AKI

Question 1

What is associated with AKI?

Answer 1

Falling urine output, rising serum urea and creatinine

Question 2

What does an AKI result from?

Answer 2

Prerenal, reduced kidney perfusion leads to falling GFR
Renal parenchymal disorders (injury to glomerulus, tubule or vessels)
Urinary tract obstruction (post renal, functioning kidneys cannot excrete urine with back pressure affecting function

Question 3

What are common causes of prerenal AKI?

Answer 3

Hypovolaemia (dehydration and haemorrhage)
Hypotension (cirrhosis or septic shock)
Low cardiac output

Question 4

What are common infrarenal causes of AKI?

Answer 4

NSAIDs
ACE inhibitors
Amphotericin B and calcineurin inhibitors

Question 5

What are common causes of post renal AKI?

Answer 5

Bladder outflow obstruction (prostate disease)

Bilateral ureteric obstruction (stones or tumours)

Question 6

What is renal parenchymal AKI?

Answer 6

Most commonly (80-90%) due to acute tubular necrosis 
Ischaemia or direct tubular toxins

Question 7

How do you tell the difference between prerenal and intrinsic causes of renal failure?

Answer 7

Urine osmolality: high in prerenal, low in intrinsic

Urine sodium: low in prerenal, high in intrinsic

Question 8

What are the causes fo acute tubular necrosis?

Answer 8

Haemorrhage
Burns 
Diarrhoea and vomiting, fluid loss from fistulae 
Acute pancreatitis 
Diuretics 
Myocardial infarction
Congestive cardiac failure 
Endotoxic shock 
Snake bite 
Myoglobinaemia 
Haemoglobinaemia (due to haemolysis, e.g. in falciparum malaria, ‘blackwater fever’) 
Hepatorenal syndrome 
Radiological contract agents 
Drugs, e.g. aminoglycosides, NSAIDs, ACE inhibitors, platinum derivatives 
Abruptio placentae 
Pre-eclampsia and eclampsia

Question 9

What are the biochemical abnormalities seen in AKI?

Answer 9

Hyperkalaemia
Metabolic acidosis (unless vomiting) 
Hyponatraemia 
Hypocalcaemia 
Hyperphosphataemia

Question 10

What are the symptoms of uraemia?

Answer 10

Weakness, fatigue, anorexia, nausea and vomiting
Mental confusion, seizures and coma
Pruritus and bruising (impaired platelets)
Breathlessness (anaemia dn pulmonary oedema secondary to fluid overload)
Pericardiits in severe untreated
Infection

Question 11

What are the investigations for a uraemic emergency?

Answer 11

Blood count- anaemia and high ESR (myeloma or vasculitis)
Urine dip- haematuria and proteinuria (glomerulonephritis)
Urinary electrolytes
Serum calcium, phosphate and uric acid
Renal USS(exclude obstruction)
Histological investigations- renal biopsy in unexplained and normal sized kidneys

Question 12

What are the complications of an AKI?

Answer 12

Sepsis- impaired immune defence and instrumentation

Renal function recovers in 1-3 weeks

Question 13

What are the indications for dialysis and/or haemofiltration in AKI?

Answer 13

Progressive uraemia with encephalopathy or pericarditis
Severe biochemical derangement, especially if there is a rising trend in an oliguric patient and in hypercatabolic patients
Hyperkalaemia not controlled by conservative measures
Pulmonary oedema
Severe metabolic acidosis: pH<7.1
For removal of drugs causing the AKI, e.g. gentamicin, lithium, severe aspirin overdose

Question 14

What criteria indicates a AKI?

Answer 14

Urine output <0.5ml/kg/h for 6 hours
>50% rise in creatinine over 7 days
>26micromol rise in creatinine over 48h

Question 15

What is stage 1 AKI?

Answer 15

Serum creatinine: 150-200% increase or 25micromol/l increase in 48h
Urine output: <0.5ml/kg/h for 6h

Question 16

What is stage 2 AKI?

Answer 16

Serum creatinine: 200-300% increase

Urine output: <0.5ml/kg/h for 12h

Question 17

What is stage 3 AKI?

Answer 17

Serum creatinine: >300% increase or >350micromol/l with acute rise of >45micromol/l in 48h
Urine output: <0.3ml/kg/h for 24h or anuria for 12h

Question 18

What is pre-renal AKI aetiology?

Answer 18

Inadequate renal perfusion (75%)
Shock: hypovolaemic, cardiogenic, distributive
Renovascular obstruction: embolus, aortic dissection, renal artery stenosis (RAS), thrombosis, ACEIs given in bilateral RAS
Prolonged = acute tubular necrosis –> pourous tubular membranes
Initially, urine osmolarity is high (>500mosmol/kg) + low sodium
If ATN occurs, urine is isotonic with plasma + high sodium

Question 19

What is post-renal AKI aetiology?

Answer 19

Urinary tract outflow obstruction –> hydronephrosis
Ureter stones, stricture, clots, malignancy
Bladder outlet obstruction (prostatic enlargement, urethral stricture, phimosis/paraphimosis)

Question 20

What causes acute tubular necrosis?

Answer 20

85% of renal AKI
Drugs/toxins damaging tubular cells
Drugs: aminoglycosides (antibiotic ‘-mycin’), cephalosporins (antibiotic ‘cef-‘), radiological contrast mediums, NSAIDs
Toxins: heavy metal poisoning, myoglobinuria, haemolytic uraemic syndrome

Question 21

What are the first line investigations for an AKI?

Answer 21

Hypotension/hypertension (CKD)
Palpable bladder? 
Bloods: FBC (renal anaemia in CKD), U&Es, bicarbonate, phosphate, CRP, clotting (hepatorenal disease may need invasive procedures), creatine kinase (raised in myoglobinurea) 
Nephritic screen if cause unclear 
ABG 
Urine dip and MCS 
ECG (risk of hyperkalaemia) 
Renal USS (post-renal causes) 
Non-contrast CT (if suspect obstucting calculus) 
Echo (if suspect uraemic pericarditis)

Question 22

What are common electrolyte abnormalities in AKI?

Answer 22

Rapidly progressing uraemia (anorexia, vomiting, pruritis, encephalopathy, haemorrhagic episodes)
Hyperkalaemia
Hypernatraemia (unless pre-renal)
Metabolic acidosis
Hypocalcaemia/hypophosphataemia (more in CKD)

Question 23

How do differentiate an AKI from dehydration?

Answer 23

AKI would present with a proportionally greater rise in creatinine than urea (very high creatinine)
Dehydration rise in urea is proportionally bigger than rise in creatinine