Renal Dose Dopamine: Not Recommended
Low-dose dopamine should not be used for renal protection or treatment of acute kidney injury, as it has been definitively shown to be ineffective and potentially harmful. 1
Guideline Consensus Against Renal Dose Dopamine
The evidence against "renal dose" dopamine is unequivocal across all major guidelines:
KDIGO (Kidney Disease: Improving Global Outcomes) provides a Level 1A recommendation—the highest grade of evidence—against using low-dose dopamine to prevent or treat acute kidney injury. 1
The Surviving Sepsis Campaign 2016 guidelines issue a strong recommendation with high-quality evidence against using low-dose dopamine for renal protection in septic shock. 2, 1
Both the Canadian Society of Nephrology and American Society of Nephrology recommend against this practice. 1
The ACC/AHA heart failure guidelines note that while they previously gave a Class IIb recommendation for low-dose dopamine to improve diuresis and preserve renal function, this recommendation was expected to be revised following the ROSE trial, which showed no effect of low-dose dopamine on decongestion or renal function. 2
Why It Doesn't Work
The physiologic rationale that seemed promising in animal models and healthy subjects has failed to translate to clinical benefit:
Low-dose dopamine (3-5 μg/kg/min) increases renal blood flow in patients with normal renal function but NOT in patients with renal dysfunction—the exact population where it's being used. 3
A comprehensive meta-analysis of 17 randomized clinical trials (n=854) demonstrated that dopamine did not prevent mortality (RR 0.90, p=0.92), onset of acute renal failure (RR 0.81, p=0.34), or need for dialysis (RR 0.83, p=0.42). 4
The statistical power was sufficient to exclude any large effect (>50%) on the risk of acute renal failure or need for dialysis. 4
Potential Harms
Beyond being ineffective, renal dose dopamine carries significant risks:
Dopamine may precipitate serious cardiovascular complications including tachyarrhythmias, increased myocardial oxygen demand, and metabolic disturbances in critically ill patients. 5
In cardiogenic shock, norepinephrine resulted in lower mortality compared to dopamine, with fewer arrhythmias. 2, 6
The drug suppresses pituitary secretion of thyroid-stimulating hormone, growth hormone, and prolactin. 7
Extravasation causes tissue necrosis and sloughing. 7
When Dopamine IS Appropriate
Dopamine has legitimate indications, but renal protection is not one of them:
Dopamine should only be used as an alternative vasopressor in highly selected patients with hypotension who have low risk of tachyarrhythmias AND absolute or relative bradycardia. 2, 1, 8
At 3-5 μg/kg/min, dopamine provides inotropic effect; at >5 μg/kg/min, it adds vasopressor effect. 6
What to Use Instead for AKI Management
For patients with or at risk for acute kidney injury:
Use isotonic crystalloids (not colloids) for initial volume expansion (Level 1B recommendation). 1
Avoid starch-containing fluids entirely due to increased AKI risk. 1
If vasopressor support is needed, norepinephrine is the first-choice agent (strong recommendation, moderate quality evidence). 2, 1, 8
Diuretics should only be used for management of volume overload, not to treat AKI itself (Level 2C recommendation). 1
Target adequate mean arterial pressure to maintain organ perfusion. 1
Common Pitfalls to Avoid
Do not confuse the outdated practice of "renal dose dopamine" (2-5 μg/kg/min for renal protection) with appropriate vasopressor dosing (5-10 μg/kg/min for hemodynamic support in selected patients with bradycardia). These are entirely different indications. 2, 8
The 2012 ESC guidelines mentioned dopamine 2.5 μg/kg/min for enhancing diuresis in acute heart failure, but noted that higher doses are not recommended for this purpose. 2 However, this recommendation predates the ROSE trial and current consensus against renal dose dopamine.
If a patient requires vasopressor support AND has renal dysfunction, use norepinephrine—not dopamine—as first-line therapy. 2, 1