History and exam

Key diagnostic factors

Hypotension and/or hypovolaemia is a common cause of reduced kidney perfusion and resulting pre-kidney AKI.[9][62]

  • 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.[3] 

    • Hypovolaemia due to reduced fluid intake is a particular risk for frail, older patients especially those with cognitive or neurological impairment.[9]

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.

Assessing volume status is a crucial part of your initial examination - signs of hypovolaemia are often present.[9][64] Check:

  • Peripheral perfusion (capillary refill)

  • Pulse rate

  • Blood pressure (including a check for postural hypotension)

  • Jugular venous pressure

  • Dry axillae/mucous membranes.

Treat hypovolaemia promptly with an immediate bolus of crystalloid intravenous fluid.[1][62][13][64]

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:[17][18][67][9]

  • Risk factors[3][9][64]

    • Age ≥65 years (frail older people are at particular increased risk).[65]

    • 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).

    • Previous AKI.

    • Myeloproliferative disorder (e.g., multiple myeloma).[5][53]

    Medication history[3][9][62]

    • 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.[9]

    • 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).[77]

    • Recreational drug use.

    • Over-the-counter drugs and herbal remedies.

Practical tip

AKI is often a ‘silent disease’ so a high index of suspicion is important, particularly in acutely ill patients.[62]

  • 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.[67]

Many cases of AKI are precipitated by a kidney insult, particularly in patients with underlying risk factors. Examples include:[1][3][9][62]

  • Sepsis or other acute illness (e.g., acute pancreatitis, burns)

    • Perform a septic screen and implement your local care bundle (e.g., Sepsis Six) if infection is suspected.[9][63] 

  • Hypovolaemia (with or without hypotension)

  • Nephrotoxins

    • Exposure within the previous week to iodinated contrast agent

    • Use of an NSAID or aminoglycoside antibiotic[1]

  • Recent surgery (especially cardiac)

  • Recent vascular intervention - raises the possibility of cholesterol embolisation (livedo reticularis), contrast-induced AKI.[52][64]

Oliguria is one of the diagnostic criteria for AKI and is an earlier indicator of impaired kidney function than rising creatinine.[1] 

  • 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).[1] 

  • Stage the AKI using whichever one of serum creatinine or urine output gives the higher stage.[1][13]

    • 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).[13]

In practice, accurate and timely measurement of urine output is difficult unless the patient is catheterised.

  • Routine catheterisation is not recommended.[1][68]

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.[4]

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.

  • Otherwise the most common cause of volume overload is overenthusiastic fluid resuscitation.[1][13]

Symptoms of volume overload that may be reported at presentation include:

  • Orthopnoea

    • 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).[64]

Vomiting may cause pre-kidney AKI or can be a later manifestation of AKI-related uraemia.[62]

If present, suspect small-vessel vasculitis (e.g., granulomatosis with polyangiitis, microscopic polyangiitis), or interstitial nephritis.[64]

Can occur with kidney stones, papillary necrosis, infection, tumour, or acute glomerulonephritis.

Point to an obstructive cause of AKI.[13][64][65]

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.

May be seen in AKI secondary to renal artery stenosis or a rapidly progressive glomerulonephritis.[18][78][79][9]

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.[13]

Acute pericarditis is a complication associated with severe AKI and worsening uraemia (most often on a background of pre-existing CKD).[13][65]

  • The presence of a pericardial friction rub on examination is an indication for renal replacement therapy (although it may be absent if there is a significant effusion).[1][13]

  • Asterixis is another possible symptom of 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).[64]

Suspect renovascular disease.

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