COMMENTARY

Renin or Lactate to Predict Hospital Death?

Tejas P. Desai, MD

Disclosures

June 13, 2019

Hypoperfused and ischemic conditions are common pathophysiologic processes in many of our hospitalized patients. Although we make every effort to reverse such conditions as quickly as possible, our ability to identify and monitor hypoperfusion has been limited.

I started my medical training relying on mean arterial pressure (MAP) as an appropriate measure of perfusion. This measure is easy to calculate, and the threshold I was taught to use (MAP > 60 mm Hg) was easy to monitor. It became apparent, however, that although the MAP was an accurate measure of large vessel perfusion, microvascular hypoperfusion could still be present.

As my training progressed, I moved away from the MAP and toward the serum lactate level. This marker was easy to measure and had a clear threshold (> 2 mmol/L) from which hypoperfusion could be identified. Over time and with more research, we learned that hypoperfusion could be present in the absence of an elevated lactate level. Nevertheless, I have continued to use the MAP and lactate levels to make a best guess regarding perfusion.

Recently, I came across a fascinating article by Gleeson and colleagues[1] that suggested that renin may be a legitimate marker of hypoperfusion. In this proof- of-concept study (this is very important to remember), researchers compared the predictive ability of renin vs lactate in the mortality of critical care patients with hemorrhagic, cardiogenic, or septic shock.

Why renin?

The theory that formed the backbone of this investigation relied on the observation that renin levels are elevated in microvascular hypoperfused states. In this extremely small study (only 110 samples from 20 patients were tested), renin and lactate levels were measured. Statistical tests were performed to determine the predictive prowess of both lab tests.

The investigators showed that renin had a greater/better predictive capability of mortality than lactate (see infographic for parameters).

Why Am I Skeptical?

This is an interesting investigation, but given my past experiences with markers of hypoperfusion, I am skeptical of the authors' conclusions.

Using a hormone as a marker is always challenging. As the authors mentioned, many factors other than hypoperfusion can influence the levels of renin. These confounding influencers are often present in hospitalized patients (eg, the use of hemofiltration, beta-blockers, or angiotensin-converting enzyme inhibitors).

Hormones are secreted at low concentrations, narrowing the diagnostic window, and small changes in renin concentration (measured in µU) may result in diagnostically false positives with no discernible physiologic alterations.

These are limitations that should not be ignored in future studies of renin as a marker of hypoperfusion. Still, the investigators have underscored the need for a more reliable and measurable marker of microvascular hypoperfusion. While we wait for such markers, share your experiences with MAP, lactate, central venous oxygen saturation, or other marker of hypoperfusion that you have used (with success or failure) in the comments section.

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