Acute Kidney Injury Flashcards
What are the main roles of the kidneys?
- Make urine – regulate salt and water in the body (3-4 pints of urine daily) and remove waste products from your blood into your urine
- Produce hormones – regulate blood pressure and create erythropoietin to control the production of red blood cells
- Activate Vitamin D
- Clean the blood – metabolise and remove drugs from the blood
Define acute kidney injury
“AKI is a clinical syndrome characterised by a rapid reduction in renal excretory function due to several different causes”
AKI is not a primary diagnosis itself but is a syndrome. It occurs on the backbone of other conditions e.g. sepsis and worsening heart failure. Usually treating the primary problem can amend the kidney problem too, but sometime additional treatment and assessment is required. Kidney damage can occur long before it is diagnosed and therefore we need to be aware of the early changes. A decrease in glomerular filtration is a late marker of damage. By the time the glomerular filtration rate decreases by enough to notice, the no. of working nephrons will have decreased by 50%.
AKI is a spectrum of damage from a mild deterioration in function to severe injury requiring renal replacement therapy – as even small rises in creatinine increase the risk of mortality.
How is AKI diagnosed?
Kidney disease: improving global outcomes (KDIGO)
- Rise in creatinine >26umol/L in 48 hours
- Rise in creatinine >1.5 x baseline
- Urine output <0.5ml/kg/hr for >6 consecutive hours
What are the stages of AKI?
Stage 1: Serum creatinine (sCr) criteria = Increase >26umol/L in 48hours OR Increase >1.5 baseline
Urine output criteria =
<0.5ml/kg/h for >6 consecutive hours
Stage 2: Serum creatinine (sCr) criteria = Increase 2-2.9 x baseline
Urine output criteria = <0.5ml/kg/h for >12 hours
Stage 3: Serum creatinine (sCr) criteria = Increase >3 x baseline OR >354umol/L OR Commenced on RRT irrespective of stage
Urine output criteria=
<0.3ml/kg/h for >24hr OR Anuria for 12h
List risk factors associated with developing AKI?
- Age >75
- Chronic kidney disease
- Cardiac failure
- Peripheral vascular disease
- Chronic liver disease
- Diabetes
- Drugs
- Sepsis
- Poor fluid intake/increased loses
- History of urinary symptoms
How can the causes of AKI be categorized?
Pre-renal (40-70%)
Intrinsic renal (10-50%)
Post-Renal (10-25%)
What are the pre-renal causes of AKI?
- Renal hypoperfusion e.g. hypotension, sepsis
- Dehydration and hypovolaemia
- Renal artery stenosis
- ACE inhibitors
- Hepatorenal syndrome
- Intra-abdominal hypertension/ Compartment syndrome
- Severe heart failure
What are the intrinsic renal causes of AKI?
Tubular
o Acute tubular necrosis, often a result of pre-renal damage or nephrotoxins, radiological contrast and myoglobinuria in rhabdomyolysis
o Crystal damage (ethylene glycol poisoning, uric acid)
o Myeloma
o Hypercalcaemia
Glomerular o SLE, o Drugs (NSAIDs, ACEi, ARB, Gentamicin) o Infections o Primary glomerulonephritides
Interstitial
o Drugs
o Infiltration with lymphoma, infection, tumour lysis syndrome
Vascular: o Vasculitis o Malignant hypertension o Thrombus o Cholesterol emboli form angiography o Large vessel occlusion
What are the post-renal causes of AKI?
Luminal:
o Stones
o Clots
Mural:
o Malignancy (e.g. ureteric, bladder, prostate)
o BPH
o Strictures
Extrinsic compression
o Malignancy (esp. pelvic)
o Retroperitoneal fibrosis
How should you assess a patient with AKI?
History
Check for risk factors, comorbidities, previous renal disease, recent fluid intake and losses, new medications. Ask about systemic features e.g. rash, joint pain, fever and other systems enquiry.
Examination:
Abdominal examination esp. for: palpable bladder, palpable kidneys (i.e. polycystic disease), abdominal/pelvic masses, renal bruits (i.e. renovascular disease), rashes
Investigations:
- Urinalysis: infection (leucocytes, nitrites), glomerular disease (blood, protein).
- Urine microscopy: crystals, cells
- Urine culture: infections
- Bloods: U and E’s, FBC, LFT, Clotting, CK, ESR, CRP, ABG, autoantibodies (ANCA, ANA, anti-GBM)
- Imaging: renal USS (obstruction vs. hydronephrosis, cysts, small kidneys, masses
When should you refer to a nephrologist?
Always refer:
• Hyperkalaemia in an oligoanuric patient
• Hyperkalaemia or fluid overload which are unresponsive to medical treatment
• Urea >40mmol/L +/- signs of uraemia
• Suspected glomerulonephritis (blood and protein in urinalysis)
• Suspected systemic disease
Consider referral;
• No obvious reversible cause
• Creatinine > 300 or rising >50umol/L per day.
How should an AKI be managed?
Monitoring:
- Assess volume status: urine output, JVP, skin turgor, BP, pulse, assess for peripheral oedema, ? gallop rhythms, ? lung crepitations.
- Daily U and E’s
- Daily fluid balance chart
- Daily weight
Stop nephrotoxic drugs: NSAIDs, ACEi, Gentamicin, amphotericin.
Aim for euvolaemia
Nutrition
Treat underlying cause:
Pre-renal:
o Volume depletion…. IV fluids
o Sepsis…. Antibiotics, fluids, oxygen
Post-renal:
o Catheterise and consider CT of renal tract
o Urology referral if obstruction likely
o Cystoscopy and retrograde stents, or nephrostomy (if obstruction/hydronephrosis on CT scan)
Intrinsic renal:
o Refer to nephrology
How to manage the complications of an AKI?
Hyperkalaemia:
10ml of 10% calcium gluconate IV, intravenous insulin +glucose, salbutamol nebulizer, IV sodium bicarbonate (if bicarb is low – acidotic).
Pulmonary oedema
Sit up and give high flow oxygen, venous vasodilator (diamorphine), furosemide. If there is no response urgent haemodialysis or hemofiltration is needed.
Uraemia:
May require dialysis if severe or complications e.g. encephalopathy, pericarditis. Otherwise symptomatic management
Acidaemia
May require dialysis, consider sodium bicarbonate
When should dialysis be considered?
Acute kidney injury by its definition will recover, anyone who persists with renal damage after a few months is redefined as having Chronic Kidney Disease and is managed as such.
Therefore, dialysis is usually not necessary and in fact can make recovery prolonged and complicated.
However, if the complications below cannot be controlled with medical therapy, dialysis is life-saving and must be started. These are:
- Hyperkalaemia
- Pulmonary Oedema
- Metabolic acidosis
- Uremic encephalopathy (confusion, myoclonic jerks, seizures, coma) or uremic pericarditis (inflammation of pericardial sac)
- Drug overdose: BLAST – Barbiturates, Lithium, Alcohol (+ ethylene glycol), Salicylate, Theophylline
