Renal elastography in kidney disease: Current evidence, limitations, and future directions

Abstract

Renal elastography has gained attention as a noninvasive way to estimate tissue stiffness and, indirectly, structural kidney damage. In general, elastography is considered a noninvasive test (NIT) for assessing liver fibrosis, and it has been widely adopted and even proposed as a potential alternative to liver biopsy in selected settings. However, its use as an NIT has not been completely translated to the kidney, largely due to fundamental differences in tissue structure and hemodynamics. Unlike the relatively homogeneous liver, the kidney is anisotropic and highly dependent on perfusion. Therefore, stiffness measurements may be affected by blood flow, vascular resistance, and interstitial pressure at the time of measurement, making them more difficult to interpret. There is growing evidence that shear-wave elastography can detect structural changes in chronic kidney disease, hypertension-related damage, acute kidney injury, and some glomerular disorders. That said, findings remain inconsistent. The reported cut-off values vary widely between studies, and reproducibility remains limited. Technical factors, such as inter-device and acquisition-protocol variability, further complicate the comparison of imaging results. In practice, elastography provides information about tissue mechanics and may be complementary to conventional imaging and laboratory markers. However, it might not be specific if used alone. Combined approaches of specifically shear-wave elastography with functional and biochemical NIT could provide better diagnostic performance and reflect a more clinically useful approach. Overall, renal elastography is better viewed as a complementary tool rather than a replacement for histology. Future research should focus on standardization, improving cross-platform validation, and generating longitudinal data to clarify its role in clinical decision-making and risk assessment.

Key Words: Shear-wave elastography; Kidney diseases; Cortical stiffness; Kidney biopsy; Serum biomarkers

Core Tip: Renal elastography is a non-invasive tool for assessing tissue stiffness and may help detect structural kidney injury earlier than traditional blood and imaging markers. But unlike the liver, kidney stiffness is greatly affected by perfusion and hemodynamic variables, making interpretation difficult. Currently, the evidence is heterogeneous, and there are no defined thresholds that limit its use as a single diagnostic tool. Elastography should preferably be combined with clinical, functional, and imaging data in a multimodal approach to improve the non-invasive assessment of kidney disease.

INTRODUCTION

Early detection of renal damage remains one of the most challenging aspects of clinical nephrology. Structural changes such as interstitial fibrosis and tubular atrophy represent the final pathway of many kidney diseases, yet they are often identified only when functional decline is already evident and, in many cases, irreversible[1]. Conventional markers such as serum creatinine and estimated glomerular filtration rate provide indirect and delayed information, while kidney biopsy, although still considered the reference standard, is invasive, prone to sampling variability, and difficult to repeat over time[1,2].

In recent years, there has been growing interest in imaging techniques or noninvasive tests (NIT) that can detect structural changes earlier in the course of a disease. In this line, elastography, specifically shear-wave elastography (SWE), has emerged as a promising NIT for measuring tissue stiffness in vivo by propagating shear waves through the tissue[3-5]. Its clinical impact has been well established in liver diseases, where stiffness closely reflects fibrosis, enabling the development of validated thresholds and reducing the need for biopsy in many settings[6]. It is therefore not surprising that similar approaches are now being explored in the kidney[3].

Preliminary studies have sought to apply this concept to renal disease, suggesting that increased cortical stiffness may indicate fibrosis and chronicity[3,7,8]. However, results have been controversial. A key issue lies in the fundamental differences between organs. Unlike the liver, the kidney is not a homogeneous structure. It is highly vascularized, anisotropic, and strongly influenced by intrarenal hemodynamics[9]. Consequently, tissue stiffness in the kidney does not solely indicate fibrosis, but rather a confluence of structural and physiological factors (Figure 1)[9]. This results in a complex situation in which stiffness may increase during inflammatory or hyperemic conditions yet decrease in advanced disease due to reduced perfusion[10,11].

Figure 1 From isolated stiffness to multiparametric decision-making. Limitations of interpreting renal shear-wave elastography in isolation and the rationale for a multiparametric approach in glomerulonephritis. In inflammatory or hyperemic kidneys, increased stiffness may be driven more by perfusion and inflammation than by fibrosis. In advanced fibrotic disease, stiffness values may vary according to renal perfusion, and a “soft” kidney does not exclude significant fibrosis. Therefore, a multiparametric model integrating shear-wave elastography-derived mechanical properties (stiffness and viscosity), renal function parameters, and selected biomarkers may provide a more accurate non-invasive renal phenotyping, risk stratification, and assessment of disease progression. SWE: Shear-wave elastography; eGFR: Estimated glomerular filtration rate; TGF-β1: Transforming growth factor beta 1; CTGF: Connective tissue growth factor; NGAL: Neutrophil gelatinase-associated lipocalin; KIM-1: Kidney injury molecule 1.

