10 - AKI

Question 1

Define AKI

Answer 1

A decline in GFR that occurs within a short space of time, measured by a rise in serum creatinine and fall in urine output

Question 2

Define oliguria

Answer 2

Less than 500ml of urine per day

Question 3

Define anuria

Answer 3

Less than 100ml of urine per day

Question 4

Why is the threshold for oliguria 500ml urine excretion per day?

Answer 4

Because the amount of cellular waste that needs excreting is 600 mOsmol/day and the kidneys can concentrate urine up to 1200 mOsmol/day. Therefore minimum excretion is 0.5 l

Question 5

What is the definition of pre-renal disease?

Answer 5

Decreased renal perfusion

Question 6

Describe the process of pre-renal disease

Answer 6

Renal perfusion decreases due to renal artery occlusion or vasculitis. Or reduced circulating volume, due to hypovolaemia or systemic vasodilation (sepsis/cirrhosis/anaphylaxis) Kidneys increase prostaglandins (to dilate AA) and decrease circulating vasoconstrictors eg Ang II (constrict EA) to maintain a normal glomerular capillary pressure. Aldosterone and ADH are released to reabsorb salt and water.

Question 7

What can affect intrinsic autoregulatory mechanisms of renal perfusion?

Answer 7

NSAIDs can block prostaglandins from vasodilating AA
Sepsis can cause AA vasoconstriction
ACE inhibitors block ang II from vasoconstricting EA
Diabetes and high BP can affect AA

Question 8

What is the consequence of untreated pre-renal disease?

Answer 8

Acute tubular necrosis

Question 9

What are the causes of acute tubular necrosis?

Answer 9

Ischaemia (depletion of ATP)
Nephrotoxins
Sepsis

Question 10

What is the order that blood flows through the kidney in?

Answer 10

Interlobular artery
Afferent arteriole
Glomerular capillary 
Efferent arterioles
Peritubular capillaries 
Interlobular veins

Question 11

What part of the kidney will be damaged in acute tubular necrosis?

Answer 11

Proximal tubules, distals will be fine due to their lower o2 demand

Question 12

How can you distinguish between pre-renal disease and acute tubular necrosis?

Answer 12

Pre-renal disease shows a high urine osmolarity, ATN will be low.
Pre-renal will have a low urinary Na, ATN will have a high urinary Na

Question 13

Where do nephrotoxins affect?

Answer 13

The epithelial lining of tubules

Question 14

Name endogenous nephrotoxins

Answer 14

Myoglobin
Urate
Bilirubin

Question 15

Name exogenous nephrotoxins

Answer 15

Endotoxin
X-ray contrast
Drugs - NSAIDs and gentamicin (antibiotic for pseudomonas, Ecoli and gram positive staphylococcus)
Poisons (antifreeze)

Question 16

What is rhabdomyolysis?

Answer 16

Muscle necrosis releasing myoglobin, causing acute tubular necrosis

Question 17

How does rhabomyolysis cause ATN?

Answer 17

Muscle necrosis releases myoglobin, a nephrotoxin, which is filtered at the kidneys and is toxic to tubule cells.

Question 18

What colour does rhabdomyolysis turn urine?

Answer 18

Very dark

Question 19

How does thrombotic microangiopathy lead to AKI?

Answer 19

Damaged endothelial cells cause turbulent blood flow, causing RBCs to become deformed and burst. This activates platelets, causing clots to form. This can block arteries perfusing the kidneys.

Question 20

What causes thrombotic microangiopathy?

Answer 20

Haemolytic uraemic syndrome
Malignant hypertension
Scleroderma
Pre-eclampsia

Question 21

What causes acute interstitial nephritis?

Answer 21

Inflammatory response

Drugs: NSAIDs, PPIs, antibiotics

Question 22

Define hydronephrosis

Answer 22

Dilation of the renal pelvis

Question 23

How do obstructions cause post-renal failure?

Answer 23

Cause an increase in intraluminal pressure, causes hydronephrosis, decreasing renal function

Question 24

What are the types of post-renal failure?

Answer 24

Within the lumen of kidney/ureter/bladder: Stones, blood clots and tumours
Within the wall: Ureter stricture post TB, congenital megaureter
Pressure from outside: Enlarged prostate, tumour, aortic aneurysm, ligation of ureter

Question 25

What are serum biochem results may indicate AKI?

Answer 25

``` High urea High creatinine Metabolic acidosis Hyperkalaemia + hyperphosphataemia Hyponatraemia + Hyphosphataemia ```

Question 26

Why is acidosis a sign of AKI?

Answer 26

Reduced GFR causes impaired reabsorption of HCO3 so acid excretion is reduced

Question 27

What are the causes of hyperkalaemia?

Answer 27

Movement out of cells: Acidosis, hypertonicity, muscle damage Reduced urine loss: Reduced GFR, reduced distal delivery of Na (oliguric AKI/obstruction) Drugs: RAAS inhibitors - ACE inhibitors and spironolactone. NSAIDs ENaC blockers- Amiloride and trimethoprim

Question 28

Describe the progressive ECG changes in hyperkalaemia

Answer 28

``` Tall T waves Absent p waves Increased p-r interval Wide QRS complex Sine wave pattern Asystole ```

Question 29

What parenchymal renal diseases causes renal AKI?

Answer 29

Pyelonephritis, glomerulonephritis, acute interstitial nephritis

Question 30

When is dialysis considered with AKI?

Answer 30

``` Hyperkalaemia despite treatment Metabolic acidosis Fluid overload despite diuretics Uraemia: Pericarditis, reduced consciousness Dialysable nephrotoxin (asprin overdose) ```

Question 31

What are the risk factors for AKI?

Answer 31

Exposure: Volume depletion/dehydration, sepsis, nephrotoxins, X ray contrast, surgery Susceptibilities: Old age, CKD, diabetes, cancer, heart and liver disease