AKI

Question 1

What is an AKI?

Answer 1

Abrupt decline in kidney function (decline in actual GFR, disrupted acid base and electrolytes, build up of urea)

Question 2

3 categories of AKI

Answer 2

Pre-renal, intrinsic, post-renal

Question 3

Name pre-renal causes

Answer 3

Hypotension, hypovolemia e.g. trauma, vomiting, dehydration, diarrhoea, sepsis, anaphylaxis (systemic vasodilation). NSAIDs make afferent constrict, ACEi/AIIR antagonists make efferent dilate.
In other countries from malaria, secondary to pregnancy.

Question 4

Explain the mechanism behind pre-renal AKIs

Answer 4

The actual GFR decreases due to decreased blood flow. PGs dilate afferent and AgII constricts efferent but if this can’t compensate enough you get AKI.

Question 5

Are pre-renal AKIs responsive to fluids?

Answer 5

Yes, at least initially. If it starts to damage the kidney it may become fluid unresponsive and progress to ATN (acute tubular necrosis)

Question 6

What is ATN?

Answer 6

Acute tubular necrosis- a cause of intrinsic AKIs. Misnomer because not actually necrosis, cells are alive but just damaged.

Question 7

Is ATN responsive to fluids?

Answer 7

No, cells are already damaged- risk of fluid overload

Question 8

Causes of ATN?

Answer 8

Sepsis, nephrotoxins, ischaemia

Question 9

Name some nephrotoxins

Answer 9

Myoglobin, urate, bilirubin, x-ray contrast, NSAIDs

Question 10

What’s the problem with myoglobin?

Answer 10

Can cause rhabdomyolysis- causes coke coloured urine ‘myoglobinuria’ and damages kidney, causing AKI from ATN. Symptoms include muscle pain, confusion, vomiting, weakness.

Question 11

Causes of rhabdomyolysis?

Answer 11

Crush injury, unconscious and immobile muscle

Question 12

In ATN which parts of the nephron get damaged first?

Answer 12

PCT and TAL of LoH because they have the highest O2 demands and aren’t close to the glomerulus

Question 13

Causes of intrinsic AKIs?

Answer 13

ATN, acute interstitial nephritis (an inflam response from toxins or infection, invasion of eosinophils), malignant hypertension, small vessel disease e.g. microangiopathic haemolytic anemia, haemolytic uremic syndrome, pre-eclampsia,

Question 14

Causes of post-renal AKIs?

Answer 14

Obstruction. More common in elderly. Must occur in both kidneys or the only functioning kidney

Question 15

Mechanism of problem with post-renal AKIs?

Answer 15

Blocked ureter, raises intraluminal pressure, renal pelvis dilatation (hydropnephrosis=swollen kidney from urine), renal function decreases

Question 16

What happens clinically in AKIs?

Answer 16

Actual GFR down, urea and creatinine up, reduction in GFR means less HCO3 reabsorbed and regenerated and less HCl- excreted, acidosis –> hyperkalemia because H K pump used more, hyperkalemia means arrythmias

Question 17

What can we do to protect the heart from hyperkalemia?

Answer 17

Calcium gluconate

Question 18

ECG changes in hyperkalemia?

Answer 18

Progressive changes- tall T waves, small P waves, wide QRS, sine waves –> arrest

Question 19

What investigations are appropriate in AKIs?

Answer 19

Urinalysis in all, microscopy if sign of infection, all USS <24hrs, CXR for fluid overload and infection. only biopsy if all pre and post renal causes have been ruled out

Question 20

When is dialysis appropriate?

Answer 20

Nephrotoxins ongoing damage, not responding to diuretics, signs of uremia, if can’t fix hyperkalemia

Question 21

Commonest cause of AKI?

Answer 21

Pre-renal- Hypotension or dehydration

Question 22

Oliguria?

Answer 22

<500ml urine/day or <20ml/hour