Acute kidney injury

Question 1

Define acute kidney injury.

Answer 1

Reversible decrease in GFR over hours, days or weeks with increases in creatinine and urea levels and decreased urine output

Question 2

Name the 4 main broad causes of a pre-renal AKI.

Answer 2

1) Sudden/ severe drop in BP (hypotension)
2) Hypovolaemia
3) Impaired cardiac pump efficiency
4) Vascular disease leading to hypo perfusion.

Question 3

Which mechanism normally allows GFR to be maintain in instances of insult to the kidneys?

Answer 3

Autoregulation.

Question 4

How is normal GFR maintained when there is severe or prolonged hypovolaemia and resultant decreased systemic pressure?

Answer 4

Prostaglandin and angiotensin-II production intrarenally.

Question 5

In a pre-renal AKI caused by hypovolaemia/ hypo perfusion, what causes an increased blood urea nitrogen level?

Answer 5

Reduced perfusion of the kidneys > reduced GFR > renin released > RAAS upregulated > reabsorption of sodium and water in renal tubules > sodium reabsorption co-exists with urea reabsorption > increased BUN levels.

Question 6

Why can NSAIDs be classed as a cause of pre-renal AKI?

Answer 6

Inhibition of prostaglandin formation causes afferent arteriole vasoconstriction which can precipitate renal ischaemia.

Question 7

How are pre-renal AKIs characterised in the early stages?

Answer 7

Lack of structural damage and rapid reversibility once perfusion is restored.

Question 8

Describe the following laboratory findings for a pre-renal AKI:

a) BUN:creatinine
b) Urine sodium
c) FeNa
d) Serum sodium
e) Urine osmolarity

Answer 8

a) high (>20:1)
b) Low (<20mEq/L)
c) <1%
d) High
e) High (>500)

Question 9

1) Why might hyaline casts be present in the urine of patients with a prerenal AKI?
2) Why is there a high urine osmolarity but low urine sodium in pre-renal AKIs?
3) What could all causes of pre-renal AKI lead to if the AKI is sustained?

Answer 9

1) Due to the presence of hypovolaemia which results in concentrated urine.
2) Urine is typically concentrated due to Na+ and water reabsorption, meaning that urine osmolarity is high.
3) Ischaemic tubule cell injury.

Question 10

What is acute kidney injury a syndrome of?

Answer 10

Decreased renal function
Increased serum urea and creatinine due to decreased GFR
Decreased urine output

Question 11

Name the 7 most common causes for AKIs in general.

Answer 11

1) Sepsis
2) Major surgery
3) Cardiogenic shock
4) Other hypovolaemia
5) Drugs
6) Hepatorenal syndrome
7) Obstruction

Question 12

1) What is true hypovolaemia?

2) Give 3 causes of true hypovolaemia.

Answer 12

1) Lower circulating blood volume, usually with a history of blood loss.
2) Diarrhoea, burns and haemorrhages.

Question 13

1) What is relative hypovolaemia?

2) Name 3 causes of relative hypovolaemia.

Answer 13

1) Normal circulating volume but low BP.

2) Heart failure, septic shock and hepatorenal syndrome.

Question 14

Describe the staging of AKIs.

Answer 14

stage 1: serum creatinine >0.3mg/dL or 1.5-1.9 x baseline and urine output <0.5mL/kg/hr for 6-12 hours.

stage 2: serum creatinine 2.0-2.9 x baseline or urine output <0.5mL/kg/hr for >12 hours.

stage 3: serum creatinine >4.0mg/dL or >3.0 x baseline or on RRT and urine output <0.3mL/kg/hr for >24 hours or anuria for >12 hours.

Question 15

1) Which type of classification of AKI is the most common?

2) How can infrarenal AKIs occur?

Answer 15

1) Infrarenal AKIs
2) Through direct damage to the kidney tubules or interstitium by inflammatory, infection, drug-related or autoimmune causes.

Question 16

What is the most common cause of infrarenal AKIs?

Answer 16

Acute tubular necrosis due to pre-renal obstruct or direct renal toxins.

