Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals. Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.

1. Acute Kidney Injury
Shibu Chacko

2. Background
• Acute kidney injury covers a wide spectrum of injury to the
kidneys, not just kidney failure
• Detection is now based on monitoring level of serum creatinine
with or without urine output
• AKI is seen in 13–18% of all hospitalised people
• Inpatient AKI-related mortality is between 25 - 30%
• Between 20 - 30% of cases of AKI are preventable; prevention
could save up to 12,000 lives each year
• Cost of inpatient NHS Kidney Care is high (estimated between
£434 - £620 million/year --- Equivalent to cost of breast cancer
or combined cost of lung & skin cancer)

4. +
NCEPOD Findings &
Recommendations
 50% of cases with AKI documented as cause of death received
satisfactory or good care
 30% of cases inadequately investigated and managed
 20% of post-admission AKI is predictable and avoidable (or hospital
acquired AKI = HAAKI)
 All emergency admissions should have electrolytes checked on admission
and appropriately thereafter
 All acute admissions should receive adequate senior reviews, with
consultant review within 12 hours of admission
 Implementation of NICE guidance CG50
RecommendationsFindings

5. Objectives
• Definition / Risk factors for AKI
• Detection
• Prevention
• AKI Management Bundle
• Guidance on seeking specialist opinion
• Summary

6. Acute Renal Failure aka Acute Kidney Injury
(Renamed following the NCEPOD 2009 report)
AKI is a rapid reduction in kidney function over days to weeks
causing an accumulation of nitrogenous products in the blood
(AZOTEMIA).
(MERCK Manual – 19th Edition-2011)

7. Glomerular Filtration Rate (GFR)
• = the volume of water filtered from the plasma per minute
• Gives a rough measure of the number of functioning nephrons.
• Normal GFR:
• Men: 130 mL/min./1.73m2
• Women: 120 mL/min./1.73m2
• Cannot be measured directly, so we use creatinine and creatinine clearance
to estimate.

8. Risk Factors
• Elderly people - Age 65years or over
• Co Morbidities - Heart failure, liver disease, diabetes
• Medications -NSAIDs, aminoglycosides, ACE inhibitors, ARBs, diuretics.
• Pre Existing CKD - eGFR <60 ml/min/1.73m2 or history of AKI
• Neurological or cognitive impairment/disability
• Hypovolemia & Sepsis
• Use of iodinated contrast agents within the past week
• Symptoms or history of urological obstruction
• Emergency surgery -when the patient has sepsis or hypovolaemia

9. Causes of AKI ?
•Pre-renal = 50-80%
•Renal = 10-40%
•Post-renal (Obstruction) = 5-10%

11. Pre renal Causes
•Decreased renal perfusion without any cellular injury –
•DEHYDRATION
•50-80% cases, potentially reversible

12. Pre renal Causes
Causes Examples
ECF Volume depletion Excessive Diuresis, haemorrhages, GI
GI loses, loss of intravascular fluid into
into the interstitial space (ascites,
Pancreatitis etc), poor oral intake
Low cardiac output Cardiomyopathy, MI, Cardiac
tamponade, PE, Pulmonary
hypertension
Low systemic vascular
resistance
Septic Shock, Liver failure,
antihypertensive drugs

13. Renal / Intrinsic Causes (10%)
• Acute tubular necrosis / Injury (ATN)
• Ischemia – Prolonged or severe pre-renal state
• Toxin – Drugs / Myoglobin / Contrast
• Tubular factors – Renal artery stenosis
• Acute interstitial Nephritis (AIN)
• Drug reactions – NSAIDs, Ciprofloxacin, Furosemide
• Pyelonephritis
• Acute Glomerulonephritis (GN) – Post infections
• Damage to filtering mechanisms
• Infilterative Diseases – Lymphoma, Leukemia

14. Aminoglycoside Toxicity
• Common in hospitalised patients
• It is not metabolised in kidney, but excreted by Glomerular
filtration
• It inhibits protein synthesis in renal cells – necrosis of cells in
proximal tubules – Acute tubular cell necrosis
• Nephrotoxicity usually produces a non-oliguric AKI- Increase in
Creatinine will appear few days later

15. Rhabdomyolytic AKI
• Diagnose with high serum CK, urine dipstick for blood, without
RBCs on microscopy, pigmented granular casts
• Common after trauma (“crush injuries”), seizures, burns etc
• Treatment is largely supportive care – Generous IV fluids
(Isotonic Saline 6-8 litres in 24 hours)
• Alkalinisation of urine

17. Post renal causes (10-15%)
Tubular precipitation
Uric acid, Myeloma protein,
Ca Oxalate (Ethylene glycol ingestion),
ingestion), Myoglobin
Ureteral obstruction
Intrinsic: Calculi, clots, sloughed renal
renal tissue, edema
Extrinsic: Cancer, Ureteral trauma
during surgery
Bladder obstruction
Mechanical: BPH, Prostate Ca, Urethral
Urethral strictures, phimosis and
paraphimosis
Neurogenic: Anticholinergic drugs,
UMN or LMN lesion

