Renal Resistive Index in Cardiac Surgery: A Narrative Review

Abstract

Cardiac surgery-associated acute kidney injury (CSA-AKI) is the most prevalent clinically significant complication in adult patients undergoing open heart surgery, closely linked to increased mortality and morbidity. Among intensive care unit (ICU) patients, CSA-AKI is the second most common type of acute kidney injury, surpassed only by sepsis-induced AKI. The Doppler-based Renal Resistive Index (RRI) measurement is a rapid and non-invasive diagnostic tool with potential for the early detection of acute kidney injury in intensive care unit patients and could also be useful as an early predictor of acute kidney injury (AKI) in the context of cardiac surgery, particularly when used in conjunction with novel biomarkers.

1. Introduction

Acute kidney injury (AKI) is the most frequent severe complication following cardiac surgery, affecting 5% to 42% of patients. Known as cardiac surgery-associated AKI (CSA-AKI), it is the second most common cause of AKI in intensive care units, following sepsis, and is independently associated with increased mortality and morbidity. Severe CSA-AKI amplifies perioperative mortality by 3- to 8-fold, prolongs ICU and hospital stays, and significantly escalates healthcare costs. Even in cases of complete renal recovery, the risk of AKI-related mortality remains elevated for up to a decade post-surgery [1].

CSA-AKI encompasses a spectrum of pathophysiological mechanisms and falls under type 1 cardiorenal syndrome (CRS), wherein acute cardiac dysfunction precipitates AKI. However, a universally accepted definition of CSA-AKI is lacking in the literature, with multiple criteria complicating diagnosis due to post-cardiac surgery fluid shifts driven by fluid resuscitation and cardiopulmonary bypass (CPB) priming.

The current classification system, including the Acute Kidney Injury Network (AKIN) criteria introduced in 2007 and the RIFLE criteria (Risk, Injury, Failure, Loss, End-stage kidney disease) from 2004, relies on serum creatinine changes and urine output. However, these criteria have limitations in cardiac surgery patients due to the complexities of fluid management. The Kidney Disease Improving Global Outcomes (KDIGO) criteria, introduced in 2012, integrate aspects of AKIN and RIFLE, providing enhanced sensitivity for AKI detection and mortality prediction.

According to KDIGO [2,3], CSA-AKI is diagnosed based on at least one of the following: (1) an increase in serum creatinine of a ≥0.3 mg/dL within 48 h, (2) a 1.5- to 1.9-fold increase in serum creatinine from baseline, within the prior seven days, and (3) a urinary output of <0.5 mL/kg/h for 6 h, or both.

Beyond conventional clinical criteria, emerging biomarkers offer promising tools for early CSA-AKI detection [4,5,6,7]. Markers such as urinary α1 microglobulin, N-acetyl-β-d-glucosaminidase, serum and urinary neutrophil gelatinase-associated lipocalin (NGAL), liver fatty acid-binding protein (L-FABP), cystatin C, and tissue inhibitor of metalloproteinase 2 (TIMP2) have been proposed for early identification of AKI. Some urinary biomarkers, such as kidney injury molecule-1 (KIM1) and inteleukin 18 (IL-18), may also indicate subclinical AKI and predict long term post-surgical mortality. However, the applicability of these biomarkers across diverse cardiac surgery population remains uncertain [8]. Combining structural and functional biomarkers may enhance diagnostic accuracy and AKI severity assessment. For instance, cystatin C (CysC), a cysteine protease inhibitor released by nucleated cells, has demonstrated predictive value in AKI among cardiac surgery and hospitalized patients [9]. The integration of damage biomarkers such as CysC, with functional markers like proenkephalin A, may further improve AKI detection and stratification [10]. Additionally, newer urinary markers, including tissue inhibitor of metalloproteinase-2 (TIMP-2) and insulin-like growth factor binding protein 7 (IGFBP7), both inducers of G1 cell-cycle arrest, have shown superior performance compared to traditional markers such as kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) [11]. Interleukin-18, a pro-inflammatory cytokine released following acute proximal tubular injury, can be detected in urine [4]. Urinary KIM-1, a transmembrane glycoprotein, is well established as an AKI biomarker in adults [12]. NGAL, present in both blood and urine, is upregulated in response to ischemic or nephrotoxic kidney injury and represents another key marker for AKI detection.