Question 17

1) When acute tubular necrosis occurs, which cells of the nephron are more commonly affected?
2) What happens to the epithelial cells when they become damaged?

Answer 17

1) Epithelial cells in the PCT and in the thick ascending limb are most affected.
2) When epithelial cells become damaged they slough off, accumulate and aggregate together in the renal tubule. This can cause an obstruction, causing high pressure behind it = reduced movement of filtrate = decreased GFR.

Question 18

Name 6 drugs which can coordinate acute tubular necrosis.

Answer 18

1) Gentamicin
2) Ciclosporin
3) Cisplatin
4) Alkaloids
5) Lead
6) Radiocontrast media

Question 19

Why may a person suffering an infrarenal AKI have brown granular casts in their urine?

Answer 19

Because an aggregation of necrotised epithelial cells may become dislodged and they are excreted as brown granular casts.

Question 20

Name the 4 categories of causation of an infrarenal AKI and give examples of each.

Answer 20

1) GLOMERULAR: glomerular nephritis, ACEi’s, ARBs, NSAIDS.
2) INTERSTITIAL: acute pyelonephritis, acute interstitial nephritis (caused by drugs/ infection).
3) TUBULAR: nephrotoxic ATN, ischaemic ATN, intratubular obstruction (crystals, myoglobin, myeloma).
4) VASCULAR: vasculitis (SLE), malignant HTN, scleroderma, microvascular obstruction (HUS, TTP, emboli), vasomotor (NSAIDs/ ACEis/ ARBs).

Question 21

In acute tubular necrosis and acute interstitial nephritis, what processes are impaired?

Answer 21

Reabsorption and secretion.

Question 22

Describe the following laboratory findings for an intrarenal AKI:

a) BUN:creatinine
b) Urine sodium
c) FeNa
d) Serum sodium
e) Urine osmolarity

Answer 22

a) <15:1 (low)
b) >40mEq/L (high)
c) >2%
d) low
e) <350 (low)

Question 23

What are post-renal AKIs most often caused by?

Answer 23

By obstruction of urine flow. Occurs when both urinary outflow tracts are obstructed or when the tract is obstructed in a patient with a single functional kidney.

Question 24

How does urinary outflow obstruction cause an AKI?

Answer 24

Obstruction > backflow of urine > increased pressure within tubules > reduced pressure gradient across glomerulus > decreased GFR.

Question 25

In a post renal AKI, what causes azotemia, hypernatraemia, low urinary sodium and a low FeNa?

Answer 25

High pressure in the tubules leads to increased reabsorption of sodium, urea and water.

Question 26

Over time, describe the changes that occur in the kidney as a result of a post renal AKI.

Answer 26

High pressures exerted on renal tubule epithelial cells > causes epithelial cells to die > impairs reabsorption and secretion.

Question 27

Describe the types of urinary sediments that can be found in the following classifications of AKIs:

1) Prerenal
2) Intrarenal
3) Postrenal

Answer 27

1) Hyaline casts
2) Muddy brown, epithelial or granular casts (ATN), RBC casts (glomerulonephritis) or fatty casts (nephrotic syndrome).
3) None

Question 28

Give 3 examination findings which would be evidence of obstruction.

Answer 28

1) Enlarged, palpable kidneys or bladder
2) Large prostate on PR
3) Pelvic masses on vaginal examination

Question 29

How is it possible to rule out bladder outflow obstruction as a differential diagnosis for postrenal AKI?

Answer 29

By flushing or inserting a urethral catheter.

Question 30

Name 5 potential causes of bladder outflow obstruction.

Answer 30

1) BPH
2) Kidney stones
3) Bladder stones
4) Bladder injury or tumour
5) Ureteric stricture
6) Retroperitoneal fibrosis
7) Foreign body
8) Neurogenic bladder

Question 31

State the 9 consequences of renal failure.

Answer 31

Metabolic Acidosis
Dyslipidaemia
Hyperkalaemia
Uraemia
Na+/H2O retention
Growth retardation
Erythropoietin failure (anaemia)
Renal ostreodystrophy

Question 32

Give 6 features that may be involved in the clinical presentation of an AKI.

