Acute Kidney Injury Flashcards
What is acute kidney injury (AKI)?
Abrupt deterioration in renal function over hours/days with evidence of rising serum urea and creatinine and low urine output.
Usually reversible over days or weeks
Renal causes can be divided according to site into pre-renal, renal and post renal.
What is the underlying pathology in each of the categories above and examples of each?
I. Pre-renal causes => reduced kidney perfusion leads to falling GFR
i. Decreased vascular volume e.g. haemorrhage, diarrhoea & vomiting, burns, pancreatitis
ii. Decreased cardiac output e.g. cardiogenic shock, MI
iii. Systemic vasodilation e.g. sepsis, drugs
iv. Renal vasoconstriction e.g. NSAIDs. ACE-i, ARB, hepatorenal syndrome
II. Renal causes:
i. Injury to glomerulus e.g. glomerulonephritis, acute tubular necrosis (prolonged renal hypo perfusion causing intrinsic renal damage)
ii. Injury to the interstitium e.g. drug reaction, infection, infiltration (e.g. sarcoid)
iii. Vessels e.g. vasculitis, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura
III. Post-renal causes
i. Within renal tract e.g. stone, renal tract malignancy, stricture, clot
ii. Extrinsic compression e.g. pelvic malignancy, prostatic hypertrophy, retroperitoneal fibrosis
What are the commonest causes of acute kidney injury?
Sepsis
Major surgery
Cardiogenic shock
Other hypovolaemia
Drugs
Hepatorenal syndrome
Obstruction
How common is AKI?
AKI is common
=> 18% of hospital patients
=> 50% of ICU patients
What are the risk factors for AKI?
Pre-existing CKD
Age
Male
Comorbidity i.e. diabetes, cardiovascular disease, malignancy, chronic liver disease, complex surgery
How is the severity of AKI staged?
AKI is classified using the 3 stage KDIGO classification based on serum creatinine and urine output.
Stage 1:
Creatinine: 1.5-1.9 x baseline or >26.5umol/L (0.3mg/dL)
Urine: <0.5mL/kg/h for 6-12h
Stage 2:
Creatinine: 2.0-2.9 x baseline
Urine: <0.5mL/kg/h for >12h
Stage 3:
Creatinine: >3.0 x baseline or renal replacement therapy
Urine: <0.3mL/kg/h for >24h or anuria for >12h
How does KDIGO classification for AKI define AKI?
Rise in creatinine >26umol/L within 48h
Rise in creatinine >1.5 x baseline (i.e. before the baseline) within 7 days
Urine output <0.5mL/kg/h for >6 consecutive hours
What is the pathophysiology underlying pre-renal AKI?
Falling renal blood flow => falling GFR due to circulation changes or infrarenal vasomotor changes
What are the causes of hypovolaemia (pre-renal AK)?
Dehydration
Reduced intake i.e. nil by mouth, confusion
Gut losses i.e. vomiting, nasogastric tube loses, diarrhoea
Renal losses i.e. diuretics, hyperglycaemia
Haemorrhage
Burns, sweating
Third space losses i.e. pancreatitis, peritonitis, bowel obstruction
Systemic vasodilation (septic shock, cirrhosis)
Cardiac failure or shock (MI, arrhythmias, cardiomyopathy, tamponade)
NORMAL PHYSIOLOGY
Normal: Kidney maintains GFR close to normal despite variation in perfusion due to autoregulation (i.e. nitric oxide, prostaglandins and angiotensin)
Stimulus:
Reduced renal perfusion => reduced transglomerular pressure and GFR
Response:
Intrarenal activation of renin-angiotensin system
=>efferent arteriolar vasoconstriction
=> increases transglomerular pressure
=> restores GFR
INFO CARD
Autoregulation fail => fall in GFR => AKI
Reduced blood flow => parenchymal injury
If renal perfusion corrected early = AKI resolved
INFO CARD
Why does urine specific gravity or osmolality rise in AKI?
Because solutes are concentrated into smaller urine volume
Fall in urine volume is due to the kidney retaining fluid to try and improve renal blood flow
Urine sodium is also low because salt is retained to help retain fluid
What is the management of pre-renal AKI?
Crystalloid fluid resuscitation
*Normal saline can lead to hyperchloraemic acidosis.
Where can obstruction occur in post-renal AKI?
Obstruction anywhere between calyces to the external urethral orifice in the urinary tract
Commonly, its bladder outflow obstruction i.e. BPH or bilateral ureteric obstruction i.e. stones or tumours
*Any unexplained AKI => ultrasound to exclude obstruction because once relieved, renal function returns to normal
What is the most common form of AKI?
Renal parenchymal AKI affecting 80-90% of AKI patients
What is the most common cause of renal parenchymal AKI?
