Does low-dose dopamine improve renal blood flow?

From the Guidelines

Low-dose dopamine does not improve renal blood flow in a clinically meaningful way. Despite its historical use for "renal protection" at doses of 1-3 mcg/kg/min, multiple randomized controlled trials and meta-analyses have demonstrated that low-dose dopamine does not prevent acute kidney injury, improve renal function, or reduce mortality in critically ill patients 1. While dopamine can transiently increase urine output through its diuretic effect, this does not translate to improved kidney function or patient outcomes. The theoretical basis for using low-dose dopamine was that it would selectively activate dopaminergic receptors in the renal vasculature, causing vasodilation and increased renal blood flow. However, this effect is minimal and inconsistent in actual clinical scenarios, particularly in patients with established kidney injury or critical illness. Some key points to consider:

• The 2016 Surviving Sepsis Campaign guidelines recommend against using low-dose dopamine for renal protection (strong recommendation, high quality of evidence) 1.
• The KDIGO Clinical Practice Guideline for Acute Kidney Injury also recommends not using low-dose dopamine to prevent or treat AKI (1A) 1.
• Current clinical practice has moved away from using low-dose dopamine for renal protection, focusing instead on maintaining adequate systemic perfusion, avoiding nephrotoxins, and other evidence-based supportive measures for patients at risk of kidney injury. It's worth noting that some studies suggest that dopamine may have adverse effects, such as increased risk of death and arrhythmias, particularly in patients with sepsis or cardiogenic shock 1. Therefore, the use of low-dose dopamine for renal protection is not recommended, and other evidence-based strategies should be prioritized to improve patient outcomes.

From the FDA Drug Label

Increased output has been associated with unchanged or decreased systemic vascular resistance (SVR). The association of static or decreased SVR with low or moderate increases in cardiac output is regarded as a reflection of differential effects on specific vascular beds, with increased resistance in peripheral beds (e.g., femoral), and concurrent decreases in mesenteric and renal vascular beds. Redistribution of blood flow parallels these changes so that an increase in cardiac output is accompanied by an increase in mesenteric and renal blood flow. In many instances the renal fraction of the total cardiac output has been found to increase Low to moderate doses of dopamine, which have little effect on SVR, can be used to manage hypotension due to inadequate cardiac output Although urine flow is apparently one of the better diagnostic signs for monitoring vital organ perfusion, the physician also should observe the patient for signs of reversal of mental confusion or coma. However, it has been observed that in some oliguric or anuric patients, administration of the drug has produced an increase in urine flow which may reach normal levels.

Low-dose dopamine may help improve renal blood flow by increasing cardiac output and redistributing blood flow to specific vascular beds, including the renal vascular bed 2. This is supported by the increase in renal fraction of the total cardiac output and urine flow observed in some patients. However, the effect of dopamine on renal blood flow may vary depending on the individual patient's response to the drug.

From the Research

Effects of Low-Dose Dopamine on Renal Blood Flow

• Low-dose dopamine has been shown to augment renal blood flow, sodium excretion, and probably glomerular filtration rate in healthy humans and experimental animals 3.
• However, the effect of dopamine on renal blood flow remains controversial, with some studies suggesting that it may not be as effective as previously thought 4.
• The increased renal blood flow associated with dopamine may be largely attributable to its inotropic (myocardial) action, even with low doses 5.
• Low-dose dopamine can decrease renal and systemic vascular resistance, suppress aldosterone secretion, and interact with atrial natriuretic factor, which may contribute to its potential renoprotective effects 6.

Clinical Evidence and Recommendations

• Most studies in humans have not demonstrated prevention of acute renal failure in high-risk patients or improved outcome in those with established acute renal failure 3.
• The use of low-dose dopamine for its systemic effects in heart failure and septic shock may still be valuable, but its use for selective renal vasodilatory and natriuretic actions is not recommended until its efficacy is established in randomized control trials 3.
• Meta-analyses and a large double-blind, prospective, multiple-center, randomized controlled trial have failed to demonstrate that dopamine protects the kidney in critically ill patients with acute renal failure 7.
• The current evidence suggests that low-dose dopamine is not clinically efficacious in preventing or altering the course of acute renal failure, and its use may be associated with multiple complications 4, 7.