International Society of Nephrology. Published by Elsevier Inc.
Doi
Abstract
The concept of the renal functional reserve stems from the observation that in normal humans, the “resting” glomerular filtration rate may be acutely raised following several stimuli. This extra excretory capacity, represented by the rise in GFR from baseline to maximum, might be regarded as a reserve upon which the kidney could call in times of stress. As a corollary it seemed likely that whenever a kidney was damaged and lost filtration capacity, this unused reserve would be depleted before the resting GFR fell. Measuring the degree to which the GFR could respond to stress—its renal functional reserve (RFR)—would therefore provide an early measure of renal damage. It would also be rational to believe that once the GFR was impaired this response would be lost.Since this hypothesis was proposed it has become obvious that it was flawed. It has been clearly shown that the response is not lost in disease states and that therefore its does not represent a true “reserve”. The response itself is also heterogeneous. The glomerular filtration rate can be induced to rise by a variety of stimuli using different mechanisms. The most commonly used stimuli to test the RFR are a high protein meal or an intravenous (or oral) amino acid infusion. Dopamine infusions have also been used to provoke the response, but there is little evidence that the response is mediated in the same way.This article will chiefly deal with the physiological mechanisms involved in the renal haemodynamic response to a meat meal or amino acid infusion and confine to these responses the convenient appellation “renal functional reserve”
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