The pathophysiology of CSA-AKI is multifactorial and highly complex, necessitating an integrated understanding of perioperative renal insults to inform effective preventive and therapeutic strategies [13,14]. A pivotal mechanism is renal hypoperfusion, particularly compromising the oxygen-sensitive medullary region [15]. During cardiopulmonary bypass (CPB), renal ischemia may result from suboptimal flow rates, non-pulsatile perfusion, hemodilution, embolism formation, and rewarming-induced injury [15,16]. Intraoperative hemodynamic disturbances such as low cardiac output, hypotension, venous congestion, and surgical bleeding further aggravate renal perfusion by activating vasoconstrictive pathways [17]. The mismatch between oxygen supply and demand during CPB is especially deleterious, as hemodilution and reduced hemoglobin concentrations impair oxygen delivery, thereby increasing susceptibility to AKI. Hemodilution-associated reductions in hemoglobin further compromise oxygen delivery. Ranucci et al. [18] demonstrated that oxygen delivery during CPB falling below 272 mL/min/m² is a critical threshold for AKI development. Although moderate hemodilution (hematocrit > 25%) may be tolerated, excessive hemodilution and blood transfusions increase the likelihood of renal dysfunction and dialysis dependence.

Beyond hypoperfusion, CSA-AKI is also driven by ischemia-reperfusion injury, mitochondrial dysfunction, oxidative stress, and systemic inflammatory response initiated by CPB-induced immune and endothelial activation [19,20]. Additional perioperative contributors include nephrotoxic agents [21], vasoactive medications, neurohormonal dysregulation, septic emboli in infective endocarditis [22], and potential genetic predispositions [23,24]. Timely identification of high-risk patients is paramount [25]. Risk factors are traditionally grouped into three categories: patient-related, procedure-related, and postoperative.

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Patient-related risk factors include advanced age, female sex, cardiogenic shock requiring intra-aortic balloon pump (IABP), reduced left ventricular ejection fraction (<35%), heart failure, COPD, diabetes, left main coronary disease, prior cardiac surgery, peripheral arterial disease, emergency surgical status, and pre-existing chronic kidney disease (CKD).

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Procedure-related risk factors encompass prolonged CPB duration (>100–120 min), aortic cross clamp time, hemolysis, hemodilution, embolism, use of CPB versus off-pump techniques, pulsatile versus non-pulsatile flow, and deep hypothermic circulatory arrest.

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Postoperative risk factors include hypotension, low cardiac output syndrome, sepsis, exposure to nephrotoxins, excessive vasoconstriction, atheroembolism, and venous congestion. These variables are incorporated into predictive models such as the Cleveland Clinic Score [26,27,28].

Renal Doppler ultrasonography has emerged as a valuable non-invasive modality for risk stratification.

The Renal Resistive Index (RRI), derived from Doppler waveform analysis, independently predicts AKI following cardiac surgery [29]. Elevated RRI values have been consistently associated with an increased risk of AKI across various studies [30,31,32]. Intraoperative and post-operative RRI measurements, particularly those obtained via transesophageal echocardiography (TEE), have demonstrated predictive value for AKI, suggesting that RRI could serve as an early warning signal for renal impairment [29,33,34].

Research indicates that an RRI > 0.7 during cardiac surgery is a significant predictor of post-operative AKI. This finding underscores the potential of RRI as an integral component of intraoperative monitoring, facilitating the identification of at-risk patients and enabling timely interventions to mitigate AKI risk [35].

The primary finding of this review is the strong predictive capability of RRI for AKI with high sensitivity and specificity in the immediate postoperative period, specifically upon admission to the intensive care unit (ICU).

This review aims to critically explore the evolving role of the Renal Resistive Index (RRI) in the context of cardiac surgery-associated acute kidney injury (CSA-AKI). To this end, it addresses four key questions: (1) the diagnostic value of RRI in detecting CSA-AKI; (2) its potential as a standalone marker; (3) whether its integration with emerging renal biomarkers improves early detection and prognostication; and (4) the clinical implication of routine RRI monitoring in perioperative risk stratification and renal protection. By synthesizing current evidence, the review seeks to clarify whether RRI can be effectively incorporated into standard perioperative care to improve renal outcomes in this high-risk population.

2. Materials and Methods

This narrative review aims to analyze the relevant literature on “cardiac surgery-associated acute kidney injury and the Renal resistive index”. A comprehensive search was conducted in PubMed and Scopus, limiting the timeframe to articles published between 2006 and 2025. The search terms “Renal resistive index AND AKI” and “renal resistive index AND cardiac surgery AKI” yielded 402 results.

