Synopsis
Distinguish true intravascular depletion from low effective arterial circulation and venous congestion, restore renal perfusion safely, and prevent haemodynamic AKI from becoming structural injury.
- Pre-renal AKI reflects reduced glomerular filtration from impaired perfusion without necessarily implying whole-body dehydration; haemorrhage, sepsis, low cardiac output and cirrhotic vasodilatation can produce different haemodynamic phenotypes.
- Effective filtration depends on systemic pressure, renal blood flow and glomerular arteriolar tone. NSAIDs impair prostaglandin-mediated afferent dilatation, while ACE inhibitors and ARBs reduce angiotensin-mediated efferent constriction.
- Diuretics can compound salt and water loss, creating the familiar ACE inhibitor or ARB plus diuretic plus NSAID risk combination, particularly during intercurrent illness.
- Examine for both depletion and congestion: mucosa, capillary refill, postural symptoms, jugular venous pressure, oedema, lung crackles, weight change, perfusion, bedside echo and passive-leg-raise response where expertise exists.
- A single fluid challenge should have a stated indication, amount and reassessment endpoint. Failure to improve should trigger diagnostic revision rather than serial unrecorded boluses.
- Sepsis-associated AKI is not purely ‘pre-renal’; inflammation, microcirculatory dysfunction and tubular injury may coexist, so treat infection and haemodynamics while avoiding false certainty from urinary indices.
- Fractional excretion of sodium and urea can be distorted by diuretics, CKD, sepsis and timing. They may support a carefully framed assessment but should not overrule examination, urine sediment and trajectory.
- Temporarily withholding a haemodynamically active medicine can be appropriate during hypotension or volume loss, but its indication must be revisited promptly once perfusion, potassium and renal function stabilise.
Key red flags
Vomiting, diarrhoea, fever, burns, polyuria, poor intake or haemorrhage with weight loss, thirst, postural symptoms, tachycardia and low filling signs favours true depletion. Older adults and people taking beta blockers may lack classic tachycardia.
Infection, hypotension, altered mentation, raised lactate or mottled perfusion may indicate distributive shock. Cardiac dysfunction and capillary leak can coexist, so early antibiotics and source control accompany measured haemodynamic support.
Raised JVP, oedema, pulmonary congestion, cool peripheries and oliguria suggest cardiac failure with poor forward flow and venous back pressure. Additional crystalloid can worsen renal congestion and gas exchange.
Investigation priorities
Identify haemodynamic compromise and quantify response to initial resuscitation.
Management branches
A compatible history and examination indicate hypovolaemia without pulmonary or systemic congestion.
- 1. Control ongoing losses, obtain urgent blood tests and cross-match when bleeding is possible, and establish reliable observations and urine measurement.
- 2. Give a locally approved isotonic crystalloid bolus, or blood products through the haemorrhage pathway when appropriate, with a pre-specified reassessment time.
- 3. Recheck perfusion, pressure, respiratory findings and dynamic response; continue cautiously only when benefit is demonstrated and stop if overload develops.
- 4. Replace continuing gastrointestinal or urinary losses thoughtfully, correct electrolytes and review medicines that worsen the current haemodynamic state.