History and exam
Key diagnostic factors
Often due to acute illness (e.g., sepsis and vasodilatation; haemorrhage; vomiting and diarrhoea), particularly in a patient with background risk factors.
Can also result from dehydration due to poor fluid intake, over-diuresis, or insufficient replacement fluids in a hospital inpatient.
Hypovolaemia due to reduced fluid intake is a particular risk for frail, older patients especially those with cognitive or neurological impairment.
Hypotension may be absolute (SBP <90 mmHg) or relative to the patient’s usual BP (a drop of >40 mmHg from baseline).
May be related to antihypertensive medications.
Peripheral perfusion (capillary refill)
Blood pressure (including a check for postural hypotension)
Jugular venous pressure
Dry axillae/mucous membranes.
Prolonged hypotension can cause pre-kidney AKI to progress to cell damage and acute tubular injury (intrinsic AKI).
AKI is commonly asymptomatic so is easily missed. Whenever a patient presents with an acute illness, ensure your history covers characteristics that increase the risk of AKI. Check for:
Age ≥65 years (frail older people are at particular increased risk).
History of any one or more of chronic kidney disease (CKD), heart failure, liver disease, diabetes, dementia (or any other neurological/cognitive impairment that may result in limited access to oral fluids).
Non-steroidal anti-inflammatory drug (NSAID) or aminoglycoside antibiotic use (nephrotoxic potential - can cause drug-induced interstitial nephritis).
ACE inhibitor/angiotensin-II receptor antagonist use.
Renin-angiotensin system modifying agents reduce the kidney’s ability to adapt to changes in perfusion pressure by lowering efferent glomerular arteriolar tone, making it more difficult for the kidney to maintain glomerular filtration pressure in the event of hypovolaemia/hypotension.
Diuretic or any other antihypertensive - particularly if started (or dose changed) in the last 7 days.
These medications increase the risk of hypovolaemia and/or hypotension.
Aciclovir, methotrexate, triamterene, indinavir, or sulfonamides (can cause tubular obstruction by forming crystals).
Recreational drug use.
Over-the-counter drugs and herbal remedies.
AKI is often a ‘silent disease’ so a high index of suspicion is important, particularly in acutely ill patients.
Most patients with AKI present asymptomatically, with non-specific symptoms or with symptoms solely related to the precipitating illness (e.g., sepsis).
A 2009 report from the UK’s National Confidential Enquiry into Patient Outcome and Death (NCEPOD) identified an unacceptable delay in post-admission diagnosis of AKI in 43% of patients who died in hospital from the condition.
Sepsis or other acute illness (e.g., acute pancreatitis, burns)
Hypovolaemia (with or without hypotension)
Exposure within the previous week to iodinated contrast agent
Use of an NSAID or aminoglycoside antibiotic
Recent surgery (especially cardiac)
Oliguria is one of the diagnostic criteria for AKI and is an earlier indicator of impaired kidney function than rising creatinine.
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).
But be aware that patients with AKI are often not oliguric.
Anuria suggests either an obstructive cause or severe AKI from a pre-kidney or intrinsic cause.
AKI can also be staged according to the extent to which urine output falls (or serum creatinine rises).
Stage 1 AKI: urine output <0.5 mL/kg/h for at least 6 consecutive hours
Stage 2 AKI: urine output <0.5 mL/kg/h for at least 12 consecutive hours
Stage 3 AKI: urine output <0.3 mL/kg/h for at least 24 consecutive hours or anuria for 12 hours
A higher stage of AKI is associated with a greater risk of death as well as increased likelihood of needing renal replacement therapy (RRT).
In practice, accurate and timely measurement of urine output is difficult unless the patient is catheterised.
Lower urinary tract symptoms such as urgency, frequency, or hesitancy are suggestive of a urinary tract obstruction.
Prostatic hyperplasia is a common cause of obstructive AKI in older men.
Symptoms and signs of volume overload may be seen at presentation if the patient has obstructive AKI or any form of AKI against a background of pre-existing heart failure.
Symptoms of volume overload that may be reported at presentation include:
From pulmonary oedema or AKI-related acidosis
Swollen ankles/other signs of peripheral oedema
From an obstructive cause or in patients with nephrotic syndrome secondary to glomerulonephritis.
Examination signs in a patient with volume overload might include:
Crackles on auscultation of lungs (suggests pulmonary oedema)
Tachypnoea (suggests fluid overload and/or acidosis).
Vomiting may cause pre-kidney AKI or can be a later manifestation of AKI-related uraemia.
If present, suspect small-vessel vasculitis (e.g., granulomatosis with polyangiitis, microscopic polyangiitis), or interstitial nephritis.
Can occur with kidney stones, papillary necrosis, infection, tumour, or acute glomerulonephritis.
Other diagnostic factors
Orthostatic symptoms and postural hypotension confirmed on blood pressure monitoring are consistent with hypovolaemia and suggest pre-kidney AKI.
Thirst is another common symptom of hypovolaemia.
A change in mental status is usually secondary to a primary kidney insult (e.g., sepsis) that precipitated AKI.
Confusion can also result from encephalopathy in a patient with AKI-related uraemia.
Suspect intrinsic AKI secondary to rhabdomyolysis and tubular toxicity from myoglobin in the setting of acidosis.
Suspect an intrinsic cause of AKI (e.g., small vessel vasculitis or anti-glomerular basement membrane antibody disease).
Suspect renovascular disease.
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