Following the application of specific inclusion and exclusion criteria, a total of 211 articles were preliminarily selected. Only peer-reviewed original research articles, including prospective and retrospective cohort studies, case–control studies, and case series that explicitly addressed the diagnostic or prognostic role of RRI in the context of CSA-AKI were considered eligible. Inclusion criteria required quantitative assessments of RRI in association with CSA-AKI, including its diagnostic accuracy, predictive value, and clinical relevance for early identification and management of AKI. To ensure methodological rigor, reproducibility, and accessibility of the findings within the international scientific community, only studies published in English were considered. While this may represent a potential limitation in terms of excluding data published in other languages, it was a pragmatic decision aimed at guaranteeing consistency, quality, and transparency in data interpretation. Conversely, expert opinions, conference abstracts, animal studies, as well as non-peer-reviewed sources and preprints, were excluded. Studies lacking a clear assessment of the diagnostic or prognostic utility of RRI in CSA-AKI were also discarded. After screening, 125 papers were deemed relevant. Ultimately, after full text assessment, 104 studies were included based on methodological and scientific quality.

3. Renal Perfusion: Hemodynamic Monitoring Through Doppler Ultrasound and Resistive Index Assessment

The kidneys have a high perfusion rate and strong self-regulatory properties; however, compared to other vital organs like the brain and the heart, they are more vulnerable to fluctuations in blood pressure due to their limited autoregulatory capacity [36]. This vulnerability makes the kidneys susceptible to damage during hemodynamic instability caused by critical illness or injury, which can lead to prolonged poor perfusion. The ultimate goal of shock resuscitation is to optimize perfusion to individuals’ organs following the reversal of systemic hypoperfusion and restoration of microcirculatory perfusion. Consequently, renal perfusion assessment should be prioritized over other organs, given its pivotal role in the early detection and prevention of acute kidney injury [37]. Currently, there is no gold-standard method for assessing renal perfusion in clinical settings. Ultrasound, due to its convenience, speed, non-invasiveness, and repeatability at the bedside, is widely used to evaluate renal hemodynamics in critically ill patients [38]. Conventional ultrasound provides reliable kidney morphology images. Doppler ultrasound is valuable for assessing arterial or venous flow abnormalities and is recommended for evaluating changes in intrarenal perfusion due to parenchymal diseases and systemic hemodynamics [39]. Although considered a valuable tool, the efficacy of the Renal Resistive Index assessment by intrarenal arterial Doppler in predicting the reversibility of renal dysfunction and guiding hemodynamic support remains a subject of ongoing debate.

Intrarenal Doppler (IRD) is a valuable tool for assessing renal hemodynamics by measuring renal artery flow velocities. These measurements are used to calculate the renal resistive index (RRI). RRI, a widely used non-invasive ultrasound marker, reflects the interplay between renal microcirculation and cardiovascular, metabolic, and inflammatory systems. Despite its limitations, namely operator dependency, lack of standardized cut-off thresholds, and potential confounding by systemic hemodynamic factors, RRI remains a sensitive and reliable predictor of overall survival in patients with renal and cardiovascular diseases. Regular serial assessment may be beneficial for monitoring patient progress in clinical practice [39].

3.1. Renal Resistive Index Examination Techniques

Performing RRI measurements requires a standardized protocol involving several steps: ultrasound tool selection (trans lumbar renal Doppler is typically the first choice, but transesophageal ultrasonography is also validated for intraoperative use) [34,40,41] (Figure 1); visualization of kidney longitudinal scan (this is achieved by optimizing the B-mode acoustic window with precise focus and gain adjustments); identification of interlobar arteries (utilizing color Doppler to locate these arteries) [42]; activation of pulsed wave Doppler (positioning the sample volume within the vessel’s lumen and recording the speed–time curve); and calculation of RRI (using the formula RRI = [(peak systolic velocity − end diastolic velocity)/peak systolic velocity]). An RRI > 0.7 is typically considered the upper normal threshold in adults [43].

