Investigation, Management and Outcome of Acute Kidney Injury

and Christopher Isles²

(1)

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK

(2)

Dumfries and Galloway Royal Infirmary, Dumfries, UK

Q1 What investigations might you consider for a patient with AKI?

Initial bloods should be FBC, U&E (including bicarbonate), LFTs, calcium, phosphate and CRP. Baseline investigations should include a urine dip for blood and protein plus a renal ultrasound scan within 24 h if the cause of AKI is not immediately obvious. Other tests which may help but are not required in every case are CXR, ECG, blood gases, clotting screen, myeloma and vasculitis screens, as clinically indicated. Urine and blood should be sent for culture if infection is suspected. CT abdomen may be required when renal ultrasound shows no evidence of obstruction in circumstances in which obstruction seems likely while renal biopsy is the only certain way of confirming diagnoses of interstitial nephritis and systemic vasculitis.

Q2 Describe the principles of management of a patient with acute kidney injury.

Management should be determined by the cause, severity and any complications that may have developed. Most patients are dry, some will be shocked and for both of these groups of patients early fluid resuscitation is key. Fluid and everything else that needs to be done to treat AKI may conveniently be considered under the following headings:

Box 16.1 Key Issues to Consider in Management of AKI

Reversible factors
Specific therapies
Organ failures
Complications
Bleeding risk
Infection risk
Nutritional
Drugs

Q3 Discuss the management of reversible factors in AKI.

Essentially this means giving fluid if dry, stopping nephrotoxins, treating sepsis and relieving obstruction. The sicker the patient the more likely they are to require a urinary catheter in order to monitor urine output. Fluid management is so important that we devote a separate chapter to it. Guidelines recommend establishing a diuresis of over 30 ml/h though nephrologists much prefer 100 ml/h!

Q4 What specific therapies may be indicated in acute kidney injury?

Specific therapies target those with specific pathologies e.g. relief of obstruction if obstructed; steroids for interstitial nephritis; steroids and cyclophosphamide for systemic vasculitis plus plasma exchange if the AKI is severe; plasma exchange with fresh frozen plasma for adult HUS-TTP. No specific treatment is required for ATN other than restoring renal perfusion, treating sepsis if present and stopping nephrotoxic drugs.

Q5 Discuss the role of frusemide, dopamine and inotropes in the management of patients with AKI.

Frusemide 100 mg IV may increase urine volume but does not reduce the need for dialysis, shorten hospital stay or improve survival, so its use is not generally recommended.
Dopamine 2 μg/kg/min is a renal vasodilator that may increase urine volume but, like frusemide, does not reduce the need for dialysis, shorten hospital stay or improve survival. It is no longer recommended.
Inotropes do have a role to play in the management of patients with AKI. Noradrenaline starting at 0.1 μg/kg/min is effective in patients who are septic and hypotensive despite adequate fluid replacement. Dobutamine starting at 5 μg/kg/min is more appropriate in those with cardiogenic shock in order to increase cardiac output.

Q6 Which organ failures may occur in patients with AKI and how are they treated?

Patients with AKI may have either single organ or multi organ failure. In those with multi organ failure the organs systems commonly affected are renal, respiratory and circulation requiring renal replacement therapy, ventilation and inotropes respectively. In our unselected series of 396 consecutive patients with AKI requiring renal replacement therapy, 56 % had single organ AKI and 44 % required ventilation. Most of those ventilated also needed inotropic support.

Q7 What are the indications for renal replacement therapy in AKI?
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