18. RIFLE and Acute Kidney Injury Network
Classification of AKI (Cruz et al, Critical care 2009, 13:211

19. Acute Kidney Injury Network Criteria
Stage Creatinine Criteria UOP Criteria
1 ↑SCr ≥ 150-200% < 0.5 mL/kg/hr for > 6 hr
2 ↑SCr > 200-300% < 0.5 mL/kg/hr for >12 hr
3
↑ SCr >300% or
SCr ≥354 μmol/L + after an
an acute rise of 44µmol/L
44µmol/L in 24 hours
< 0.3 mL/kg/hr for 24 hr
or
anuria for 12 hr
Mehta et al. Crit Care 2007;11:R31

20. Signs & Symptoms of AKI
• Oliguria (70%) (Anuria usually occurs only in obstructive uropathy)
• Oedema, esp. lower extremity
• Weight gain
• Later signs (Accumulation of Nitrogenous products): anorexia,
nausea, vomiting, weakness, seizures, confusion.
• Fluid accumulation in lungs- crackles
• Colour of urine & a palpable bladder

21. Lab findings
• Rising Creatinine and Urea
• Rising potassium
• Progressive acidosis (HCO3 15-20)
• Hyponatremia (correlates with surplus of water)
• Hypocalcaemia (Reduced Calcitrol production / resistance of bone to
Parathyroid hormone)
• Reduced GFR
• Anemia (Hct 25-30) (normal:37-51)

22. Management
Points of Intervention
Patient
Event AKI
Resultant
Sequelae
Intervention
Prevention Early
Management

23. Record
Observations
Diagnosis of
AKI Made
AKIN 3 - discuss
with renal registrar
(see referral
protocol)
Note patient’s usual
BP. Is their BP low
for them?
If present
Medication
Review
Assess fluid balance
and look for signs of
shock or
hypoperfusion
Check for signs
of sepsis
Initially 30 minute
observations, moving to
hourly then 2 hourly and 4
hourly observations when
stable
Pyrexia, tachycardia,
hypotension, peripheral
vasodilatation, raised
inflammatory markers
Stop NSAID / ACEi / ARB /
metformin / K-sparing
diuretic.
Modify drug doses
dependent on renal
function
Assess BP, P, JVP,
capillary refill, GCS, urine
output
Consider antibiotics
early, at correct
doses
Take cultures
Move to
Investigation
If hypovolaemia, give
250mls fluid bolus and
observe response
If volume replete and
remains hypotensive,
consider ITU referral for
inotropic support
If response, continue fluid
replacement until volume
replete
AKI Treatment Pathway -
Assessment
SAKI
Stop Acute Kidney Injury

24. Urinary Tract
Ultrasound
Consider whether
referral to Renal /
ITU / Urology is
appropriate
Bloods Consider Acute
Renal Screen
Within 24 hours of AKI
recognition to rule out
obstruction
See Referral Protocol
Ensure all bloods taken
including:
FBC, CRP, CK, LFTs, Ur,
Cr, Na, K, Ca, Mg,
bicarbonate
Correct electrolytes (see
management of
complications)
If electrolyte disturbance
consider twice daily
repeats or after treatment
Ensure renal function
checked daily
AKI Treatment Pathway -
Investigation
Continued
Management
ANCA and
ANA if:
Anti-GBM if:
Bence Jones +
Serum
Electrophoresis if:
• Raised calcium or
globulin fraction
• Known MGUS /
myeloma
• Short prodrome
• Rapid rise in
creatinine
• No signs of sepsis
• +/- haemoptysis
• Raised CRP
• Without signs of
sepsis
• +/- vasculitic rash
/ haemoptysis
SAKI
Stop Acute Kidney Injury

25. Regular
observations and
assessment
Fluid Balance
Assess and Treat
Complications of
AKI
Fluid assessment, BP, P,
JVP, capillary refill, GCS,
urine output, daily weight
Minimum 4 hourly
observations
Hyperkalaemia
K > 6.5
Reverse Hypovolaemia
When fluid replete give
maintenance fluids
(estimated output plus
500mls)
AKI Treatment Pathway -
Management
Acidosis
Fluid Overload
• 10mls of 10% calcium
gluconate
• Insulin / dextrose (10-15 IU
in 50mls of 50% dextrose
over 30 minutes)
• Salbutamol 2.5mg
nebulisers 6 hourly
Repeat K post
treatment
If K remains >6.5 after
3 treatments consider
renal / ITU referral for
RRT
Note insulin / dextrose and
salbutamol reduce ECF
potassium for < 4 hours
If bicarbonate <22 and no fluid
overload consider 500mls of
1.26% sodium bicarbonate
over 2hrs (consider repeat
dependent on level of
acidosis)
Oxygen therapy and
consider CPAP for
pulmonary oedema
Give Frusemide 80mg IV
If no response consider
frusemide infusion (10mg/hr
If no response, anuria or
oliguria, consider referral to
Renal Physician / ITU to
consider RRTRegular assessment of
fluid status
SAKI
Stop Acute Kidney Injury