In this context, renal elastography should be regarded as a complementary tool rather than a replacement for histology. This review evaluates current evidence, significant limitations, and the prospective role of elastography within a multiparametric approach to non-invasive renal assessment.

PRINCIPLES OF ELASTOGRAPHY

The noninvasive evaluation of tissue stiffness has gained interest as a tool to detect fibrosis, inflammation, and neoplastic processes[12]. Instead of relying solely on structural imaging, elastography complements conventional ultrasonography with information about tissue dynamics[12,13]. Moreover, biological tissues are viscoelastic, anisotropic, and heterogeneous, which leads to a mechanical response that depends on the magnitude, duration, and direction of the applied force in the tissue[14]. These properties influence the propagation of mechanical waves and limit the use of simplified elastic models[14,15]. Elastography is based on the use of shear waves, which propagate slower than conventional ultrasound waves and are therefore more sensitive to differences in tissue stiffness[16,17]. Overall, stiffer tissues allow faster wave propagation. In clinical practice, results are reported either as shear wave velocity in meters per second or as stiffness values in kilopascals (kPa), which may reflect resistance to deformation[13,15].

Elastography has evolved substantially in recent years, with new methods now available to obtain additional diagnostic information. Some methods estimate how tissue changes shape after compression and provide qualitative or semi-quantitative data, whereas others generate and track shear waves in the tissue, enabling quantitative measurements[16,18-20]. Acoustic radiation force impulse is a well-established technique that uses focused ultrasound pulses to generate localized displacement and to measure shear wave velocity in a given area[18]. In this context, SWE allows for the visualization and mapping of stiffness in real time across a larger area[17,21].

On the other hand, vibration-controlled transient elastography uses external mechanical impulses, and it has been widely used in liver disease[21,22]. Unfortunately, it is less flexible for targeting specific areas. Although increased stiffness is often associated with fibrosis, elastographic measurements are not specific and may also be influenced by inflammation, vascular congestion, and interstitial pressure[13,20]. Therefore, stiffness values should be carefully interpreted considering the right underlying physiology.

DIFFERENCES BETWEEN LIVER AND KIDNEY ELASTOGRAPHY

Elastography has been widely validated in liver disease, but its use in the kidney is more complicated. While both organs are highly vascularized and receive a significant proportion of cardiac output, their structural organization and hemodynamic behavior are fundamentally distinct[9,10,23]. The liver is relatively uniform and stiffness is more consistently linked to fibrosis[23,24]. However, the kidney is structurally more complex, and the cortex and medulla display different mechanical properties, thus making measurements less reliable[5,25,26]. This complexity is also associated with anisotropy (Figure 2). In the kidney, tubule and vessel orientations vary by region, so shear wave propagation depends on the measurement direction[27,28]. Consequently, stiffness values are not only dependent on tissue composition but also on probe positioning, which may influence reproducibility[29,30]. Renal hemodynamics adds another layer of complexity. Although both organs require adequate perfusion, the kidney operates under higher and more tightly regulated pressures, whereas hepatic circulation is driven primarily by low-pressure portal flow[9-11,23]. Changes in blood flow can directly affect stiffness measurements, as reduced perfusion tends to decrease shear-wave velocity, whereas increased pressure can elevate it, even in the absence of fibrosis[31,32].

Figure 2 Effect of renal anisotropy on shear wave elastography measurements. Renal tissue anisotropy significantly influences shear wave propagation and, consequently, stiffness measurements obtained by shear wave elastography. When the ultrasound beam is aligned parallel to the corticomedullary axis, shear waves travel along tubular and vascular structures with less resistance, resulting in higher measured velocities and increased apparent stiffness. In contrast, perpendicular orientation results in slower wave propagation and lower stiffness due to higher structural impedance. These orientation-dependent differences highlight the impact of renal architecture on elastographic measurements and underscore the need for standardized probe positioning to improve reproducibility and interpretation in clinical practice. SWE: Shear-wave elastography; SWS: Shear-wave speed.

For this reason, renal stiffness should not be interpreted in the same manner as liver stiffness. In the kidney, stiffness reflects not only structural changes but also dynamic factors such as perfusion, vascular resistance, and interstitial pressure. For example, advanced fibrosis may be associated with lower stiffness because of hypoperfusion, whereas obstructive or congestive conditions may increase stiffness in the absence of structural damage[26,33]. Taken together, these differences make it difficult to directly apply liver-based stiffness thresholds to the kidney. This highlights the need for caution when using elastography to assess kidney disease.