3.2. Factors Impacting Renal Resistive Index

Although termed “resistive”, RRI essentially measures blood pulsatility. The relationship between RRI and renal vascular resistance (VR) is debated. Bude and Rubin, 1999, in an in vitro study indicated that RRI depends on VR when vascular compliance is present but is independent of VR in its absence [44]. Both systemic and intrarenal factors can significantly influence the Renal Resistive Index. Among systemic determinants, pulse pressure plays a central role, as it is modulated by vascular compliance and cardiac function [45]. For instance, reduced aortic compliance, often observed in conditions such as arterial stiffness, leads to an increase in pulse pressure, which in turn elevates the RRI [46]. Similarly, alterations in cardiac function, including bradycardia, aortic valve insufficiency, and increased stroke volume, can also modify pressure dynamics and consequently raise RRI values. On the other hand, intrarenal factors, such as renal capillary wedge pressure (RCWP), exert a direct effect on RRI. RCWP may be elevated in various pathological scenarios including renal parenchymal injury, urinary tract obstruction, intra-abdominal hypertension, and systemic venous congestion [47]. These conditions compromise renal perfusion dynamics and contribute to increased resistance within the renal microcirculation, thus impacting RRI measurements. In summary, RRI reflects both intrarenal factors (RCWP) and systemic hemodynamic conditions (PP).

3.3. Applicability and Clinical Utility of the Renal Resistive Index

The Renal Resistive Index (RRI) is a valuable non-invasive tool used in diagnosing and prognosticating renal disease such as urinary obstruction [48], renal artery stenosis [49], and diabetic nephropathy [50]. It offers benefits in critically ill patients by predicting the reversibility of renal dysfunction and aiding in fluid resuscitation, thereby serving as a hemodynamic window for monitoring organ perfusion [51].

Darmon et al. [52] found that a RRI > 0.795 had 92% sensitivity and 85% specificity for predicting persistent AKI in mechanically ventilated patients. However, a larger study by Darmon et al. in 2018 [53] reported lower sensitivity (50%) and specificity (68%) for RRI in predicting persistent AKI in broader population.

3.4. Renal Resistive Index in Cardiac Surgery

In recent years, the Renal Resistive Index has gained significant attention as a predictive marker for acute kidney injury (AKI), particularly in the context of cardiac surgery.

Several studies [54,55,56,57,58,59,60] have underscored its utility in detecting AKI early, facilitating timely interventions and potentially improving patients’ outcomes (Table 1).

Identifying the timing of primary renal insult intraoperatively has facilitated research on the rapidity of the Renal Resistive Index as an early biomarker for acute kidney injury [61]. Elevated intraoperative RRI, also measured by Transesophageal Echocardiography (TEE), has been associated with subsequent AKI diagnosis [55,62,63,64,65]. Similarly, increased RRI predicts AKI shortly after various surgical procedures in critically ill patients [54]. The expectation is that early identification of AKI risk through elevated RRI (prior to the rise in other biomarkers) will pave the way for future development of renal-protective interventions in both surgical and nonsurgical patients.

Kajal et al. [62] demonstrated that an RRI > 0.68 during CABG was significantly associated with postoperative AKI, suggesting its potential as a threshold for intraoperative risk stratification via standard TEE. Similarly, Zhou et al. [66] reported that elevated RRI values, particularly at the end of cardiopulmonary bypass in the immediate postoperative period, were predictive of AKI, highlighting the temporal sensitivity of RRI to dynamic changes in renal perfusion. Kararmaz et al. [55] further validated the reliability of intraoperative RRI, demonstrating a strong correlation between TEE and translumbar ultrasound derived measurements, thereby supporting its diagnostic consistency across different modalities. Collectively, these findings suggest that intraoperative RRI is not merely a diagnostic surrogate, but also a physiologically relevant marker of renal hemodynamic stress during cardiac surgery, particularly in procedures such as CABG, characterized by fluctuating perfusion pressures. Importantly, the predictive value of RRI extends beyond the immediate perioperative window. Renberg et al. [56] found that preoperative RRI ≥ 0.70 was independently associated with long-term adverse outcomes, including persistent renal dysfunction, major adverse kidney events (MAKE), and major adverse cardiovascular events (MACE) at five year follow up, thereby positioning RRI as a potential biomarker for both acute and chronic postoperative risk stratification.

Complementing these findings, Wybranic et al. [67] demonstrated that elevated RRI values, both pre- and post-coronary angiography, were independent predictors of major cardiac and cerebrovascular events (MACCE) in coronary artery disease (CAD) patients, with a pre-procedural RRI > 0.645 showing high predictive value over a 24-month period. Higher RRI was also associated with increased risk of contrast-induced AKI (CI-AKI), arterial stiffness, and heightened sympathetic activity, suggesting its dual role as a marker of renal and cardiovascular vulnerability. This integrative role of RRI is further corroborated by Valeri et al. [68], who identified a ≥7% postoperative increase in RRI as a highly specific predictor of AKI in aortic surgery patients (specificity 90%, AUC: 0.75). Similarly, Hertzberg et al. [57] confirmed that elevated preoperative RRI in cardiac surgery patients is independently associated with postoperative AKI, advocating for its inclusion in perioperative risk stratification protocols. Beyond predictive capacity, RRI reflects underlying hemodynamic and oxygenation disturbances. Corradi et al. [69] demonstrated that higher postoperative RRI was associated with decreased SvO2 and increased oxygen extraction, indicating a renal vascular response to systemic hypoperfusion.

