The maximum capacity of a functioning renal mass is not reflected by the baseline GFR of a given individual. Bellomo et al used an example of 4 different patients to explain this concept. Patients A (animal protein consumer) and B (vegetarian) have the same renal mass but different baseline GFRs owing to different basal protein in-takes levels. Patient A has a GFR of 120 ml/min that can be stimulated to 170 ml/min. Patient B has a baseline GFR of 65 ml/min that also can be stimulated to 170 ml/min. Therefore, the RFR in these two patients is different because they are using their GFR capacity at a different level. Patient C had a unilateral nephrectomy. His baseline GFR corresponds to his maximal GFR under unrestricted dietary conditions. If a moderate protein restriction is applied to his diet, his baseline GFR may decrease and some degree of RFR become evident. Patient D, who is a vegetarian who underwent unilateral nephrectomy, will have a lower baseline compared to patient C but a higher RFR. Therefore, in general, restoring some RFR requires a severe protein restriction, and hence baseline GFR does not always correspond to the extent of functioning renal mass unless we place it in the context of maximal capacity. Bellomo et al concluded the section about GFR by using a very interesting, possibly true, statement:
“In this regard GFR is not unlike a resting ECG for the kidney. When it is grossly abnormal, renal function is impaired, but when it is normal, a stress test is required.”
The GFR rises considerably during pregnancy. This physiological rise is multifactorial and is mainly attributed to increase in cardiac output and renal blood flow. It becomes apparent from the 1st month and peaks at 40% – 50% above baseline levels by the 4th or 5th month of pregnancy. This increase in GFR is referred to as renal hyperfiltration. The RFR is consumed as a part of adaptation to this physiological demand that occur during pregnancy. This was demonstrated by Ronco et al. They assessed GFR changes in pregnant women, with normal kidneys, before and after protein load. After acute protein load, all women had a significant increase in GFR. This rise was more in the first than in the last trimester. This finding explains, at least partially, renal hyperfiltration in pregnancy.
RFR allow for an increase in GFR during stressful conditions to ensure maintenance of adequate kidney function. When RFR is lost or fully utilized and the kidney insult continues, changes in baseline GFR and serum creatinine occur. After an AKI episode, creatinine and GFR may return to normal, displaying an apparent complete recovery of the kidney. Unfortunately, this recovery might be at the expense of reduction or loss of the RFR. In my opinion, without performing a kidney stress test to assess the RFR post-AKI, it will remain unclear whether the recovery from AKI was complete or was it just a biochemical recovery (reflected by creatinine level) at the expense of RFR utilization. Conceptually, recovering baseline GFR and creatinine level post-AKI without recovering the RFR should be labelled as new-onset CKD because it actually reflects an irreversible loss of nephrons/RFR. I have no evidence to support this, but I would hypothesize that these patients who lose their RFR post-AKI are the ones who were shown to progress to CKD in previous studies.
I think the following are potential benefits for using a kidney stress test/ checking RFR:
- Assessment of recovery post-AKI: It will help to detect patients who are likely to progress to CKD.
- Assessment of living kidney donors prior to donation: It is likely that a low RFR might increase the long-term risk of CKD during the post-donation period.
- To assess the risk of AKI in patients undergoing contrast studies and high-risk surgeries.
Post by Mohammed Kaballo