Acute Kidney Injury (Acute Renal Failure)
Definition and demographics
Acute Kidney Injury (AKI) formerly known as acute renal failure, refers to the deterioration of renal function acutely over hours or days. It is characterised by a rise in plasma urea and creatinine ratios. This may occur without clinical symptoms, however tends to be associated with oliguria (urine output less than 400ml/day or 0.5ml/kg/h).
Acute kidney injury is common amongst people admitted to hospital.
Causes and risk factors
The causes of acute renal failure may be divided into pre-renal, renal and post renal causes.
An acute rise in urea and creatinine from baseline due to the accumulation of metabolic waste is the primary biochemical sign of renal failure.
Patients with acute kidney injury may present with normal urine output, but more commonly they will be oliguric. However the increased osmolality due to the waste products may also cause polyuria. In patients who are anuric, consider an obstructive cause.
When differentiating chronic renal failure from acute renal failure, patients with chronic renal failure may have a history and signs of chronic renal failure, or previous abnormal tests. They tend to have small kidneys non ultrasound. They may also have anaemia, decreased calcium and raised phosphate, although this may occur in acute renal failure as well. Acute renal failure may also occur on a background of chronic renal failure.
In prerenal failure, patients may also present with signs or symptoms related to volume depletion, although fluid overload from failure to excrete fluids may also occur.
In post renal failure, patient may have a distended bladder and signs and symptoms of obstruction.
Differential diagnosis
Chronic renal failure
Acute on chronic renal failure
Investigations
Urine - dipstick for leucocytes, nitrites, blood, protein, glucose, ketones and specific gravity. Protein and blood in the absence of trauma or an infective cause suggests an acute renal cause.
Microscopy for red cells, white cells, crystals and casts.
Urine cultures and sensitivity
Biochemistry for U+E, Creatinine, osmolarity, and bence jones protein.
Bloods - FBC (may show anaemia or raised WCC, haematological conditions may also affect renal function)
U+Es, LFTs, clotting (DIC in sepsis may affect clotting), Creatinine kinase (raised in rhabdomyolysis), ESR, CRP.
Arterial blood gasses
Blood cultures
Serum immunoglobulins, autoantibodies, and complement concentrations, and serum protein electrophoresis (for myeloma) may show renal causes.
Imaging:
In postrenal failure, and ultrasound may show the site of obstruction, dialation/hydronephrosis above the level of obstruction and cortical thinning may occur in prolonged obstruction. Renal size may be decreased in chronic renal failure.
ECG may show changes if patient has electrolyte abnormalities, and chest x ray may show infection or pulmonary oedema. Doppler ultrasound may show renal artery stenosis, and Abdominal/pelvic x ray may show an obstructing stone. Imaging with contrast should be avoided.
Management
General measures:
Assess and monitor the patient's fluid status. Start fluid balance and weight charts. Insert a urinary catheter and a central line if necessary and monitor urine output and patient status hourly initially. Correct any fluid imbalances, using IV fluids if necessary, and stop any nephrotoxic drugs. Ensure that the patient recieves adequate nutrition, inserting a nasogastric tube if necessary. Monitor electrolyte levels regularly and monitor glucose levels.
Stage 1 - Baseline +28 - 2x baseline or less than 0.5ml/kg/h for over 6 hours
Stage 2 - 2x baseline - 3x baseline or less than 0.5ml/kg/h for 12-24 hour
Stage 3 - 3x baseline + or anuria or 0.3ml/kg/h for over 24 hour.
Treat the underlying cause
Diagnose and treat the underlying cause. This may include blood cultures/septic screen and antibiotics in suspected sepsis, fluid resuscitation in hypovolaemic shock, or relieving any obstructive causes with a catheter initially and more definitive treatment after. Refer to nephrologists or urologists if necessary.
Treat any complications
Hyperkalaemia
Pulmonary oedema
metabolic acidosis
Bleeding
Indications for dialysis:
Perisistent hyperkalaemia
Worsening/severe acidosis
Persistent fluid overload/pulmonary oedema
Complications of uraemia including uraemic pericarditis and encephalopathy.
Prognosis
Mortality and prognosis is dependent on the severity of the AKI and the cause. It may be 20-30% in the UK. Patients with chronic kidney disease are more likely to have poorer outcomes and less likely to recover. Other risk factors include age, and multiorgan failure. Long term renal replacement therapy may be needed in some patients.
http://www.patient.co.uk/doctor/acute-kidney-injury-pro
http://www.renal.org/guidelines/modules#sthash.3O4uNuvj.dpbs
The medics handbook - acute kidney injury.
Acute Kidney Injury (AKI) formerly known as acute renal failure, refers to the deterioration of renal function acutely over hours or days. It is characterised by a rise in plasma urea and creatinine ratios. This may occur without clinical symptoms, however tends to be associated with oliguria (urine output less than 400ml/day or 0.5ml/kg/h).
Acute kidney injury is common amongst people admitted to hospital.
Causes and risk factors
Prerenal causes includes causes which reduce renal perfusion:
- Sepsis (often due to post surgical or due to pneumonia)
- Haemorrhage
- Burns
- Dehydration due to diarrhoea and vomiting etc.
- Drug induced hypotension (NSAIDs, ACE inhibitors, COXibs, AIIRAs)
- Cardiogenic shock
- Hepatorenal syndrome
- Renal artery stenosis, obstruction due to abdominal aortic aneurysm, malignant hypertension.
