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Renal functional reserve (RFR) is a physiological parameter defined as the difference between the maximal glomerular filtration rate (GFR) and the baseline GFR [1, 7]. It represents the kidney's capacity to increase its filtration rate in response to stimuli such as a high-protein meal or amino acid infusion [13]. In healthy individuals, the kidneys typically operate at approximately 75% of their maximum capacity, providing a reserve that can be recruited during metabolic stress [7]. A decline in RFR is considered an early indicator of subclinical kidney damage, often preceding changes in baseline GFR or serum creatinine levels [1, 11]. While RFR is not a single molecular target, it is modulated by various pharmacological agents that affect renal hemodynamics, including SGLT2 inhibitors, ACE inhibitors, and dopamine [1, 12]. Monitoring RFR is clinically significant for predicting the risk of acute kidney injury (AKI) and the progression of chronic kidney disease (CKD) [3, 7]. Therapeutic strategies often aim to preserve RFR by reducing pathological hyperfiltration and protecting the remaining nephron population [1, 6].
Modulation of renal hemodynamics and tubuloglomerular feedback to alter glomerular filtration rate [1, 13]
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