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 3

Stages of CKD Stage 1 eGFR ≥ 90 Kidney damage, normal or increased GFR 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

The UK eCKD Guide - Renal

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 10 10 10

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 Urine output is <0.5 mL/kg/hr for >6 consecutive hours

Serum Creatinine criteria 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 SCr increase ≥354 µmol/L initiated on RRT (irrespective of stage at time of initiation) <0.3 mL/kg/hr for 24 hr anuria for 12 hr 13 13

Epidemiology

Epidemiology based on old definitions based on new 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

AKI is a Syndrome Pre-renal AKI Intrinsic AKI Post-renal AKI Sepsis Hypovolemia Intrinsic AKI Acute tubular injury Tubulointerstitial injury Glomerulonephritis Vasculitis Post-renal AKI Kidney stones Prostatic hypertrophy Retroperitoneal fibrosis

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 cardiovascular gastrointestinal hyperkalaemia cardiovascular pulmonary oedema, arrhythmias, pericarditis gastrointestinal nausea, vomiting, gastritis, ulceration, malnutrition

Complications of AKI neurological infectious haematological 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? 39

Royal Society of Medicine 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 Provide better support for people to self-care Self-treatment options & care plan to know what to do and who to contact when deterioration Help people with urgent care needs get right advice in right place, first time Highly responsive urgent care services outside hospital People with serious and life threatening emergency care needs receive treatment in centres with facilities and expertise 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

1.2 million 300,000 $7,500 12.5 days (3.5 times) $9,000,000,000/YR (3 to 14,000) PER ADMISSION EXCESS HOSPITAL COSTS $9,000,000,000/YR Your length of stay in the hospital increases by 12.5 days (3.5 times) if you get AKI 22 3.5% ADMISSIONS 5 1.2 million People per year get AKI during a hospital stay 300,000 people die in the US annually from AKI ODDS OF DEATH DEATH RATE/YR More than breast cancer, prostate cancer, heart failure and diabetes, combined Severity of AKI 60

Think Functional Reserve ! 50% loss of function before serum creatinine rises above the upper limit of normal

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

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?