Renal causes:
- Acute tubular necrosis -caused by prerenal disease - The kidneys are very sensitive to changes in blood flow, and as the medulla has recieves the least blood, it is often the first to become ischaemic. in acute tubular necrosis, the ability for the kidneys to concentrate urine is lost. This can be distinguished from prerenal AKI by urine sodium, osmolality and urine/plasma ratios of creatine and urea. In prolonged ischaemia, the cortex may become necrotic, and function may not recover.
- Glomerular causes (glomerulonephritis, vasculitis)
- Nephrotoxic durgs (aminoglycosides ,amphotericin B, tetracyclines, NSAIDs, ACE inhibitors)
- Poisoinous chemicals (heavy metals)
- myoglobinuria (eg. in rhabdomyolysis)
- Intrarenal obstruction (urate, oxalate crystals, calcium, tubular casts (myeloma))
- Acute interstitial nephritis (drug induced hypersensitivity, infection, autoimmune)
- Hypercalcaemia
- Haemolytic uraemic syndrome
- Thrombotic thrombocytopenic purpura
Post renal causes:
Presentation - Stones
- Clots
- Prostate hypertrophy or carcinoma
- Pelvic malignancy
- Urethral Stricture
- Bladder cancer
- renal cancer
- Fibrosis
- Neuromuscular dysfunction
- Schitosomiasis
Risk factors
Risk factors for developing AKI include old age ( above 65), coexisting comorbidities such as heart failure, liver disease, or existing chronic renal failure. In addition, any condition which increases the risk of reduced renal perfusion such as sepsis, diarrhoea and vomiting, poor oral intake due to other disabilities (eg. dementia patients) may increase this risk. Drugs and contrast agents may also increase the risks of AKI.
An acute rise in urea and creatinine from baseline due to the accumulation of metabolic waste is the primary biochemical sign of renal failure.
Patients with acute kidney injury may present with normal urine output, but more commonly they will be oliguric. However the increased osmolality due to the waste products may also cause polyuria. In patients who are anuric, consider an obstructive cause.
When differentiating chronic renal failure from acute renal failure, patients with chronic renal failure may have a history and signs of chronic renal failure, or previous abnormal tests. They tend to have small kidneys non ultrasound. They may also have anaemia, decreased calcium and raised phosphate, although this may occur in acute renal failure as well. Acute renal failure may also occur on a background of chronic renal failure.
In prerenal failure, patients may also present with signs or symptoms related to volume depletion, although fluid overload from failure to excrete fluids may also occur.
In post renal failure, patient may have a distended bladder and signs and symptoms of obstruction.
Differential diagnosis
Chronic renal failure
Acute on chronic renal failure
Investigations
Urine - dipstick for leucocytes, nitrites, blood, protein, glucose, ketones and specific gravity. Protein and blood in the absence of trauma or an infective cause suggests an acute renal cause.
Microscopy for red cells, white cells, crystals and casts.
Urine cultures and sensitivity
Biochemistry for U+E, Creatinine, osmolarity, and bence jones protein.
Bloods - FBC (may show anaemia or raised WCC, haematological conditions may also affect renal function)
U+Es, LFTs, clotting (DIC in sepsis may affect clotting), Creatinine kinase (raised in rhabdomyolysis), ESR, CRP.
Arterial blood gasses
Blood cultures
Serum immunoglobulins, autoantibodies, and complement concentrations, and serum protein electrophoresis (for myeloma) may show renal causes.
Imaging:
In postrenal failure, and ultrasound may show the site of obstruction, dialation/hydronephrosis above the level of obstruction and cortical thinning may occur in prolonged obstruction. Renal size may be decreased in chronic renal failure.
ECG may show changes if patient has electrolyte abnormalities, and chest x ray may show infection or pulmonary oedema. Doppler ultrasound may show renal artery stenosis, and Abdominal/pelvic x ray may show an obstructing stone. Imaging with contrast should be avoided.
Management
General measures:
Assess and monitor the patient's fluid status. Start fluid balance and weight charts. Insert a urinary catheter and a central line if necessary and monitor urine output and patient status hourly initially. Correct any fluid imbalances, using IV fluids if necessary, and stop any nephrotoxic drugs. Ensure that the patient recieves adequate nutrition, inserting a nasogastric tube if necessary. Monitor electrolyte levels regularly and monitor glucose levels.
Stage 1 - Baseline +28 - 2x baseline or less than 0.5ml/kg/h for over 6 hours
Stage 2 - 2x baseline - 3x baseline or less than 0.5ml/kg/h for 12-24 hour
Stage 3 - 3x baseline + or anuria or 0.3ml/kg/h for over 24 hour.
Treat the underlying cause
Diagnose and treat the underlying cause. This may include blood cultures/septic screen and antibiotics in suspected sepsis, fluid resuscitation in hypovolaemic shock, or relieving any obstructive causes with a catheter initially and more definitive treatment after. Refer to nephrologists or urologists if necessary.
Treat any complications
Hyperkalaemia
Pulmonary oedema
metabolic acidosis
Bleeding
Indications for dialysis:
Perisistent hyperkalaemia
Worsening/severe acidosis
Persistent fluid overload/pulmonary oedema
Complications of uraemia including uraemic pericarditis and encephalopathy.
Prognosis
Mortality and prognosis is dependent on the severity of the AKI and the cause. It may be 20-30% in the UK. Patients with chronic kidney disease are more likely to have poorer outcomes and less likely to recover. Other risk factors include age, and multiorgan failure. Long term renal replacement therapy may be needed in some patients.
http://www.patient.co.uk/doctor/acute-kidney-injury-pro
http://www.renal.org/guidelines/modules#sthash.3O4uNuvj.dpbs
The medics handbook - acute kidney injury.
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