Synonym(s)
DefinitionThis section has been translated automatically.
The current diagnosis of Acute Renal Failure is based on the 2012 KDIGO criteria (Kidney Disease: Improving Global Outcome") and is considered to be present if one of the following criteria is met:
Increase in serum creatinine by ≥0.3 mg/dL (26.5 μmol/L) within 48 hours
Increase in serum creatinine to ≥1.5-fold within the last 7 days
Newly occurred reduction of the urine quantity <0.5 mL/kgKG/h over 6 hours
ClassificationThis section has been translated automatically.
Stadium | Serum Creatinine | Urinary excretion |
---|---|---|
1 |
1.5 to 1.9 times increase (within 7 days) or Increase by 0.3 mg/dL (26.5 μmol/L) (within 48 hours) |
<0.5 mL/kgKG/h for 6-12 h |
2 | 2 to 2.9 times increase (within 7 days) |
<0.5 mL/kgKG/h for ≥12 h |
3 |
≥6-fold? increase (within 7 days) or Increase to ≥4 mg/dL (353.6 μmol/L) or Start of a renal replacement therapy or Patients <18 years: decrease of eGFR to <35 mL/min/1.73 m2 |
<0.3 mL/kgKG/h for ≥24 h or Anuria for ≥12 h |
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EtiologyThis section has been translated automatically.
Prerenal acute renal failure (60%):
- Reduced perfusion is the cause of loss of function, e.g. due to hypovolaemia or reduced circulating blood volume, for example in the context of shock, sepsis or nephrotic syndrome. A long-lasting prerenal genesis can additionally lead to intrarenal kidney versgene through tubule necrosis.
Intrarenal acute renal failure (35%); the cause is an O2 deficiency of the renal parenchyma due to reduced perfusion:
- tubular causes:
- Acute tubule necrosis (mainly) due to ischemia or drug toxicity
- Pigment nephropathy, for example due to haemolysis or rhabdomyolysis (crush syndrome)
- macrovascular causes:
- Renal vein thrombosis
- Renal artery stenosis
- Renal infarctions
- Artery dissections
- microvascular/glomerular causes:
- Glomerulonephritides
- thrombotic microangiopathies (e.g. HUS, HELP syndrome)
- Cholesterol Embolism
- local bacterial infections
Postrenal acute kidney failure (5%)
- an obstruction is the cause of acute renal failure (acquired: e.g. renal pelvic stones, tumours or congenital: e.g. urethral strictures, malformations of the bladder)
Clinical pictureThis section has been translated automatically.
The clinic of acute kidney failure is non-specific. Asymptomatic courses are possible.
Possible leading finding: oligo- or anuria
Three phases of acute kidney failure are described (Herold 2019):
- asymptomatic initial phase or symptoms of the underlying disease
- Phase of manifest renal failure characterised by an increase in retention parameters
- Diuretic/polyuretic phase
DiagnosisThis section has been translated automatically.
Diagnosis based on the amount of urine excreted or the increase in creatinine.
Staging according to KDIGO
Determination of the cause by:
- anamnesis (loss of fluid, intake of nephrotoxic drugs...)
- physical examination (signs of hypervolemia, hypovolaemia)
- Laboratory (blood: creatinine, urea, electrolytes, blood count, BGA, CK, LDH, lipase, possibly BK, electrophoresis; urine: urine sediment, urine status, determination of fractional sodium excretion to differentiate between prerenal and intrarenal acute renal failure)
- Imaging mainly by sonography
- Renal biopsy to exclude a rapid progressive form
Complication(s)This section has been translated automatically.
- fluid lung, pleural effusions
- Anemia, Uremia
- upper gastrointestinal bleeding
- Cardiac arrhythmias, pericarditis
- encephalopathy, seizures
- Infections, sepsis
TherapyThis section has been translated automatically.
- Treatment of the underlying disease,
- Avoid nephrotoxic drugs
- Balanced volume output
- depending on the genesis: immunosupressive therapy, revascularization, removal of the obstruction
- renal replacement therapy if necessary
LiteratureThis section has been translated automatically.
- Gudsoorkar PS et al (2019) Acute Kidney Injury, Heart Failure, and Health Outcomes. Cardiol Clin 37:297-305.
- Zarbock A et al. (2014) New KDIGO guidelines on acute kidney injury. Practical recommendations.
Anaesthesiologist 63:578-88.