Clinical applications of shear wave elastography in kidney disease

Chronic kidney disease (CKD) remains one of the primary areas in which SWE has been explored as a NIT. Current clinical evaluation relies largely on serum creatinine, estimated glomerular filtration rate, and structural imaging changes, all of which provide indirect and often delayed indicators of chronic disease[3,5]. Likewise, renal biopsy is often of limited utility in end-stage CKD, where the kidneys may be too small or the tissue obtained may be insufficient to determine the underlying etiology[34]. Although elastography cannot establish disease etiology, it may offer a non-invasive assessment of tissue stiffness that reflects early structural alterations[3,4].

Several studies have demonstrated significant differences in renal stiffness between individuals with CKD and healthy controls, suggesting a potential role for SWE as a marker of parenchymal damage[3,35-38]. However, findings have been inconsistent, and interpretation remains challenging because measurements are affected by perfusion, inflammation, and other disease-specific factors. For example, in transplanted kidneys, measurements are generally more reproducible because of the superficial location of the graft. In this setting, elastography has been investigated as a tool for detecting graft dysfunction, including fibrosis and rejection, although its specificity remains limited[2,11].

In another context, elastography may help identify early cortical changes associated with hypertension-related renal damage that are not detected by traditional NITs[7,39-41]. Increased renal stiffness has also been reported in patients with chronic hypertension, suggesting structural alterations such as arteriolar sclerosis and interstitial fibrosis[39]. However, its clinical application in this setting remains limited by measurement variability, the lack of standardized acquisition protocols, and the influence of factors such as blood pressure control and renal perfusion.

Acute kidney injury represents a distinct and more common clinical scenario in which elastography has primarily been explored as a NIT for detecting changes in tissue mechanics associated with inflammation, edema, and altered perfusion[42-44]. Qiang et al[44] reported increased renal stiffness in critically ill patients with acute kidney injury, with area under the receiver operating characteristic curve values of 0.736 to 0.784 and cutoff values of 9.9 kPa for the medulla and 2.9 kPa for the cortex, suggesting moderate diagnostic performance. However, the study was limited by a small sample size and incomplete reporting of factors such as fluid status (volemia) and renal perfusion.

In glomerular diseases, elastography has been explored as a noninvasive method for assessing chronic damage, with some studies suggesting that increased stiffness reflects cumulative structural alterations rather than active inflammation. However, one of the major limitations across studies is the wide variability in reported cutoff values. This variability in absolute measurements warrants careful consideration in clinical practice (Table 1). For example, Prasad et al[7] proposed a cutoff of approximately 14 kPa, whereas Leong et al[3] suggested 5.81 kPa, and Maralescu et al[45] reported cutoff values as high as 20.77 kPa for detecting any degree of fibrosis.

Table 1 Comparative summary of shear-wave elastography cutoff values for renal fibrosis across different devices and study populations.

Ref.	Population	Device/technique	Diagnostic target	Cutoff (kPa)	AUC	Sensitivity	Specificity
Prasad et al[7], 2026	Chronic glomerulonephritis	2D-SWE (Supersonic Mach 30, Hologic)	Any fibrosis vs none (IF/TA ≥ I)	13.98	0.986	98%	73%
Maralescu et al[45], 2023	Chronic glomerulonephritis	2D-SWE PLUS	Fibrosis vs no fibrosis	< 20.77	0.860	88.89%	75%
Maralescu et al[45], 2023	Chronic glomerulonephritis	2D-SWE PLUS	> 40% fibrosis vs < 40%	< 19.75	0.789	100%	74.29%
Leong et al[3], 2021	CKD (biopsy-proven)	Philips EPIQ 7 (ElastPQ)	Moderate vs mild histologic impairment	5.81	0.702	67.3%	61.5%
Wang et al[43], 2025	CKD	ACUSON Sequoia (Siemens)	Mild vs moderate-severe fibrosis	6.70	0.824	91.5%	59.3%

Cutoff values correspond to the optimal thresholds reported by each study for the specified diagnostic target. Sensitivity and specificity are those reported at the selected cutoff. Differences across studies may reflect variability in device platform, acquisition protocol, fibrosis definition, and study population characteristics. AUC: Area under the receiver operating characteristic curve; CKD: Chronic kidney disease; SWE: Shear-wave elastography; 2D-SWE PLUS: Two-dimensional shear-wave elastography PLUS; IF/TA: Interstitial fibrosis and tubular atrophy.

These discrepancies likely reflect differences not only in the technological platforms used (Aixplorer, Siemens, or Philips) but also in acquisition techniques[4]. Renal anisotropy, defined as variation in wave velocity depending on whether measurements are obtained parallel or perpendicular to the medullary pyramids, represents a major confounding factor[8,10]. Studies by Early et al[46] and Kuttancheri et al[37] have emphasized the importance of strict acquisition protocols to control transducer depth and pressure, as obesity and increased skin-to-kidney distance may attenuate the shear wave and alter results. In addition, limited data on interobserver reproducibility and the lack of standardized acquisition parameters, including region-of-interest placement, imaging depth, and probe pressure, remain important barriers to the clinical implementation of renal SWE. Without addressing these sources of variability, the generalizability of proposed cutoff values across centers and platforms will remain limited.

