Hypovolaemic Acute Kidney Injury
Also known as: Hypovolemic Acute Kidney Injury, Prerenal Acute Kidney Injury
Hypovolaemic acute kidney injury is a fall in glomerular filtration caused by reduced effective circulating volume, which lowers renal perfusion pressure. In the early phase the kidney is structurally intact and the injury is functional, reversible within 24 to 72 hours of volume restoration. If hypoperfusion persists beyond this window, ischaemic tubular necrosis follows.
The kidney defends filtration through afferent arteriolar dilation (prostaglandins) and efferent arteriolar constriction (angiotensin II), and increases proximal reabsorption of sodium, water and urea under the influence of angiotensin II, noradrenaline and vasopressin. This produces concentrated, sodium avid urine with a raised urea:creatinine ratio. Drugs that blunt these defences (NSAIDs, ACE inhibitors, angiotensin receptor blockers, SGLT2 inhibitors, diuretics) convert tolerated volume depletion into acute kidney injury.
Causes:
- Gastrointestinal: vomiting, diarrhoea (including cholera), high output stoma, fistula
- Renal: diuretics, osmotic diuresis in uncontrolled diabetes, post-obstructive diuresis, polyuric recovery phase, salt wasting disorders, adrenal insufficiency
- Skin and insensible: burns, heat exposure, fever, excessive sweating
- Third space sequestration: pancreatitis, bowel obstruction, peritonitis, crush injury, hypoalbuminaemia
- Inadequate intake: dementia, sedation, fasting, poor access to water
Elevated risk groups are older adults, patients with chronic kidney disease, diabetes, heart failure and infants.













