Acute kidney injury Flashcards
what is the definition of AKI?
Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output.
what is the epidemiology of AKI?
Becoming more common
what is the aetiology of AKI?
Pre-kidney AKI can be due to various causes of reduced kidney perfusion, such as hypovolaemia, haemorrhage, sepsis, third spacing of fluid (such as in severe pancreatitis), overdiuresis, or other causes of reduced kidney perfusion such as heart failure. Hepatorenal syndrome, a form of pre-kidney AKI not responsive to fluid administration, is seen in cases of severe liver disease. Renovascular disease, especially with the recent addition of an ACE inhibitor to a patient with bilateral renal artery stenosis, is also a consideration, as this sometimes leads to acute tubular necrosis (ATN).
Intrinsic kidney failure may be multifactorial. ATN, rapidly progressive glomerulonephritis, and interstitial nephritis are the most common aetiologies. Vascular diseases, including haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura, scleroderma renal crisis, atheromatous embolisation, and thrombosis, are also potential causes. Severe ischaemic injury may result in cortical necrosis.
Post-kidney AKI results from mechanical obstruction of the urinary outflow tract. Retroperitoneal fibrosis, lymphoma, tumour, prostate hyperplasia, strictures, renal calculi, ascending urinary infection (including pyelonephritis), and urinary retention are common causes.
what are the risk factors for AKI?
Age Kidney disease DM Sepsis Iodinated contrast Nephrotoxins Excessive fluid loss Surgery Haemorrhage Vascular intervention Cardiac arrest Pancreatitis Trauma Malignant hypertension Myeloproliferative disorders Connective tissue disorders Sodium-retaining states Drug overdose Nephrolithiasis
what is the pathophysiology of AKI?
Pre-kidney AKI results from impaired kidney perfusion and the changes seen are appropriate physiological responses. The kidney’s response to a lower perfusion pressure is to enhance sodium and water reabsorption. Baroreceptors in the carotid artery and aortic arch respond to lower blood pressure with sympathetic stimulation. This, along with vasoconstriction of the glomerular efferent arteriole and dilation of the afferent arteriole, is intended to maintain glomerular filtration within a relatively narrow range. Decreasing perfusion promotes activation of the renin/angiotensin/aldosterone system. Angiotensin II, a potent vasoconstrictor, stimulates aldosterone release, promoting sodium and water resorption at the collecting duct. Low blood volume is also a stimulus to the hypothalamus promoting antidiuretic hormone release and increased tubular water re-absorption, concentrating the urine
what are the key presentations of AKI?
Hypotension Risk factors Kidney insults Reduced urine production LUT symptoms Symptoms of volume overload, pulmonary oedema, vomiting, fever, rash, haematuria, palpable bladder
what are the signs of AKI?
Hypotension Risk factors Kidney insults Hypertension Altered mental status Pericardial rub Haemoptysis Abdominal bruit
what are the symptoms of AKI?
Reduced urine production LUT symptoms Symptoms of volume overload, pulmonary oedema, vomiting, fever, rsh, haematuria, palpable bladder Dizziness Muscle tenderness
what are the first line and gold standard investigations for AKI?
Basic metabolic profile - acutely elevated serum creatinine, high serum potassium, metabolic acidosis, confirm the diagnosis of AKI if there is: a rise in serum creatinine of ≥26 micromol/L (≥0.3 mg/dL) within 48 hours OR a rise in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the past 7 days, LFTs will be deranged in hepatorenal syndrome
Serum potassium - elevated in hyperkalaemia, 5.5 to 5.9 mmol/L indicates mild hyperkalaemia, 6.0 to 6.4 mmol/L indicates moderate hyperkalaemia, ≥6.5 mmol/L indicates severe hyperkalaemia
FBC - anaemia, leukocytosis, thrombocytopenia
Bicarbonate - low bicarbonate suggests acidosis
C-reactive protein - elevated in infection and also in vasculitis
Blood culture - positive for bacterial pathogen
Urinalysis - RBCs, WBCs, cellular casts, proteinuria, positive nitrite, and leukocyte esterase
Urine culture - bacterial growth with antibiotic sensitivity
Urine output monitoring - confirm a diagnosis of AKI if urine output <0.5 ml/kg/hour for at least 6 consecutive hours (at least 8 hours in children/young people), if catheterisation is considered appropriate: significant urine volume released after catheter placement points to bladder outlet obstruction, minimal residual urine after catheter placement suggests a non-obstructive cause of AKI or higher level urinary tract obstruction
Fluid challenge - kidney function improves rapidly in pre-kidney AKI
Venous blood gases - an anion gap acidosis occurs in a number of different scenarios
CXR - may show signs of infection, fluid, cardiomegaly, or haemorrhage
ECG - ECG changes associated with hyperkalaemia: peaked T waves, increased PR interval, widened QRS, atrial arrest, and deterioration to a sine wave pattern
what are the differential diagnoses for AKI?
CKD, increased muscle mass, drug side effects
how is AKI managed?
Hypovolemic:
Fluid revascularization, stop nephrotoxins, identify and treat cause, vasoactive drug, blood transfusion, specialist referral
With hyperkalaemia:
Identify and treat cause, insulin and glucose, salbutamol, calcium
Hypervolaemia:
Loop diuretic, sodium restriction, treat cause, renal replacement therapy
With pulmonary oedema:
Upright positioning, high flow oxygen, glyceryl trinitrate
With hyperkalaemia:
Identify and treat cause, insulin and glucose, salbutamol, calcium
how is AKI monitored?
If recovery of function is complete and a normal glomerular filtration rate is re-established with no evidence of residual kidney injury, no kidney follow-up is required.
what are the complications of AKI?
Hyperphosphataemia, uraemia, hyperkalaemia, CKD and end stage kidney disease
what is the prognosis of AKI?
Recovery for AKI is variable and depends on cause of injury and the severity and duration of AKI.
There is an independent association of AKI with a higher risk of death. In-hospital mortality rates associated with AKI vary from 6% to 80%, and there is increased long-term mortality in those with AKI surviving hospitalisation
