The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Renal Functional Reserve and Renal Recovery after Acute Kidney Injury
Abstract
Renal functional reserve (RFR) represents the capacity of the kidney to increase glomerular filtration rate (GFR) in response to certain physiological or pathological stimuli or conditions. Once baseline GFR is determined, RFR can be assessed clinically after an oral protein load or intravenous amino acid infusion. In clinical practice, baseline GFR displays variable levels due to diet or other factors. RFR is the difference between peak ‘stress' GFR induced by the test (p.o. or i.v.) and the baseline GFR. In clinical scenarios where hyperfiltration is present (high baseline GFR due to pregnancy, hypertension or diabetic nephropathy, in solitary kidney or kidney donors), RFR may be fully or partially used to achieve normal or supranormal renal function. Since commonly used renal function markers, such as GFR, may remain within normal ranges until 50% of nephrons are lost or in patients with a single remnant kidney, the RFR test may represent a sensitive and early way to assess the functional decline in the kidney. RFR assessment may become an important tool to evaluate the ability of the kidney to recover completely or partially after a kidney attack. In case of healing with a defect and progressive fibrosis, recovery may appear complete clinically, but a reduced RFR may be a sign of a maladaptive repair or subclinical loss of renal mass. Thus, a reduction in RFR may represent the equivalent of renal frailty or susceptibility to insults. The main aim of this article is to review the concept of RFR, its utility in different clinical scenarios, and future perspective for its use.
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Cites
Assessing Kidney Function — Measured and Estimated Glomerular Filtration Rate
Stevens, L. A., Coresh, J., Greene, T., & Levey, A. S. (2006) · New England Journal of Medicine · doi:10.1056/nejmra054415 · Cited by 2,952
Cited by
Ronco, C., Bellomo, R., & Kellum, J. A. (2019) · The Lancet · doi:10.1016/s0140-6736(19)32563-2 · Cited by 1,910
Self-citationGlomerular hyperfiltration in diabetes: mechanisms, clinical significance, and treatment
Tonneijck, L., Muskiet, M. H. A., Smits, M. M., van Bommel, E. J., Heerspink, H. J. L., van Raalte, D. H., & Joles, J. A. (2017) · Journal of the American Society of Nephrology · doi:10.1681/asn.2016060666 · Cited by 887
Doig, G. S., Simpson, F., Bellomo, R., Heighes, P. T., Sweetman, E. A., Chesher, D., Pollock, C., Davies, A., Botha, J., Harrigan, P., et al. (2015) · Intensive Care Medicine · doi:10.1007/s00134-015-3827-9 · Cited by 232
Cortinovis, M., Perico, N., Ruggenenti, P., Remuzzi, A., & Remuzzi, G. (2022) · Nature Reviews Nephrology · doi:10.1038/s41581-022-00559-y · Cited by 214
Shear stress-induced alteration of epithelial organization in human renal tubular cells
Maggiorani, D., Dissard, R., Belloy, M., Saulnier-Blache, J.-S., Casemayou, A., Ducasse, L., Grès, S., Bellière, J., Caubet, C., Bascands, J.-L., et al. (2015) · PLOS ONE · doi:10.1371/journal.pone.0131416 · Cited by 74
Metadata
- Authors
- Sharma, A., Mucino, M. J., & Ronco, C.
- Venue
- Nephron Clinical Practice
- Publisher
- S. Karger AG
- Published
- 2014-09-24
- Volume
- 127
- Issue
- 1-4
- Pages
- 94-100
- ISSN
- 1660-2110 (ISSN-L)
- OpenAlex
- W2030557766
- Cited by
- 296
- References
- 1
- FWCI
- 12.28
- Type
- journal article
- Language
- en
- Open access
- closed
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