This positions RRI as a surrogate marker of oxygen supply–demand mismatch, offering a dynamic index of organ perfusion adequacy. The diagnostic performance of RRI is further enhanced when combined with molecular markers. The Bordeaux University Hospital group [70] reported improved accuracy for early CSA-AKI detection when RRI was used alongside urinary tissue inhibitor of metalloproteinases 2 (TIMP-2) and insulin-like growth factor binding protein 7 (IGFBP7) levels. Additional investigations have explored novel applications and technical developments related to RRI. Kararmaz et al. [71] demonstrated the diagnostic value of postoperative RRI and serum cystatin C in predicting AKI, while IRRIV (Intraparenchymal RRI Variation) testing, a non-invasive bedside ultrasound technique assessing renal functional reserve, showed high sensitivity and specificity in forecasting subclinical AKI [72]. Efforts to enhance clinical applicability include automation: Andrew et al. [73] developed a computer vision algorithm for intraoperative RRI analysis, achieving strong concordance with expert assessments and significantly reducing processing time. This technological advancement facilitates integration into real-time perioperative workflows. Multiple studies confirmed the feasibility and prognostic accuracy of intraoperative RRI measurement. Bossard et al. [74] showed early postoperative RRI could reliably predict AKI. Zhang et al. [75] identified RRI thresholds >0.74 and >0.79 post CPB as strongly predictive, with the latter offering superior specificity. Dhawan et al. [76] reported that intraoperative TEE-based RRI assessment was feasible in >90% of cases and that values >0.75 post chest closure correlated with AKI. Similarly, Andrew B.Y. et al. [77] confirmed that intraoperative RRI > 0.70 post CPB in aortic valve surgery patients was predictive of AKI. Furthermore, combining arterial (RRI) and venous (venous impedance index, VII) Doppler parameters enhanced predictive capacity, as shown by Giles et al. [78], where elevated intraoperative RRI and VII were strongly associated with postoperative AKI. Finally, Vo and Boodhwani [79] advocated for integrating RRI into preoperative evaluation protocols in aortic valve surgery, emphasizing its non-invasive nature and capacity to refine perioperative AKI risk stratification.

3.4.1. Renal Resistive Index in Advanced Surgical and Percutaneous Techniques

The predictive utility of the Renal Resistive Index (RRI) extends to patients undergoing transcatheter and mechanical circulatory support interventions. In the setting of transcatheter aortic valve implantation (TAVI), elevated RRI values post-procedure were significantly associated with acute kidney injury (AKI) and paravalvular aortic regurgitation, with an RRI threshold > 0.85 demonstrating superior specificity compared to serum creatinine [80]. In patients supported by continuous-flow left ventricular assist devices (CF-LVADs), RRI decreased significantly after device implantation, reflecting improved renal vascular resistance and correlating with enhanced renal function [81]. These findings suggest that RRI serves as a dynamic biomarker of renal perfusion changes in advanced surgical and percutaneous cardiovascular procedures.

3.4.2. Renal Resistive Index in Neonatal and Pediatric Population

RRI also demonstrated prognostic value in neonatal and pediatric cohorts. In children undergoing cardiac surgery, both RRI and renal pulsatility index (RPI) were independently associated with early detection of severe AKI, offering high diagnostic accuracy [82]. Among neonates receiving extracorporeal membrane oxygenation (ECMO), elevated RRI values preceded clinical diagnosis of AKI, highlighting its potential as an early non- invasive biomarker for renal injury in critically ill neonates [83]. Furthermore, in patients with Fontan physiology, RRI was significantly elevated and correlated with adverse hemodynamic parameters, including increased central venous pressure and reduced cardiac output. Elevated RRI in this population was associated with increased mortality, underscoring its prognostic relevance in complex congenital heart disease [84].