Acute tubular necrosis (ATN)
Any cause of pre-renal if prolonged to the point of autoregulation failure => ischaemic ATN
ATN can also result from direct tubular toxins
What causes acute tubular necrosis?
Sustained under-perfusion and reduced renal blood flow of renal tubules => tubular cell death
Nephrotoxins => direct injury and cell death in renal tubules
What is the pathology following acute tubular necrosis?
Reduced renal blood flow
=> reduced GFR as glomeruli contract through afferent arteriolar spasms
=> filtrate leaks backward toward the glomerulus
=> tubular obstruction
How is pre-renal diagnosed?
Mostly a clinical diagnosis based on clinical examination and assessing the volume status
=> large palpable bladder suggests longstanding outflow obstruction
=> draining large urine volumes after inserting a urethral catheter
=> ultrasound of the kidneys and bladder
What investigations are carried out in AKI?
Urinalysis: red blood cells indicative of glomerulonephritis
Blood tests: serum urea, creatinine, electrolytes, calcium, phosphate, albumin, alkaline phosphatase and urate concentration.
Coagulation, blood cultures and nephrotic drug blood level measurements.
Urinary & plasma biomarkers i.e. kidney injury molecule 1, insulin like growth factor binding protein 7, tissue inhibitor of metalloproteinases-2 rise within a few hours of AKI
Ultrasound is key: renal size (measured pole-pole length) and echogenicity (increased in scarring)
=> small scarred kidney suggests long term insult
What are the complications of AKI?
Hyperkalaemia
Pulmonary oedema
Sepsis
How do you manage hyperkalaemia as a result of AKI?
Hyperkalaemia can be life-threatening => cardiac dysrhythmias i.e. ventricular fibrillation
Treatment:
IV sodium bicarbonate reduces potassium by correcting acidosis
=> should not be used in volume overloaded patients as can trigger/exacerbate pulmonary oedema
How do you manage pulmonary oedema as a result of AKI?
IV furosemide diuresis
Dialysis
Haemofiltration
How do you manage sepsis as a result of AKI?
Blood cultures + septic screen + U&E
Urine output - monitor hourly + urea
Fluid resuscitation
Antibiotics IV - avoid nephrotoxic antibiotics
Lactacte - ABG
Oxygen - to correct hypoxia
How should fluid and nutrition be managed in an AKI patient?
Fluid: Daily assessment x2
Bolus crystalloid fluid 250-500mL in 15 mins until volume replete
*if 2L given without response, seek help
Once patient is euvolaemic, daily fluid intake = urine output
Nutrition: salt and potassium restriction
When may renal replacement therapy be indicated?
Main indication for blood purification and/or fluid removal are:
i. Symptomatic uraemia (including pericarditis or tamponade)
ii. Hyperkalaemia not controlled conservatively
iii. Pulmonary oedema not controlled by diuresis
iv. Severe acidosis
v. to remove nephrotoxic drugs i.e. gentamicin, lithium, severe aspirin overdose
What types of renal replacement therapy may be used in AKI?
- Haemodiafiltration (intermittent haemodialysis)
- Continuous venovenous haemofiltration (CVVHF)
- Peritoneal dialysis
How does continuous venovenous haemofiltration (CVVHF) work to treat AKI?
CVVHF achieves blood flow using a blood pump to draw and return blood from the lumen of dual-lumen catheter placed in the jugular, subclavian or femoral vein.
Ultrafiltrate (i.e. plasma) is continuously removed from the patient (at rates of 1000mL/h), combined with simultaneous infusion of replacement solution
Peritoneal dialysis is used in resource poor countries - it has low efficiency (removes fluid slowly).
INFO CARD
What general measures are taken in AKI?
Infection control
Physiotherapy
Fluid balance (intake and urine output) => key to recovery ; consider urinary catheter + hourly urine output
Daily measurements of weight esp in patients receiving fluid (prevent fluid overload)
Daily measurements of lying and standing BP
Medication review - stop nephrotoxin meds => diuretics only in symptomatic fluid overload, otherwise not at all, esp not k+ sparing diuretics
Obs every 4 hours
What are the ECG changes seen in AKI?
Hyperkalaemia:
Tall tented T waves
Increased PR interval
Small/absent p wave
Widened QRS complex
Treat K+ >6.5mmol/L or any with ECG changes
Do ECG for all k+ >6.0mmol/L)
How do you treat hyperkalaemia ?
- Give 10ml of 10% calcium chloride or 30ml of 10% calcium gluconate IV via big vein over 5-10 mins => cardioprotective but doesn’t reduce K+ levels
- IV insulin in 25g glucose => insulin stimulates intracellular uptake of K+, lowering serum K+.
Monitor hourly for hypoglycaemia - Salbutamol => intracellular K+ shift but high dose required and tachycardia can limit the use
- Definitive treatment = K+ removal via renal replacement therapy
