acute kidney injury

Question 1

what causes acute interstitial nephritis?

Answer 1

drugs: the most common cause, particularly antibiotics; penicillin; rifampicin; NSAIDs; allopurinol; furosemide
systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci

Question 2

what is the histology of AIN?

Answer 2

histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

Question 3

what are features of AIN?

Answer 3

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

Question 4

what are the ix in AIN?

Answer 4

sterile pyuria
white cell casts

Question 5

describe epidemiology, symptoms + ix for tubulointerstitial nephritis with uveitis

Answer 5

Tubulointerstitial nephritis with uveitis (TINU) usually occurs in young females. Symptoms include fever, weight loss and painful, red eyes. Urinalysis is positive for leukocytes and protein.

Question 6

what is acute kidney injury?

Answer 6

a reduction in renal function following an insult to the kidneys

Question 7

what are the 3 types of AKI causes?

Answer 7

prerenal, intrinsic and postrenal causes

Question 8

what causes pre-renal + examples?

Answer 8

One of the major causes of AKI is ischaemia, or lack of blood flowing to the kidneys.

Examples
hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis

Question 9

what causes intrinsic AKI?

Answer 9

The second group of causes relate to intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves. This may be due to toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.

Examples
glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome

Question 10

what causes post renal AKI?

Answer 10

This is where there is an obstruction to the urine coming from the kidneys resulting in things ‘backing-up’ and affecting the normal renal function.

Examples
kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter

Question 11

what are RF for AKI?

Answer 11

chronic kidney disease
other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
history of acute kidney injury
use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
use of iodinated contrast agents within the past week
age 65 years or over

Question 12

what are features of AKI?

Answer 12

reduced urine output
pulmonary and peripheral oedema
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia (for example, pericarditis or encephalopathy)

Question 13

what imaging is needed?

Answer 13

renal USS

Question 14

how do you dx AKI?

Answer 14

by using any of the following criteria:

a rise in serum creatinine of 26 micromol/litre or greater within 48 hours

a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days

a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than

Question 15

what drugs are safe to continue in AKI?

Answer 15

Paracetamol
* Warfarin
* Statins
* Aspirin (at a cardioprotective dose of 75mg od)
* Clopidogrel
* Beta-blockers

Question 16

what drugs should be stopped in AKI?

Answer 16

• NSAIDs
• Aminoglycosides
• ACE inhibitors
• Angiotensin II receptor antagonists
• Diuretics

Question 17

what drugs may have to be stopped in AKI as increased risk of toxicity?

Answer 17

Metformin
* Lithium
* Digoxin

Question 18

what is the mx for AKI?

Answer 18

fix the case ie remove stones, stop drugs
manage electrolyte abnormalities
Renal replacement therapy (e.g. haemodialysis) is used when a patient is not responding to medical treatment of complications, for example hyperkalaemia, pulmonary oedema, acidosis or uraemia (e.g. pericarditis, encephalopathy).

Question 19

what stabilises cardiac membrane in hyperkalaemia mx?

Answer 19

Intravenous calcium gluconate

Question 20

what causes Short-term shift in potassium from extracellular to intracellular fluid compartment?

Answer 20

• Combined insulin/dextrose infusion
• Nebulised salbutamol

Question 21

what removes K+ from body?

Answer 21

• Calcium resonium (orally or enema)
• Loop diuretics
• Dialysis

Question 22

what is stage 1 AKI defined by?

Answer 22

Increase in creatinine to 1.5-1.9 times baseline, or
Increase in creatinine by ≥26.5 µmol/L, or
Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours

Question 23

what is stage 2 AKI defined by?

Answer 23

Increase in creatinine to 2.0 to 2.9 times baseline, or
Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours

Question 24

what is stage 3 AKI defined by?

Answer 24

Increase in creatinine to ≥ 3.0 times baseline, or
Increase in creatinine to ≥353.6 µmol/L or
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2

Question 25

what is acute tubular necrosis?

Answer 25

he most common cause of acute kidney injury (AKI) seen in clinical practice. Necrosis of renal tubular epithelial cells severely affects the functioning of the kidney. In the early stages ATN is reversible if the cause if removed.

Question 26

what are the 2 main causes of ATN?

Answer 26

ischaemia: shock, sepsis
nephrotoxins: aminoglycosides, myoglobin secondary to rhabdomyolysis, radiocontrast agents, lead

Question 27

features of ATN?

Answer 27

features of AKI: raised urea, creatinine, potassium
muddy brown casts in the urine

Question 28

what are histopathological features of ATN?

Answer 28

tubular epithelium necrosis: loss of nuclei and detachment of tubular cells from the basement membrane
dilatation of the tubules may occur
necrotic cells obstruct the tubule lumen

Question 29

what are the phases of ATN?

Answer 29

oliguric phase
polyuric phase
recovery phase

Question 30

what causes rhabdomyolysis?

Answer 30

seizure
collapse/coma (e.g. elderly patient collapses at home, found 8 hours later)
ecstasy
crush injury
McArdle’s syndrome
drugs: statins (especially if co-prescribed with clarithromycin)

Question 31

features of rhabdomyolysis?

Answer 31

acute kidney injury with disproportionately raised creatinine
elevated creatine kinase (CK) at least 5 times the upper limit of normal
myoglobinuria: dark or reddish-brown colour
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia (may develop before renal failure)
metabolic acidosis

Question 32

how do you manage rhabdomyolysis?

Answer 32

IV fluids to maintain good urine output
urinary alkalinization is sometimes used

Question 33

what is urine sodium in pre-renal vs ATN?

Answer 33

pre-renal < 20 mmol/L
ATN > 40 mmol/L

Question 34

what is urine osmolality in pre-renal vs ATN?

Answer 34

pre-renal > 500 mOsm/kg
ATN < 350 mOsm/kg

Question 35

what is response to fluid challenge in pre-renal vs ATN?

Answer 35

pre-renal good
ATN poor

Question 36

what is serum UCR in pre-renal vs ATN?

Answer 36

pre-renal raised
ATN normal

Question 37

what is appearance of urine in pre-renal vs ATN?

Answer 37

pre-renal Normal/ ‘bland’ sediment
ATN Brown granular casts

Question 38

why do kidneys hold onto sodium in pre-renal?

Answer 38

to preserve volume