Table 1. Summary of included studies on Renal Resistive Index and acute kidney injury in cardiac surgery population. RRI: Renal Resistive Index; AKI: acute kidney injury; CABG: coronary artery bypass grafting; CAD: coronary artery disease; ECMO: extracorporeal membrane oxygenation; LVAD: left ventricular assist device.

Author (Year)	Population	Surgical Context	RRI Cut-Off	Key Findings
Guinot et al. (2013) [54]	82 patients	Cardiac Surgery	>0.73	RRI predicts AKI progression (AUC 0.93)
Kararmaz et al. (2015) [55]	60 patients	Cardiac Surgery	-	RRI correlates with AKI; good method agreement
Renberg et al. (2024) [56]	96 patients	Cardiac Surgery	>0.70	Preop. RRI linked to long-term renal/cardiovascular outcomes
Hertzberg et al. (2017) [57]	96 patients	Cardiac Surgery	>0.70	RRI > 0.74 increases AKI risk
Kajal et al. (2022) [62]	115 patients	Cardiac Surgery (CABG)	>0.68	RRI associated with AKI (AUC 0.705)
Zhou et al. (2020) [66]	74 patients	Cardiac Surgery	>0.68	RRI predicts AKI
Wybraniec et al. (2020) [67]	111 patients	Cardiac Surgery (CAD patients)	>0.645	Elevated RRI predicts long-term mortality
Valeri et al. (2022) [68]	73 patients	Cardiac Surgery (aortic surgery)	>0.75	RRI associated with AKI
Corradi et al. (2015) [69]	61 patients	Post-cardiac surgery	-	RRI reflects renal oxygen supply-demand mismatch
Zaouter et al. (2018) [70]	50 patients	Cardiac Surgery	-	RRI + biomarkers improve early AKI detection
Kararmaz et al. (2021) [71]	42 patients	Cardiac Surgery	-	RRI + biomarkers improve early AKI detection
Samoni et al. (2022) [72]	31 patients	Pre-cardiac surgery	-	RRI variation predicts AKI risk
Andrew et al. (2018) [73]	318 patients	Cardiac Surgery	-	Algorithm for RRI estimation from automatically processed intraoperative renal Doppler waveforms
Bossard et al. (2011) [74]	125 patients	Cardiac Surgery	>0.74	RRI > 0.74 predicts AKI
Dhawan et al. (2024) [76]	80 patients	Cardiac Surgery	>0.75	Elevated RRI associated with AKI
Andrew et al. (2018) [77]	100 patients	Cardiac Surgery (valve)	>0.70	High RRI linked to AKI development
Giles et al. (2024) [78]	150 patients	Cardiac Surgery	-	Combined Doppler improves AKI prediction
Vo et al. (2018) [79]	Review	Cardiac Surgery (aortic valve surgery)	>0.75	RRI useful in high-risk patients
Sinning et al. (2014) [80]	132 patients	TAVI	>0.85	RRI detects AKI and paravalvular regurgitation
Barua et al. (2024) [81]	-	LVAD	-	Elevated RRI in LVAD patients
De Souza et al. (2024) [82]	58 children	Pediatric cardiac surgery	>0.85	RRI predicts AKI in children
Sun et al. (2024) [83]	16 neonates	ECMO	>0.79	Elevated RRI associated with neonatal AKI
Ohuchi et al. (2017) [84]	280 Fontan patients	Fontan follow-up	>0.71	RRI predicts mortality in Fontan patients

Table 1. Summary of included studies on Renal Resistive Index and acute kidney injury in cardiac surgery population. RRI: Renal Resistive Index; AKI: acute kidney injury; CABG: coronary artery bypass grafting; CAD: coronary artery disease; ECMO: extracorporeal membrane oxygenation; LVAD: left ventricular assist device.

