Acute renal failure has been renamed ‘acute kidney
injury’ (AKI), defined as an abrupt and sustained
decrease in kidney function. AKI in the critically
ill patient is often due to pre-renal elements such
as hypovolaemia, hypotension and ischaemia resulting
in reduced renal DO2. Sepsis is often present. Potentially
nephrotoxic drugs liable to contribute to AKI include
non-steroidal anti-inflammatory drugs (NSAIDs),
angiotensin- converting enzyme (ACE) inhibitors,
angiotensinII receptor antagonists, radiological contrast
media and some antibiotics. Oliguria is frequently an
early sign of systemic problems in critical illness and
successful resuscitation is associated with restoration of
good urine output, an improving acid–base balance and
correction of plasma potassium, urea and creatinine.
Oliguria is also a normal physiological component of the
stress response to major surgery, and care should be taken
not to overfill the post-operative patient with oliguria
who is otherwise cardiovascularly and biochemically well.
In any patient with AKI, renal tract obstruction
(including a blocked urinary catheter) must be excluded.
Acute glomerulonephritis and vasculitis associated with
connective tissue diseases such as microscopic polyarteritis
or Goodpasture’s disease must always be considered
and appropriate investigations such as urine microscopy
and immunopathological tests must be carried
out early.
Diagnostic criteria for acute kidney injury:
An abrupt (within 48 hours) decline in kidney function defined as:
• An absolute increase in serum creatinine of ≥ 26.4 μmol/L
(0.3 mg/dL)
• A percentage increase in serum creatinine of ≥ 50%
(1.5-fold from baseline)
• A reduction in urine output (documented oliguria of
< 0.5 mL/kg for > 6 consecutive hours)
injury’ (AKI), defined as an abrupt and sustained
decrease in kidney function. AKI in the critically
ill patient is often due to pre-renal elements such
as hypovolaemia, hypotension and ischaemia resulting
in reduced renal DO2. Sepsis is often present. Potentially
nephrotoxic drugs liable to contribute to AKI include
non-steroidal anti-inflammatory drugs (NSAIDs),
angiotensin- converting enzyme (ACE) inhibitors,
angiotensinII receptor antagonists, radiological contrast
media and some antibiotics. Oliguria is frequently an
early sign of systemic problems in critical illness and
successful resuscitation is associated with restoration of
good urine output, an improving acid–base balance and
correction of plasma potassium, urea and creatinine.
Oliguria is also a normal physiological component of the
stress response to major surgery, and care should be taken
not to overfill the post-operative patient with oliguria
who is otherwise cardiovascularly and biochemically well.
In any patient with AKI, renal tract obstruction
(including a blocked urinary catheter) must be excluded.
Acute glomerulonephritis and vasculitis associated with
connective tissue diseases such as microscopic polyarteritis
or Goodpasture’s disease must always be considered
and appropriate investigations such as urine microscopy
and immunopathological tests must be carried
out early.
Diagnostic criteria for acute kidney injury:
An abrupt (within 48 hours) decline in kidney function defined as:
• An absolute increase in serum creatinine of ≥ 26.4 μmol/L
(0.3 mg/dL)
• A percentage increase in serum creatinine of ≥ 50%
(1.5-fold from baseline)
• A reduction in urine output (documented oliguria of
< 0.5 mL/kg for > 6 consecutive hours)
No comments:
Post a Comment