History and exam
Key diagnostic factors
common
presence of risk factors
Key risk factors include low renal perfusion, underlying renal disease, diabetes mellitus, hypotension, multiple myeloma, exposure to nephrotoxins or radiocontrast media, excessive fluid loss, sepsis, muscle trauma, major surgery, cardiac arrest, haemolysis, hyperuricaemia, mechanical ventilation, chronic hypertension, and advanced age.
oliguria or anuria
Oliguria and anuria, although not diagnostic, may be present in ATN. Oliguria is usually present in the maintenance phase. Nephrotoxic ATN is less prone to show oliguria than ischaemic ATN due to fluid depletion.
hypotension
Common in ATN due to fluid depletion.
tachycardia
Common in ATN due to fluid depletion.
Other diagnostic factors
common
poor oral intake and anorexia
Patients may have poor oral intake, and anorexia.
malaise
Patients may have malaise.
uncommon
thirst
Excessive fluid loss (due to haemorrhage, burns, gastrointestinal losses, or sweating) may present with symptoms of hypovolaemia, including thirst.
dizziness
Excessive fluid loss (due to haemorrhage, burns, gastrointestinal losses, or sweating) may present with symptoms of hypovolaemia, including dizziness.
orthopnoea/dyspnoea
May occur if advanced cardiac failure is present leading to reduced renal perfusion.
oedema
Patients with fluid loss, sepsis, or pancreatitis may have signs of circulatory collapse including oedema.
Risk factors
strong
chronic kidney disease (CKD)
Pre-existing CKD increases susceptibility to acute kidney injury (AKI). Lower levels of glomerular filtration rate are associated with higher risk of AKI.[13]
chronic hypertension
Patients with chronic hypertension are more vulnerable to situations of hypoperfusion as the kidney’s autoregulation processes are impaired. Due to chronic structural changes in renal arterioles and small arteries, afferent arteriolar resistance does not decrease as it should, or may even increase in situations of hypoperfusion, increasing the susceptibility of renal ischaemia.[2]
diabetes mellitus
advanced age
Advanced age is associated with a higher prevalence of chronic kidney disease, underlying renal vascular disease, and other comorbid medical conditions that predispose to ATN.[18]
low-perfusion states
Hypotension and/or excessive fluid loss from haemorrhage, the gastrointestinal tract (e.g., vomiting and diarrhoea), sweating, or burns may cause a decrease in renal blood supply, which can lead to ischaemic injury and result in ATN. Anasarca (severe and generalised oedema), such as may occur in congestive heart failure or cirrhosis, may cause reduced kidney perfusion. Cardiac arrest or mechanical ventilation can lead to alterations of haemodynamics and worsen renal function.
The sensitivity of individual patients to a decrease in renal perfusion is variable. For example, some patients suffer from ATN after a few minutes of hypoperfusion, while others tolerate several hours of ischaemia without structural damage to the kidney. In fact, several studies have shown how acute kidney injury may develop with normal or even increased renal perfusion due to a dysfunction of the intrarenal microcirculation, which appears to play an important role in the pathogenesis.[19][20] It is not clear whether this is a direct cause of kidney injury as a result of inflammatory diseases such as sepsis, or an adaptive mechanism.[20]
sepsis
Sepsis is the most common condition associated with acute kidney injury (AKI) in hospital and intensive care units (ICUs).[1] Globally, it has been reported in almost 50% of patients with severe AKI in ICUs. In Europe, AKI has been reported in up to 51% of patients with sepsis, with a mortality up to 41% in ICUs. Sepsis is characterised by a systemic inflammatory response to an infection. The pathogenesis of septic AKI is still not fully understood. Systemic vasodilation leads to a decrease in renal blood supply and resulting ischaemia. There is also direct toxic injury generating an inflammatory response, with vascular injury (endothelial dysfunction, microvascular obstruction, vasoconstriction, coagulopathy, and vascular oedema) as well as tubular injury.[1]
major surgery
Certain types of surgery are associated with higher risks of renal hypoperfusion, such as in vascular surgery, where the aorta is cross-clamped above the renal arteries. Cold ischaemia can occur during renal transplantation, renal surgery, or renal artery thrombosis and can lead to ischaemic injury and ATN. The pathophysiology of acute kidney injury following cardiac surgery is complex and involves multiple factors (including pre-, intra-, and post-operative factors). Hypoperfusion, ischaemia-reperfusion injury, neurohormonal activation, oxidative stress, and inflammation leads to vasoconstriction that leads to a reduction in renal perfusion and renal ischaemia.[20]
exposure to nephrotoxic agents
Examples include non-steroidal anti-inflammatory drugs, amphotericin-B, aminoglycosides, chemotherapeutic agents (e.g., cisplatin), calcineurin inhibitors (tacrolimus, ciclosporin), and poisons (e.g., ethylene glycol). ATN occurs in 10% to 20% of patients receiving aminoglycosides.[5]
exposure to radiocontrast media
Exposure to radio-isotopic contrast media may cause ATN within 7 days after exposure.[3][5][21] Incidence is variable and influenced by patient-related factors, such as pre-existing chronic kidney disease and diabetic nephropathy. The type and volume of contrast (>350 mL), as well as repeated administration within 72 hours can also increase the risk.[21]
exposure to endogenous toxins
Muscle trauma (e.g., crush injury) may cause rhabdomyolysis, which will produce an increased myoglobin release that can occlude the renal filtration. Haemolysis, increased haemoglobin release, can lead to ATN. In patients with multiple myeloma there may be increased light chain proteins precipitated into the tubular lumen associated with myeloma of the kidney. Bacterial toxins may also cause toxic injury and result in ATN. Hyperuricaemia (e.g., gout, tumour lysis syndrome) leads to acute crystal-induced nephropathy, which may result in ATN.
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