Author (Year)	Population	Surgical Context	RRI Cut-Off	Key Findings
Guinot et al. (2013) [54]	82 patients	Cardiac Surgery	>0.73	RRI predicts AKI progression (AUC 0.93)
Kararmaz et al. (2015) [55]	60 patients	Cardiac Surgery	-	RRI correlates with AKI; good method agreement
Renberg et al. (2024) [56]	96 patients	Cardiac Surgery	>0.70	Preop. RRI linked to long-term renal/cardiovascular outcomes
Hertzberg et al. (2017) [57]	96 patients	Cardiac Surgery	>0.70	RRI > 0.74 increases AKI risk
Kajal et al. (2022) [62]	115 patients	Cardiac Surgery (CABG)	>0.68	RRI associated with AKI (AUC 0.705)
Zhou et al. (2020) [66]	74 patients	Cardiac Surgery	>0.68	RRI predicts AKI
Wybraniec et al. (2020) [67]	111 patients	Cardiac Surgery (CAD patients)	>0.645	Elevated RRI predicts long-term mortality
Valeri et al. (2022) [68]	73 patients	Cardiac Surgery (aortic surgery)	>0.75	RRI associated with AKI
Corradi et al. (2015) [69]	61 patients	Post-cardiac surgery	-	RRI reflects renal oxygen supply-demand mismatch
Zaouter et al. (2018) [70]	50 patients	Cardiac Surgery	-	RRI + biomarkers improve early AKI detection
Kararmaz et al. (2021) [71]	42 patients	Cardiac Surgery	-	RRI + biomarkers improve early AKI detection
Samoni et al. (2022) [72]	31 patients	Pre-cardiac surgery	-	RRI variation predicts AKI risk
Andrew et al. (2018) [73]	318 patients	Cardiac Surgery	-	Algorithm for RRI estimation from automatically processed intraoperative renal Doppler waveforms
Bossard et al. (2011) [74]	125 patients	Cardiac Surgery	>0.74	RRI > 0.74 predicts AKI
Dhawan et al. (2024) [76]	80 patients	Cardiac Surgery	>0.75	Elevated RRI associated with AKI
Andrew et al. (2018) [77]	100 patients	Cardiac Surgery (valve)	>0.70	High RRI linked to AKI development
Giles et al. (2024) [78]	150 patients	Cardiac Surgery	-	Combined Doppler improves AKI prediction
Vo et al. (2018) [79]	Review	Cardiac Surgery (aortic valve surgery)	>0.75	RRI useful in high-risk patients
Sinning et al. (2014) [80]	132 patients	TAVI	>0.85	RRI detects AKI and paravalvular regurgitation
Barua et al. (2024) [81]	-	LVAD	-	Elevated RRI in LVAD patients
De Souza et al. (2024) [82]	58 children	Pediatric cardiac surgery	>0.85	RRI predicts AKI in children
Sun et al. (2024) [83]	16 neonates	ECMO	>0.79	Elevated RRI associated with neonatal AKI
Ohuchi et al. (2017) [84]	280 Fontan patients	Fontan follow-up	>0.71	RRI predicts mortality in Fontan patients

4. Renal Resistive Index in Focus: A Valuable Diagnostic Tool for CSA-AKI

Acute kidney injury following cardiac surgery, known as cardiac surgery-associated AKI (CSA-AKI), remains a prevalent and severe complication, affecting a significant proportion of patients and substantially increasing perioperative mortality, morbidity, ICU and hospital stay durations, and healthcare costs [85]. Despite advancements in surgical techniques and perioperative care, the incidence of CSA-AKI and its long-term mortality risk post-surgery remain troublingly high, necessitating improved diagnostic and therapeutic approaches [25].

Early identification of patients at risk is pivotal for the prevention of CSA-AKI. Recognized risk factors encompass demographic characteristics (age, sex) and pre-existing conditions such as chronic kidney disease (CKD) and diabetes (Figure 2). Although these factors are non-modifiable, optimizing the management of comorbidities prior to surgery remains a crucial strategy in mitigating the risk of CSA-AKI [25].

Given the limitations of traditional diagnostic criteria, such as KDIGO [3,4], RIFLE and AKIN classifications [86,87,88,89], which rely on delayed functional markers like serum creatinine (sCr) and urine output, there is an urgent need for more sensitive and timely indicators of renal injury. In this context, the RRI has gained increasing attention as a promising non-invasive tool for early risk stratification and diagnosis of AKI in cardiac surgical patients.

4.1. The Role of Renal Resistive Index in Diagnosis of CSA-AKI

The Renal Resistive Index (RRI), measured via Doppler ultrasound, has emerged as a non-invasive and dynamic marker for evaluating renal perfusion in patients undergoing cardiac surgery. Numerous studies have demonstrated a strong correlation between elevated intraoperative and early postoperative RRI values and subsequent development of CSA-AKI [55,56,66]. In particular, RRI values > 0.7 have shown significant predictive power for postoperative AKI, especially when measured upon ICU admission [29,90,91]. Intraoperative and postoperative RRI measurements, particularly those obtained via transesophageal echocardiography (TEE), have demonstrated predictive value for AKI suggesting that RRI could serve as an early warning signal for renal impairment [29,33,34].

