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Acute Kidney Injury Dr Andrew Lewington Consultant Renal Physician/Honorary Clinical Associate Professor Leeds Teaching Hospitals

Acute Kidney Injury Dr Andrew Lewington Consultant Renal Physician/Honorary Clinical Associate Professor Leeds Teaching Hospitals

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Acute Kidney Injury

Dr Andrew Lewington Consultant Renal Physician/Honorary Clinical

Associate Professor Leeds Teaching Hospitals

What is AKI?

Functions of the Kidney

• maintenance of body composition– osmolality, electrolyte content, acidity

• excretion of metabolic end products– urea, drugs

• secretion of erythropoietin– maturation of erythrocytes

• secretion of activated form of vitamin D3

– calcium and phosphate balance

• renin secretion– angiotensinogen→angiotensin I

Stage 1 eGFR ≥ 90• Kidney damage, normal or increased GFR

Stage 2 eGFR 60-89• Kidney damage, mildly reduced GFR

Stage 3A eGFR 45-59• Moderately reduced GFR ± other evidence of kidney damage• GFR < 60 ml/min for ≥ 3 months ± kidney damage

Stage 3B eGFR 30-44

Stage 4 eGFR 15-29• Severely reduced GFR ± other evidence of kidney damage

Stage 5 eGFR < 15• Established kidney failure

• Kidney damage (presence of structural abnormalities and/or persistent haematuria, proteinuria or microalbuminuria) for ≥ 3 months

Stages of CKD

What is Acute Kidney Injury?

Acute Kidney Injury

• Term encompasses all forms of AKI– rapid reduction in kidney function– occurs over hours to days– no specific symptoms

• exception – stones

– failure to regulate • fluid and electrolyte balance• acid/base balance

– failure to excrete some drugs

Acute Kidney Injury

– Most commonly associated with acute illness (hypoperfusion)• recovery usual if patient recovers from primary

cause• severe AKI may progress to chronic kidney

disease

– Rarer forms • require rapid recognition for specific therapy

Increased mortality associated with changes in serum creatinine

Chertow et al: JASN 2005

0

10

20

30

40

25-35 44-80 88-170 176

change in SCr (umol/l)

Odd

s of d

eath

Unadjusted Age- and sex-adjusted Multivariable-adjusted

New Definitions

www.renal.org

Definition of AKI – Kidney Disease Improving Global Outcomes

• Serum creatinine rise ≥26 µmol/L within 48 hours

or• Serum creatinine rise ≥1.5 fold from the

baseline value, which is known or presumed to have occurred within one week

or• Urine output is <0.5 mL/kg/hr for >6

consecutive hours

AKI Staging – KDIGO

AKI stage Serum Creatinine criteria Urine output criteria

1

SCr increase ≥26 µmol/L within 48 hrs

or

SCr increase ≥1.5–2 fold from baseline

<0.5 mL/kg/hr for 6 consecutive hrs

2 SCr increase ≥2–3 fold from baseline <0.5 mL/kg/hr for 12 hrs

3

SCr increase ≥3 fold from baseline

or

SCr increase ≥354 µmol/L

or

initiated on RRT (irrespective of stage at time of initiation)

<0.3 mL/kg/hr for 24 hr

or

anuria for 12 hr

Epidemiology

Epidemiology• based on old definitions

– 5% of hospital admissions– 30% of ICU admissions

• based on new definitions– 18% of hospital admissions– 30-80% of ICU admissions

Aetiology

Aetiology

• essential to establish aetiology • aetiology determines treatment• not all AKI is secondary to ischaemia

/reperfusion injury• important to identify rarer causes

• Sepsis• Hypovolemia

• Acute tubular injury• Tubulointerstitial injury• Glomerulonephritis• Vasculitis

• Kidney stones• Prostatic hypertrophy• Retroperitoneal fibrosis

Pre-renal AKI

Intrinsic AKI

Post-renal AKI

AKI is a Syndrome

Clinical Presentation of AKI

Clinical Presentation of AKI

• Risk factors for AKI (some)– chronic kidney disease – cardiac failure– peripheral vascular disease– diabetes mellitus (with proteinuria)– liver disease– myeloma