26. AKI Referral Protocol
Renal Referral Intensive Care
Referral
Urology Referral
• All AKI with confirmed
obstruction on imaging
• If K > 6.0 also discuss with
Renal Registrar as may
require renal replacement
prior to intervention
• All AKIN 3
• AKIN 1/2/3 if blood and
protein on urine dip
• AKIN 1/2/3 if known
myeloma or BJP positive
• AKIN 1/2/3 if possible
HUS / TTP
• AKIN 1/2/3 with
hyperkalaemia resistant
to medical treatment
• AKIN 1/2/3 with anuria
despite adequate volume
replacement / fluid
overload
• AKIN 1/2/3 with other
organ failure
(hypotension despite
adequate volume
replacement, or
respiratory failure)
• AKIN 1/2/3 with
hyperkalaemia / fluid
overload resistant to
medical treatment and
not safe for transfer to
Renal Unit (see
Transfer Policy)
SAKI
Stop Acute Kidney Injury

27. Managing AKI - key priorities
• Follow AKI management bundle
• Relieve urological obstruction
• Refer to a urologist immediately if following is present:
• Pyelonephrosis
• an obstructed solitary kidney
• bilateral upper urinary tract obstruction
• complications of AKI caused by urological obstruction.
• When you see an abnormal creatinine or AKI alert
• Confirm the results
• Simply follow Seven Steps (8S of AKI)

28. AKI Management Bundle Step 1
• “AKI Alert” (checking blood result)

29. AKI Management Bundle – Step 2
Urgent Senior Review
• You do not have to be as
old as an SpR to provide a
sound advice ….

30. AKI Management Bundle Step 3
Assess fluid status & begin fluid therapy
• Regularly assess
fluid status.
• Maintain Fluid
balance chart
• Reverse
Hypovolemia &
Hypotension

31. AKI Management Bundle Step 4
NEWS Chart and maintain fluid balance chart
ESCALATE YOUR CONCERNS
• Look for and Treat infection
early.
• Recognise and treat hypoxia

32. AKI Management Bundle Step 5
Urine dip

33. AKI Management Bundle Step 6
Remove ‘The usual suspects’, Assess drug doses with respect to kidney function
NSAIDS ACE I /ARBs Gentamicin Spironolactone X-ray contrast

34. AKI Management Bundle Step 7
Monitor daily U&Es and urine output
Check for Acidosis
and Hyperkalemia
!

35. AKI Management Bundle Step 8
Consider ultrasound and urinary catheter

36. ARF: Life Threatening Conditions
• Hyperkalemia
• Volume overload
• Vascular access

37. Hyperkalemia Symptoms
• Dysrhythmias
• Weakness
• Lethargy
• Muscle cramps
• Paresthesias
• Hypoactive reflexes

38. Hyperkalemia & ECG
•K > 5.5 -6
•Tall, peaked T’s
•Wide QRS
•Prolong PR
•Diminished P
•Prolonged QT
•QRS-T merge – sine
wave

41. Hyperkalemia Treatment
•Calcium Gluconate (10% - 10mls – 10mins)
•Insulin AND Glucose (50% Dextrose with 15u Actrapid)
•Salbutamol Nebs (increase cellular potassium uptake)
•Sodium Bicarbonate
•Ca.Resonium (15gm tds to bind k+ in the gut, long term management)
•Haemofiltration

42. Local Initiatives

43. Qlik View screen shot

44. AKI Sticker

45. Prevention
• Maintain a normal fluid balance, blood volume, BP in patients
with trauma, burns, haemorrhage, D&V, surgical patients.
• Minimise the use of contrast agents
• Avoid NSAIDS
• HYDRATION, HYDRATION, HYDRATION!!!!!
• Monitor I/O Charts
• Monitor drug levels
• Get help early !!!

46. Summary: AKI
• Identify the risk
• Risk assessment - Early identification of sick patients (AKI and risk assessment)
• Prevention
• Follow principles of managing acutely ill patients
• Basic steps in management: Physiological monitoring, fluid balance chart, urinalysis
• Detection
• Investigation - Early identification and management of hypovolaemia and sepsis
• Management
• Remember to follow the Check List
• Early senior review, critical care outreach team and nephrology referral
• Monitor the response to treatment and consider in people not responding for
• Renal Replacement therapy /ITU
• Nephrology opinion / referral