This index reflects real time alterations in renal vascular resistance, offering a sensitive assessment of renal hemodynamic status before the appearance of classical functional impairments such as reduced urine output or elevated serum creatinine (sCr) [61,92]. Unlike conventional diagnostic criteria, such as KDIGO, RIFLE and AKIN, which rely on delayed biochemical changes (which may lag behind actual renal damage by up to 48 h), RRI can provide an earlier indication of evolving renal dysfunction, thereby facilitating more timely interventions [35]. Moreover, RRI alterations often precede biochemical abnormalities and are capable of capturing transient or subclinical reductions in renal perfusion, which might otherwise go undetected [93]. Thus, its utility lies not only in detection but potentially also in anticipation of functional decline, making it particularly valuable in the perioperative setting where hemodynamic fluctuations are frequent and often abrupt.

4.2. Can RRI Serve as a Standalone Diagnostic Marker?

Although RRI has demonstrated superior diagnostic performance in the immediate postoperative period compared to serum creatinine-based markers, current evidence does not support its use as standalone diagnostic tool [94,95]. While its sensitivity and specificity are high, RRI may be influenced by extrarenal factors such as vascular compliance, systemic vascular resistance, and intra-abdominal pressure, which may confound interpretation [6,96,97,98]. Therefore, while RRI offers valuable real-time insights into renal perfusion, its isolated use may lead to either over- or underestimation of AKI risk in certain clinical contexts. As such, it should be interpreted in conjunction with other clinical parameters and not as an autonomous diagnostic endpoint [99]. Additionally, its measurement is operator-dependent, and while interobserver variability has been reported as acceptable, standardization and training are essential for reliable clinical application. As such, RRI should be viewed as part of a multimodal diagnostic strategy rather than a solitary determinant of renal dysfunction [33].

4.3. The Synergistic Role of RRI and Novel Biomarkers in Early AKI Detection

Emerging evidence supports the integration of RRI with biomarkers of tubular and glomerular injury, such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), cystatin C and the combination of tissue inhibitor of metalloproteinase-2 and insulin-like growth factor-binding protein 7 (TIMP-2/IGFBP7) [5,6,7]. While RRI captures the perfusion component of renal stress, these biomarkers provide biochemical evidence of cellular injury, inflammation or apoptosis. The pathophysiology of CSA-AKI is multifactorial, encompassing ischemia–reperfusion injury, inflammation, oxidative stress, and nephrotoxin exposure. Hence, a multidimensional diagnostic approach, combining functional, hemodynamic, and structural markers, is more reflective of the underlying mechanism. Studies employing combined RRI and biomarker assessment have shown improved predictive accuracy, particularly for subclinical AKI or in patients with borderline RRI values [35,100,101]. This combinatorial strategy allows for early initiation of renal protective interventions, such as fluid resuscitation, avoidance of nephrotoxins, and optimization of cardiac output, potentially modifying the clinical course before irreversible injury ensues.

4.4. Is Routine Quantification of RRI Clinically Beneficial?

Routine perioperative quantification of RRI in high-risk patients may represent a paradigm shift in the management of CSA-AKI. Real-time monitoring of RRI can facilitate early identification of renal hypoperfusion, guiding tailored hemodynamic interventions even before overt signs of kidney dysfunction appear. Integration of RRI assessment into standard care protocols could allow for dynamic decision-making during key perioperative phases, especially weaning from CPB or titration of vasopressors, in order to preserve renal perfusion and oxygen delivery. Furthermore, repeated RRI measurements can offer prognostic value: persistently elevated RRI in the early postoperative period has been linked to prolonged ICU stay, greater incidence of renal replacement therapy, and increased mortality. Technological innovation, such as automated RRI calculation and artificial intelligence-driven interpretation algorithms, may soon overcome current barriers to routine implementation and make RRI assessment more accessible, reproducible and scalable [102,103].

5. Conclusions

The Renal Resistive Index (RRI) has demonstrated significant predictive value for AKI and long-term renal and cardiovascular outcomes in cardiac surgery patients. Both preoperative and intraoperative RRI assessment provide critical insights, facilitating early detection and enabling targeted interventions. Integrating RRI into standard perioperative assessment protocols can significantly improve patient management and outcomes. However, large-scale, multi-center studies are required to validate these findings and refine RRI thresholds. Furthermore, investigating the integration of RRI with other biomarkers and establishing standardized protocols for its clinical application will be essential to maximize its predictive utility for AKI and optimize perioperative care.