Clinical Presentation

• poor fluid intake– nausea, vomiting– ↓ functional capacity

• excessive fluid losses– fever– diuretics– diarrhoea– high stoma output– haemorrhage– burns

Clinical Presentation

• drug history– nephrotoxic drugs– radiocontrast media

• urinary tract symptoms– prostatic disease– renal calculi

Clinical Presentation

• volume status – core temperature– heart rate– JVP– postural hypotension

• cardiovascular status– peripheral perfusion– BP– heart rate and rhythm

Clinical Presentation

• palpable bladder– prostatic hypertrophy– carcinoma of cervix

• bruits/absent pulses– renovascular disease

• rash – vasculitis– interstitial nephritis

Complications

Complications of AKI

• metabolic– hyperkalaemia

• cardiovascular– pulmonary oedema, arrhythmias, pericarditis

• gastrointestinal– nausea, vomiting, gastritis, ulceration,

malnutrition

Complications of AKI

• neurological– seizures, mental status changes

• infectious• haematological

– anaemia, bleeding

Investigations

Investigations

• Full Blood Count and clotting• U&Es and bicarbonate (previous renal function)• Liver Function Tests and bone• urinalysis (prior to urinary catheter)• immunological screen – if vasculitis suspected

Investigations

• ultrasound of renal tract within 24hrs if– obstruction suspected– isoteric cause suspected requiring a kidney

biopsy• consider blood film, LDH

– (if ↓ Hb and ↓ Pl)• consider creatine kinase

– (rhabdomyolysis)

Management

No Specific Therapy For Most Forms of AKI

Prevention of AKI is Essential

• Risk of complications– increased length of stay– increased mortality– chronic kidney disease

• Cost– £1.2 Billion

Prevention

• identify risk factors– > 75 years– pre-existing chronic kidney disease– vascular disease– diabetes mellitus (with proteinuria)– cardiac failure– hypovolaemia– sepsis– nephrotoxins

• drugs• contrast media

Prevention

• treat sepsis promptly• optomise volume status• stop/avoid

– nephrotoxic medications– minimise volume of contrast

Treatment

Treatment of AKI

dependent upon the cause– supportive therapy

• stabilise haemodynamics• treat complications• renal replacement therapy - dialysis• avoid further renal insults

– nephrotoxins– Hypotension

» Hold antihypertensives/diuretics

Treatment of AKI

• specific therapy– e.g. vasculitis –

• Immunosuppression• If suspected – refer immediately

How Good Are We at Caring for Patients with AKI in the UK?

June 11, 2009

Royal Society of Medicine

London

Key findings

• < 50% of AKI care considered good

• poor assessment of risk factors• 43% of post-admission AKI -

unacceptable delay in recognition

What is the relevance of AKI to the GP?

• Patients with c-AKI sustain more severe AKI than h-AKI

• Patients with c-AKI have better short term and long term outcomes than h-AKI

The Context:Addressing vulnerability & Transforming Urgent Care

1. Provide better support for people to self-care

Self-treatment options & care plan to know what to do and who to contact when deterioration

2. Help people with urgent care needs get right advice in right place, first time

3. Highly responsive urgent care services outside hospital

4. People with serious and life threatening emergency care needs receive treatment in centres with facilities and expertise

5. Connect all urgent and emergency care services

Acute kidney injury: prevention, detection and management up to the

point of renal replacement therapy (CG169)

• Guidance from the National Institute for Health and Care Excellence

• August 2013

• Dr Andy Lewington• Leeds Teaching Hospitals

NICE AKI Guideline

• stresses the importance of risk assessment and prevention, early recognition and treatment

• it is primarily aimed at the non-specialist clinician, who will care for most patients with AKI in a variety of settings

