A multinational European working group produced the following evidence-based recommendations for preventing acute kidney injury (AKI). Read the full guideline before criticising – some are just suggestions, some recommendations; I have not included the strength of recommendation or grade of evidence in my summary below.
Volume expansion

Controlled fluid resuscitation in true or suspected volume depletion

There is little evidence-based support for the preferential use of crystalloids or colloids

Avoid 10% HES 250/0.5 as well as higher-molecular-weight preparations of HES and dextrans in sepsis

Prophylactic volume expansion by isotonic crystalloids in patients at risk of contrast nephropathy. Use isotonic sodium bicarbonate solution, especially for emergency procedures

Prophylactic volume expansion with crystalloids to prevent AKI by certain drugs (amphotericin B, antivirals including foscarnet, cidofovir, and adefovir, as well as drugs causing crystal nephropathy such as indinavir, acyclovir, and sulfadiazine)

Diuretics

1. Do not use loop diuretics to prevent or ameliorate AKI

Vasopressors and inotropes

1. Maintain mean arterial pressure (MAP) at least 60–65 mmHg, however, target pressure should be individualized where possible, especially if knowledge of the premorbid blood pressure is available.
2. In case of vasoplegic hypotension as a result of sepsis or SIRS use either norepinephrine or dopamine (along with fluid resuscitation) as the first-choice vasopressor agent to correct hypotension.
3. Do not use low-dose dopamine for protection against AKI.

Vasodilators

1. Use vasodilators for renal protection when volume status is corrected and the patient is closely hemodynamically monitored with particular regard to the development of hypotension.
2. Prophylactic use of fenoldopam, if available, in cardiovascular surgery patients at risk of AKI. Do not use fenoldopam for prophylaxis of contrast nephropathy.
3. Use theophylline to minimize risk of contrast nephropathy, especially in acute interventions when hydration is not feasible.
4. Do not use natriuretic peptides as protective agents against AKI in critically ill patients, while its use may be considered during cardiovascular surgery.

Hormonal manipulation and activated protein C

1. Avoid routine use of tight glycemic control in the general ICU population. Use “Normal for age’’ glycemic control with intravenous (IV) insulin therapy to prevent AKI in surgical ICU patients, on condition that it can be done adequately and safely applying a local protocol which has proven efficacy in minimizing rate of hypoglycemia.
2. Do not use thyroxine, erythropoietin, activated protein C or steroids routinely to prevent AKI.

Metabolic interventions

1. All patients at risk of AKI should have adequate nutritional support, preferably through the enteral route
2. Do not use N-acetylcysteine as prophylaxis against contrast induced nephropathy or other forms AKI in critically ill patients because of conflicting results, possible adverse reactions, and better alternatives.
3. Do not routinely use selenium to protect against renal injury.

Extracorporeal therapies

1. Use periprocedural continuous veno-venous hemofiltration (CVVH) in an ICU environment to limit contrast nephropathy after coronary interventions in high-risk patients with advanced chronic renal insufficiency

Prevention of acute kidney injury and protection of renal function in the intensive care unit
Expert opinion of the working group for nephrology, ESICM
Intensive Care Med. 2010 Mar;36(3):392-411