MANAGEMENT OF ACUTE KIDNEY INJURY

PREVENTION OF AKI

Identify those at risk

• Many patients are already developing AKI on admission and many others during admission.
• To prevent AKI and recognize AKI early, consider these risk factors on admission and on every review:
• General: age >65, known CKD, previous AKI
• Acute events: sepsis, falls with long lie, dehydration (vomiting, diarrhoea, high fever, ileostomy),
haemorrhage, shock, major surgery, overnight or repeated fasting
• Comorbidities: diabetes, vascular disease, heart disease, liver disease, malignancy
• Drugs/toxins: ACEI/ARBs, NSAIDs, diuretics, aminoglucosides, contrast

Monitor those at risk

• Assess volume status daily with clinical monitoring

• Fluid balance chart and weight daily
• U+Es every 1-2 days

Protect those at risk

• Individualize volume status targets. Avoid dehydration/hypovolaemia by NG and/or IV fluid supplementation.

• 500ml 0.9% saline over 6-8 hrs before and after contrast exposure
• Review drugs: adjust doses, stop nephrotoxins, once daily renal dose aminoglycosides if unavoidable •
Early treatment for sepsis

MOHW August 2020

What is AKI ?
• AKI is a sudden decline in kidney function over hours or days
• Most often seen during episodes of acute illness
• Can occur on top of chronic kidney disease
• It is diagnosed by either a rise in serum creatinine or a fall in urine output (see table below)
KDIGO AKI Staging

Stage Serum creatinine Urine Output

1 1.5 to 1.9 x baseline OR increase by ≥ 26 μmol/L within 48hrs <0.5 mL/kg/hr for > 6 consecutive
hrs

2 2 to 2.9 x baseline <0.5 mL/kg/ hr for > 12 hrs

3 ≥3 X baseline OR increase to ≥ 354 μmol/L <0.3 mL/kg/ hr for > 24 hrs

OR initiation on renal replacement therapy OR anuria for 12 hrs

WHY IS AKI IMPORTANT?

 AKI occurs in 10-20% of emergency hospital admissions

 Increased length of hospital stay and morbidity
 >20% of these will die during hospital admission, usually due to cardiovascular events,sepsis or upper GI bleed
 AKI can progress to CKD later in life (may lead to needing long term dialysis)
 AKI can accelerate progression of pre-existing CKD (may lead to needing long term dialysis)
 Pre-renal AKI is rapidly reversible if treated early. If not, it l0eads to a more serious acute tubular injury
SEEK EXPERT HELP

Refer to nephrology team if:

●
There is no clear cause of AKI
●
New finding of blood and/or protein on urine dipstick (in absence of UTI, regardless of stage) ●

Systemic symptoms e.g. vasculitic rash, epistaxis, haemoptysis, polyarthralgia

●
Patient has a kidney transplant
 ●
Inadequate response to initial treatment
●
AKI Stage 3 or serum creatinine >300umol/l
●
Dialysis is indicated: Life-threatening or intractable pulmonary oedema
Uncontrollably rising K+
Severe (pH < 7.2) or worsening acidosis

Refer to urology if obstruction suspected. Refer to ICU if patient critically ill .

MANAGEMENT OF AKI

Fluid management. Assess fluid status. Correct hypovolaemia using 0.9% saline with continuous monitoring of
pulse, BP, JVP, chest auscultation and urine output. If urine output remains low after 2 litres of fluid seek Sp
advice. Once patient is adequately volume resuscitated maintain fluid intake at a rate of urine output + 30 ml/hr.
Use diuretics ONLY if volume overload is present.
Optimise blood pressure. If patient remains hypotensive (SBP<100 mm Hg) after fluid therapy consider
inotropic agent (not renal dose dopamine) and ICU advice. CVP monitoring is useful only in ICU.
Check for palpable bladder. Urethral catheterisation NOT mandatory. Only indicated if patient immobile,
obstructed, uncooperative or critically ill.
Treat sepsis with appropriate antibiotics. Put on PPI as stress ulcers likely.
Treat hyperglycaemia with sliding scale insulin but stop metformin, sulphonylureas, SGLT2I
Stop all nephrotoxins: ACEI, ARB, NSAIDs, aminoglycosides
Adjust drug doses to allow for reduced renal clearance (eg opiates, vancomycin)
Watch out for complications: fluid overload (see protocol), hyperkalaemia ( see protocol), metabolic acidosis,
hypoglycaemia not rare in AKI patients (IV dextrose infusion)
Baseline Investigations
Urine: dipstick, microscopy, ACR, culture and sensitivity
Blood: U+Es, LFTs, calcium, uric acid, Fbc with differential. ABG if clinically indicated
Imaging: USS of kidneys and urinary tract

FIND THE CAUSE oF AKI

Most causes will be obvious from history, examination and the above investigations. If not consider the following:

PRE-RENAL INTRINSIC

Decreased effective Acute tubular injury

Circulating volume Ischaemic (from prolonged or severe pre-renal AKI)
Haemorrhage Toxins
Volume depletion - Nephrotoxic drugs
Sepsis Full culture screen, CRP - Radiocontrasts
Cardio-renal syndromes
Troponin, cardiac imaging - Haemoglobinuria Full haemolysis screen
Liver failure - Myoglobinuria CK, urinary myoglobin
- Intratubular crystal
Arterial narrowing - Myeloma casts BJP, serum protein electrophoresis,
free light chains, kidney biopsy
Vasomotor
NSAIDs
Glomerulonephritis/ANCA, ANA, Anti-GBM, Anti dsDNA,
ACEI/ARBs
Vasculitis C3/C4, ENA
, Immunoglobulins, cryoglobulins,
hep B,C HIV serology, kidney biopsy

Interstitial nephritiseosinophilia,eosinophiluria, kidney biopsy

POST-RENAL CT imaging, cystoscopy
Bladder Outlet obstruction Vascular
Bilateral ureteric obstruction HUS/TTP Full haemolysis screen
Ureteric obstruction of single kidney Accelerated hypertension