Acute kidney injury is a spectrum of disease ranging from those at risk of renal injury (manifested by a slight elevation of creatinine or transient oliguria) through renal injury (greater elevation of creatinine and more prolonged oliguria) to frank renal failure.
Acute renal failure is manifested as:
It is important to realize that both risk and injury can often be rapidly reversed by treatment, but reversal of established renal failure is usually dependent on spontaneous renal recovery. It is, therefore, vital to intervene early in the patient with acute kidney injury.
As a result adults with urine output <0.5 mL/kg/h should be urgently assessed for reversible causes of oliguria and acute renal failure.
Under normal circumstances the oxygen extraction of the outer medulla of the kidney is near maximal. As a result, this part of the kidney is very susceptible to hypoxia as a result of decreased blood flow.
Some factors that increase the risk of developing ARF in critically ill patients include:
The causes of acute renal failure are numerous. The most important are those which are readily reversible such as hypovolaemia, low cardiac output, drugs, sepsis, abdominal compartment syndrome, hypercalcaemia and post-renal obstruction. In addition, causes for which there are specific supportive treatments (eg rhabdomyolysis) need to be identified early. Finally urinary retention must be excluded as a cause for oliguria.
In critically ill patients a number of causes may combine to produce acute renal failure.
Urea and creatinine are insensitive markers of glomerular filtration rate as they become abnormal only when there has been a huge (>50%) drop. They are affected by nutrition, muscle injury, steroids or gastrointestinal bleeding, conditions that commonly occur in the critically ill. Creatinine clearance is more accurate, but less readily available. Routine urgent investigations in patients with acute renal failure should include serum urea, creatinine, sodium, potassium, calcium and creatine kinase, arterial blood gases and urine dipstick testing for haematuria (this is also positive in the presence of myoglobinuria). Renal ultrasound should be carried out in all patients with unexplained acute renal failure.
Renal biopsy is of limited value in the ICU unless vasculitis or glomerulonephritis are suspected.
Some of the principles of supportive management of ARF include:
It is, of course, essential to treat the underlying cause.
This involves prompt and adequate resuscitation with rapid and carefully monitored restoration of intravascular filling, cardiac output and blood pressure. Reasonable haemodynamic targets (in the absence of cardiac disease) are a central venous pressure of 8-12 mmHg and a mean arterial pressure of > 70-75 mmHg (>80 mmHg for patients with underlying hypertension or renovascular disease).
Prevention can be divided into primary (before a known renal insult occurs eg. aortic surgery, antibiotic nephrotoxicity, cardiopulmonary bypass, at risk patients with diabetes, volume depletion) or secondary (after a renal insult).
Aim is to maintain renal perfusion, medullary oxygenation and glomerular filtration by a combination of volume resuscitation, vasopressors and avoidance of further iatrogenic injury.
Treat the cause, in particular, think of sepsis.
If obstruction is suspected, perform a bedside ultrasound. Patients with post renal obstruction should be managed in conjunction with a urologist.
Treatment strategies depend on severity. For moderate hyperkalaemia (5.5-6.5 mmol/L) use ion-exchange resins, loop diuretics and potassium restriction. For severe hyperkalaemia (>6.5 mmol/L), use glucose-insulin, intravenous sodium bicarbonate and intravenous calcium while starting renal replacement therapy.
Bicarbonate infusion may be a useful temporizing measure but most patients with acute renal failure and severe metabolic acidosis require renal replacement therapy.
Loop diuretics may increase urine output (without an increase in creatinine clearance) facilitating management of fluid and electrolyte balance. This may reduce the need for renal replacement therapy. Diuretics should NOT be used unless the patient has been adequately fluid and haemodynamically resuscitated (see above).
The indications for referral for urgent renal replacement therapy are:
If the cause of ARF is removed, recovery may start to occur within 4-5 days but may take weeks. However, a number of patients, especially those with pre-existing chronic renal failure,may progress to requiring long term renal replacement therapy.
The mortality of critically ill patients with ARF is high There is an increased length of ICU and hospital stay and the cost of therapy is high. These negative implications should encourage clinicians to aim for early detection and treatment and employ renal protective strategies where possible.