Acute Kidney Injury Flashcards
What is acute kidney injury?
Sudden deterioration of renal function over hours or days
What is oliguria?
Production of small amounts of urine
100-400ml
What is anuria?
Failure of kidneys to produce urine
<100ml
Three categories of causes of acute kidney injury
Pre renal
Intrinsic renal
Post renal
Risk factors of AKI
- older age >65
- sepsis
- CKD
- heart failure
- diabetes
- liver disease
- cognitive impairment > leading to reduced fluid intake
- meds e.g. diuretics, ACE inhibitors, NSAIDs
- radiocontrast agents
Causes of pre renal cute kidney injury
- Sepsis
- Hypovolaemia
- Shock
- Renal artery stenosis
- NSAIDs
- Congestive cardiac failure
- ACE inhibitors
. generally cause a decreased blood supply to kidneys
Causes of intrinsic renal acute kidney injury
Acute tubular necrosis
Acute interstitial nephritis
Glomerulonephritis
Rhabdomyolysis
Haemolytic uraemic syndrome
Causes of post renal acute kidney injury
Obstruction of urine
Bilateral calculus of ureters
Ureteric/urethra stricture
Tumour
Retro-peritoneal fibrosis
Benign prostatic hyperplasia
Diagnosis of AKI
- rise in creatinine for >25mmol/L in 48 hours
- rise in creatinine of >50% in 7 days
- urine output <0.5nl/kg/hr over >6 hours
Complications of acute kidney injury
- Metabolic acidosis
- Hyperkalaemia
- Ureamia > encephalopathy + pericarditis
- Volume overload > heart failure + pulmonary oedema
Urine volume in oliguria
100-400ml a day
Urine volume in anuria
<100ml a day
Staging of acute kidney injury
Stage 1
- serum creatinine: 1.5-1.9 times baseline
- urine output: <0.5ml/kg/h for 6-12 hours
Stage 2
- serum creatinine: 2-2.9 times baseline
- urine output: <0.5 ml/kg/h for >12 hours
Stage 3
- serum creatinine: 3 times baseline
- urine output: <0.3ml/kg/h for >24hours or anuria for >12 hours
Stage 1 AKI
- serum creatinine: 1.5-1.9 x baseline
- urine output: 0.5ml/kg/h for 6-12 hours
Stage 2 AKI
- serum creatinine: 2-2.9 x baseline
- urine output: <0.5ml/kg/h for >12 hours
Stage 3 AKI
- serum creatinine: 3 x baseline
- urine output: <0.3ml/kg/h for >24hours or anuria for >12 hours
Treatment of pre-renal AKI
Treat the cause
- IV fluids for hypovolaemia
- stop potentially nephrotoxic meds e.g. NSAIDs, ACEi
- diuretics
Treatment of intrinsic renal AKI
- correct electrolytes
- renal replacement therapy (dialysis)
- call nephrology
Treatment of post renal AKI
- urinary or supra-pubic catheter
- ureteric stents
- nephrostomy
Management of AKI
- stop nephrotoxic agents
- treat underlying cause
- fix any electrolyte imbalances
- ensure volume status + perfusion pressure (IV fluids if dehydrated | diuretics if overloaded)
- monitor urine output + daily bloods
How can AKI cause metabolic acidosis?
Unable to make more bicarbonate in intercalated cells or glutamine
Symptoms of a patient with failing kidneys?
- palpitations
- deceased urine output
- fatigue
- vomiting (to resolve acid base imbalance)
- oedema (volume overload)
- confusion (end stage)
What meds do you want to stop if a patient has an AKI?
Stop the DAMN meds
Diuretics
ACE inhibitors
Metformin
NSAIDs
What is acute tubular necrosis?
What is it due to?
Damage + necrosis of the epithelial cells of renal tubules due to:
- ischaemia due to hypoperfusion
- nephrotoxins e.g. gentamicin, radiocontrast agents
What is used to confirm acute tubular necrosis?
Muddy brown casts on urinalysis
Renal tubular epithelial cells may also be seen
What is acute interstitial nephritis?
What is it due to?
Acute inflammation of the interstitium due to an immune reaction assocaited with:
- drugs e.g NSAIDs
- infection e.g. E.coli, HIV
- autoimmune conditions e.g. SLE, sarcoidosis
Management of acute interstitial nephritis
Treat underlying cause
Steroids can reduce inflammation + improve recovery
Are ACEi nephrotoxic?
- No but they should be stopped during an AKI as they reduce filtration pressure
- They have a protective effect on the kidneys long term
Investigations of AKI
- urine dipstick
- daily FBCs, U&Es, LFTs, bone profile (phosphate + Ca) + CRP
- urine PCR
- USS KUB - to rule out obstruction
Indications for renal replacement therapy in AKI
- hyperkalaemia refractory to medical therapy
- metabolic acidosis refractory to medical therapy
- fluid overload refractory to diuretics
- uraemic pericarditis
- uraemic encephalopathy
What further investigations are needed if protein + blood are detected on urine dipstick in patient with AKI and why?
- c-ANCA + p-ANCA - vasculitis
- anti-GBM, ANA, C3 + C4 - lupus nephritis
- serum immunoglobulins + electrophoresis - myeloma
What is haemolytic uraemic syndrome?
What is it due to?
What is the classic triad?
- Involves thrombosis in small blood vessels in the body due to shiga toxins from E.coli or shigella.
.
Triad of: - microangiopathic haemolytic anaemia
- acute kidney injury
- thrombocytopenia
How can haemolytic uraemic syndrome cause the classic triad?
- formation of blood clots uses platelets > thrombocytopenia
- the thrombi partially obstructs small blood vessels + damage RBCs > microangiopathic haemolytic anaemia
- the thrombi reduces kidney perfusion + damage the RBCs > acute kidney injury
Presentation of haemolytic uraemic syndrome
- E. coli + shigella cause gastroenteritis > bloody diarrhoea
- fever
- pallor or jaundice
- bruising
- abdominal pain
- oliguria
- lethargy
- confusion
Management of haemolytic uraemic syndrome
- stool culture to establish causative organism
- blood transfusion
- IV fluids
- anti hypertensive meds
- haemodialysis
What does muscle cell death release?
Myoglobin
Potassium
Phosphate
Creatine kinase
Causes of Rhabdomyolysis
- prolonged immobility
- extremely rigorous exercise beyond person’s fitness level
- crush injuries
- statins
- seizures
Presentation of Rhabdomyolysis
- muscle pain, swelling + weakness
- oliguria
- red-brown urine (Myoglobinuria)
- fatigue
- N+V
- confusion
Investigations of Rhabdomyolysis
- Creatine kinase levels
- U&Es
- potassium levels + ECG
- urine dipstick for presence of blood (for myoglobin in urine)
Management of Rhabdomyolysis
- IV fluids
-
treatments of hyperkalaemia
.
Possible options but have risks: - IV sodium bicarbonate to increase urinary pH
- IV mannitol to increase urine output + reduce oedema
Prevention of AKI
- regular creatinine monitoring if at risk
- review for neprhotoxic drugs
- educate patient on symptoms of AKI
- explain risk of AKI is increased with acute illness, diarrhoea, vomiting