Answer 32

1) Oliguria/ anuria (early stages) - <0.5ml/kg/hour
2) Nausea and vomiting
3) Confusion
4) HTN
5) Abdominal/ flank pain
6) Signs of fluid overload (oedema/ high JVP).

Question 33

Give 5 biochemical changes seen in AKI.

Answer 33

1) hyperkalaemia
2) metabolic acidosis
3) hyponatraemia
4) hypocalcaemia
5) hyperphosphataemia

Question 34

Define uraemia.

Answer 34

A raised level in the blood of urea and other nitrogenous waste compounds that are normally eliminated by the kidneys.

Question 35

Name the 10 possible symptoms of uraemia, from those present in mild uraemia to those present in severe uraemia.

Answer 35

Anorexia
Change in taste
Nausea
Vomiting 
Pruritis
Neuropathy
Pericarditis
Confusion
Encephalopathy
Coma

Question 36

Describe the relevant investigations you would perform for a patient with an AKI in the following categories:

a) bloods
b) urine
c) imaging
d) histology

Answer 36

a) GFR, FBC, U&Es, Creatinine, Calcium, Phosphate, ESR, CRP, immunology, virology.
b) Urinalysis: blood, protein, glucose, leukocytes, nitrites, BJPs.
c) USS: to exclude obstruction and assess kidney size.
d) Renal biopsy in every patient with an unexplained AKI and normal sized kidneys.

Question 37

Name the 5 general steps in the management of an AKI.

Answer 37

1) Maintain renal blood flow and fluid balance.
2) Monitor electrolytes
3) Stop nephrotoxic drugs
4) Treat the underlying cause
5) Refer to renal team if appropriate

Question 38

1) Describe the pathophysiology behind sodium retention in patients with an AKI.
2) Name 3 consequences of sodium and water retention.
3) What can long term HTN lead to which increases mortality rates in those with longstanding AKIs/ CKD?

Answer 38

1) Decreased GFR leads to the up regulation of RAAS which causes sodium and water retention.
2) HTN (early manifestation), peripheral and pulmonary oedema (late manifestations).
3) HTN > LVH > CCF.

Question 39

What causes the manifestation of anaemia in patients with longstanding AKIs/ CKD?

Answer 39

The kidneys produce less EPO so the bone marrow produces fewer red blood cells.

Question 40

1) Overall, what causes patients with a longstanding AKI or CKD to develop bone disease?
2) What do these mechanisms lead to?
3) What causes decreased Calcium absorption from the gut?
4) What is the overall management aim for these patients with bone disease?

Answer 40

1) A fall in serum calcium and increase in serum phosphate. This causes PTH release, leading to 2o hyperparathyroidism.
2) Renal osteodystrophy and vascular calcification.
3) Decreased levels of calcitriol.
4) To maintain vitamin D levels to encourage production of the active form of vitamin D (calcitriol).

Question 41

1) What 2 factors can cause metabolic acidosis to occur in patients with a long-standing AKI or CKD?
2) Name 2 signs or symptoms of Hyperkalaemia.
3) In these patients, what is the basic treatment of acidosis and hyperkalaemia?

Answer 41

1) Diminished ability to excrete H+ and decreased ability to generate bicarbonate.
2) Muscle weakness and fibrillations/
3) Loop diuretics for hyperkalaemia and sodium bicarbonate for acidosis.

Question 42

Describe the ECH changes that might be seen on an ECG of a patient with hyperkalaemia.

Answer 42

Tall tented/ peaked T waves (first sign on ECG)
Prolonged PR interval
P wave widens and flattens leading to absent P waves
Widened QRS complex
Progression to a sine wave

Question 43

1) In longstanding AKI or CKD, what might impaired platelet function cause?
2) In longstanding AKI or CKD, what might immunosuppression cause?

Answer 43

1) Bruising and/or worsening of GI bleed.

2) Increased risk of infection.