruction of RBCs = microangiopathic haemolytic anaemia

Question 14

Outline the pathophysiology of post-renal AKI

Answer 14

Obstruction with continues urine prod = rise in intraluminal pressure = dilation of renal pelvis = decreased renal function

Question 15

What causes post-renal AKI?

Answer 15

Within the lumen = stones, clots, tumours

Within the wall = congenital megaureter

Pressure from outside = enlarged prostate, tumour, aortic aneurysm

Question 16

Regarding AKI what is seen in a serum biochem test?

Answer 16

Raised urea

Raised creatinine

Question 17

What diagnostic approach is used to establish AKI?

Answer 17

Dipstick = detection of blood, protein, leucocytes

Urine microscopy = culture is dipstick +ve

USS = looking for obstruction

CXR = look for fluid overload, +/- infection

Kidney biopsy

Question 18

If blood and protein is present on a urine dip what is likely?

Answer 18

Intrinsic renal disease

Question 19

Outline the management for AKI

Answer 19

Vol over load = restrict dietary Na/water

Hyperkalaemia = calcium gluconate, restrict dietary K, stop K sparing diuretic

Dialysis = if other treatment isnt working

Question 20

In what diff disorders can renal ischaemia lead to reduced GFR?

Answer 20

Acute tubular necrosis