• in view of its frequency and mortality rate, prevention or amelioration of just 20% of cases of AKI would prevent a large number of deaths and substantially reduce complications and their associated costs

NICE AKI Guidelines

Rajib Pal (expert adviser)

GP Principal, Hall Green Health, West Midlands

Demographics• 25% of general population > 60yrs• >85yrs age group will double in next 20

years• 37% rise in admissions over last 10 years• 66% of patients admitted > 65yrs• 25% of patients have dementia• Patients > 85yrs account for 22% of bed

days in NHS

Patient Population

• Many patients have – multiple co-morbidities– in nursing homes– more complex management issues– decreased functional reserve

• Cardiac• Respiratory• Kidney

– polypharmacy – e-presribing• Need to recognise at risk population

NHS England - Workstreams

AKI – sits under Patient safety• Detection• Risk Assessment

• Chair AJPL• Co-Chairs

• Fiona Loud (Patient)• Tom Blackmore (GP)

• Management• Education

Identifying AKI in patients with acute illness

Investigate for acute kidney injury, by measuring serum creatinine and comparing with baseline, in adults with acute illness if any of the following are likely or present:

– chronic kidney disease (adults with an estimated glomerular filtration rate [eGFR] less than 60 ml/min/1.73 m2 are at particular risk)

– heart failure – liver disease – diabetes – history of acute kidney injury – oliguria (urine output less than 0.5 ml/kg/hour) – neurological or cognitive impairment or disability, which may mean limited

access to fluids because of reliance on a carer – hypovolaemia – use of drugs with nephrotoxic potential (such as non-steroidal anti-

inflammatory drugs [NSAIDs], aminoglycosides, angiotensin-converting enzyme [ACE] inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week, especially if hypovolaemic

– use of iodinated contrast agents within the past week – symptoms or history of urological obstruction, or conditions that may lead to

obstruction – sepsis – deteriorating early warning scores – age 65 years or over

Identifying AKI in patients with no obvious acute illness

• Be aware that in adults, children and young people with chronic kidney disease and no obvious acute illness, a rise in serum creatinine may indicate acute kidney injury rather than a worsening of their chronic disease. [1.1.3 ]

• Ensure that acute kidney injury is considered when an adult, child or young person presents with an illness with no clear acute component and has any of the following: – chronic kidney disease, especially stage 3B, 4 or 5, or urological

disease – new onset or significant worsening of urological symptoms – symptoms suggesting complications of acute kidney injury – symptoms or signs of a multi-system disease affecting the kidneys

and other organ systems (for example, signs or symptoms of acute kidney injury, plus a purpuric rash). [1.1.4]

AKI is a Global Problem

$9,000,000,000/YR

1.2 million 300,000 people die in the USannually from AKI

People per yearget AKI during ahospital stay

5

22

Your length of stay in the hospital increases by

12.5 days(3.5 times)if you get AKI

Prostate cancer

Breast cancer

Heart failure

Diabetes AKI0

50,000100,000150,000200,000250,000300,000350,000

More than breast cancer, prostate cancer, heart failure and diabetes, combined

0.3-0.4 0.5-0.9 1.0-1.9 >=2.00

102030405060708090

unadjustedage adjustedmultivariableODDS OF

DEATHDEATH RATE/YR

3.5% ADMISSIONS

$7,500(3 to 14,000)

PER ADMISSIONEXCESS HOSPITAL

COSTS

Severity of AKI

ThinkFunctional Reserve !

50% loss of function before serum creatinine rises above the

upper limit of normal

“It is morally inexcusable that people - mostly young people - still die of untreated acute kidney failure. ”

Giuseppe Remuzzi

ISN President Giuseppe Remuzzi

0 by 25 initiative

This initiative has one clear and concise aim: that no one should die of untreated acute kidney failure in the poorest parts of Africa, Asia and South America by 2025.

Discussion Points

• Sick Day rules – NIHR funded• Vulnerable patients – how to identify

– Electronic alerts• Map of Medicine – other resources• Y&H AKI Patient Care Initiative

QUESTIONS?