“Pre-renal”: What It Is and What It Isn’t
I often hear residents and attending physicians characterize a patient as “pre-renal”. By that, they usually mean that the patient needs additional fluids because they think the circulation is volume-depleted. And they usually make that conclusion based upon a fractional excretion of sodium (FENa) determination. Unfortunately, this is a situation where oversimplification has distorted critical thinking.
First, the term “pre-renal” is an incomplete term. It is a short-cut for “pre-renal azotemia”, which is a term that was coined several decades ago. Pre-renal azotemia was one of the three types of azotemia originally developed to characterize renal disorders, the others being “renal azotemia” and “post-renal azotemia”.
“Azotemia”, in turn, refers to the presence of higher than normal levels of nitrogenous compounds in the bloodstream as determined by laboratory analyses. While there are numerous nitrogen-containing molecules normally found in the blood, azotemia usually refers to an elevation of the blood urea nitrogen (BUN) concentration. Because urea is excreted by the kidney, its elevation in the bloodstream usually indicates some type of renal dysfunction.
However, this, too, is occasionally an erroneous assumption, as patients with gastrointestinal hemorrhage can also elevate their BUN levels due to the increased intestinal absorption and digestion of blood.
The concepts of “pre-renal”, “renal”, and “post-renal” with respect to the cause of the azotemia refer to where the defect lies in the kidney’s excretory process. In a pre-renal problem, the kidney is receiving inadequate blood flow to be able to excrete waste products adequately. In renal azotemia, the problem lies within the tubular epithelium responsible for the molecular exchanges that get urea to stay in the excreted urine instead of reabsorbed like the non-waste materials (i.e., sodium, bicarbonate, glucose, etc.). And post-renal azotemia indicates the presence of an obstruction somewhere in the collecting system responsible for eliminating waste materials through the urethra.
Where I have a real problem with the use of the term “pre-renal” by itself is that the presence of an elevated BUN and/or creatinine level (i.e., the azotemia) is often completely ignored. In fact, both of those laboratory values will be absolutely normal, and yet those physicians will still label the patient as “pre-renal” simply because the FENa is less than 1%. They may even administer a bolus of intravenous fluids to correct what they think is a sign of hypovolemia.
While modern medicine is very advanced with respect to its management of the human body, it would be a real paradigm shift for us to fully understand the full meaning of the terms we use..