Steiner1 poses an interesting question related to the interpretation of eGFR. In our study, eGFR, on the basis of the Chronic Kidney Disease Epidemiology Collaboration formula, was primarily used to exclude patients at increased risk for contrast nephropathy. The main goal of the regression analysis, as reported in our article, was to determine whether the estimated glomerular pressure (Pglom) had correlations consistent with current knowledge about glomerular hyperfiltration.2 As described in the supplemental material, we found that an increased estimated Pglom was associated with the prevalence of diabetes, renal perfusion pressure, and body mass index, but not with eGFR. We agree with Steiner that use of eGFR may complicate the interpretation of our results for multiple reasons, including the notion that eGFR is indexed for body surface area (BSA).
Indexation of GFR to the individual patient’s body size is appropriate when using estimates based on serum creatinine in the identification of patients with CKD.
We agree with Steiner that, in case of obesity, indexation of GFR for BSA can conceal obesity-related hyperfiltration.3 However, (e)GFR and other surrogates used for Pglom are affected by other factors, such as kidney mass and the loss of functional nephrons. This makes it cumbersome to identify patients with hyperfiltration on the basis of (e)GFR.2
We reanalyzed our data using an eGFR unindexed for BSA; this did not change our findings. In our population, we did find a large spread in the renal fractional flow reserve and estimated Pglom; suggesting there are meaningful intraindividual differences between renal function in patients with normal eGFR.4 To acquire a better understanding in the fundamental relation between GFR, filtration fraction, and Pglom, we plan to perform iodine-125–iothalamate and iodine-131–hippuran clearance measurements in combination with intrarenal hemodynamic measurements in patients undergoing percutaneous renal revascularization.
Disclosures
D. Collard, L. van de Velde, L. Vogt, and B.J.H. van den Born are supported by an innovation grant (project number 19OI18) from the Dutch Kidney Foundation. L. Vogt reports having consultancy agreements with AstraZeneca (The Hague, The Netherlands), ISIS Pharmaceuticals (Carlsbad, CA), and Vifor Pharma (Breda, The Netherlands); and being the associate editor of BMC Nephrology.
Funding
None.
References
1. Steiner R: Complexities of eGFRs in a study of glomerular physiology. J Am Soc Nephrol 32: 256–257, 2021
2. Tonneijck L, Muskiet MHA, Smits MM, van Bommel EJ, Heerspink HJL, van Raalte DH, et al.: Glomerular hyperfiltration in diabetes: Mechanisms, clinical significance, and treatment. J Am Soc Nephrol 28: 1023–1039, 201728143897
3. Delanaye P, Radermecker RP, Rorive M, Depas G, Krzesinski JM: Indexing glomerular filtration rate for body surface area in obese patients is misleading: Concept and example. Nephrol Dial Transplant 20: 2024–2028, 200516030047
4. van Brussel PM, van Lavieren MA, Wijntjens GW, Collard D, van Lienden KP, Reekers JA, et al.: Feasibility and reproducibility of renal flow reserve with combined pressure and flow velocity measurements in humans [published online ahead of print April 9, 2019]. EuroIntervention 10.4244/EIJ-D-18-0110130967361