Current controversies and limitations

One of the biggest barriers to the routine clinical implementation of renal elastography is inter-platform variability. Differences in hardware, insonation frequency, and proprietary processing algorithms mean that stiffness measurements are often not directly comparable across devices, making it difficult to establish universal cutoff values[25,47-49]. Even within the same imaging system, measurements may vary depending on the transducer used or specific acquisition settings, further underscoring the current lack of standardization[3,4,50-52].

Part of this challenge is inherent to the kidney itself[9-11,53]. Renal tissue is anisotropic and highly influenced by hemodynamic conditions, meaning that shear-wave propagation depends not only on tissue structure but also on perfusion and tissue orientation[26,54]. Experimental studies have demonstrated that changes in vascular flow, such as occlusion or congestion, can produce stiffness variations that may exceed those caused by fibrosis alone[54]. Consequently, distinguishing structural damage from physiological influences remains difficult.

Not surprisingly, this complexity is reflected in the literature. Some studies have reported increased stiffness in the presence of fibrosis, whereas others have observed lower stiffness values in more advanced stages of disease, potentially due to hypoperfusion and capillary rarefaction[41,55]. Additional variability arises from differences in region-of-interest selection and measurement techniques, which can affect both reproducibility and interobserver agreement[37,56]. Taken together, these limitations highlight the need for cautious interpretation of elastography findings and emphasize the importance of further standardization of acquisition and analysis techniques.

Comparison with other imaging modalities

Conventional ultrasound remains the first-line imaging modality in nephrology because of its wide availability and favorable safety profile[57]. However, its diagnostic utility is often limited to detecting late structural changes, such as cortical thinning or increased echogenicity[25,57]. Other Doppler-derived parameters, including the resistive index, can provide additional hemodynamic information but are influenced by systemic factors such as age, vascular stiffness, and blood pressure, thereby reducing their specificity for parenchymal disease[25,26].

Advanced imaging techniques, such as diffusion-weighted magnetic resonance imaging and blood oxygen level-dependent imaging, offer complementary insights into microstructure and oxygenation[58]. Although these modalities have demonstrated correlations with fibrosis, their interpretation is also influenced by perfusion and interstitial factors, and their availability in routine practice remains limited[58,59].

Magnetic resonance elastography overcomes some of the technical limitations of ultrasound-based methods, particularly those related to imaging depth, and enables whole-organ assessment. Nevertheless, it remains susceptible to similar hemodynamic confounding factors and lacks standardized thresholds, limiting its role as a definitive staging tool[60,61]. Overall, no single imaging modality currently provides a comprehensive assessment of renal fibrosis, underscoring the need for integrated approaches that combine structural, functional, and biomechanical information.

AUTHOR PERSPECTIVES

Elastography is a promising and evolving tool in nephrology from a clinical perspective. Its principal advantage lies in the ability to provide noninvasive, real-time information on tissue mechanics that may complement established markers of renal function. However, emerging evidence suggests that stiffness measurements are not direct surrogates for fibrosis, as they are strongly influenced by hemodynamic and technical factors.

In clinical practice, elastography may prove more useful for longitudinal monitoring and trend assessment than for reliance on absolute cutoff values. Its integration with with clinical data, laboratory findings and other imaging modalities is likely to enhance the diagnostic information obtained beyond its use as a standalone tool. At present, elastography should be considered an adjunctive technique, particularly in cases where biopsy is not feasible or carries substantial risk.

CONCLUSION

Looking ahead, one of the main factors limiting the broader clinical adoption of elastography is the lack of consistency across imaging platforms. Until measurements become more comparable between systems, interpreting results with confidence outside controlled research settings will remain challenging. As the evidence base grows and becomes more robust, it is likely that future clinical guidelines will incorporate recommendations regarding renal elastography, although the filed has not yet reached that stage.

In routine clinical practice, elastography is unlikely to function as a standalone diagnostic tool. Rather, its value will likely depend on integration with imaging findings, laboratory parameters, and the overall clinical context. Similarly, the expanding use of artificial intelligence in diagnostics may facilitate the integration of these diverse sources of information, although this potential remains largely unexplored.

A major unmet need in the field is the availability of longitudinal evidence. Future studies following patients over time are necessary to determine whether elastography measurements correlate with clinically meaningful outcomes. Until such evidence becomes available, renal elastography should be regarded as a promising but still evolving tool whose precise role in clinical decision-making remains to be defined.

ACKNOWLEDGEMENTS

We thank the medical staff of the Department of Internal Medicine at Hospital General and Dr. Manuel Gea González for their continuous academic support and commitment to resident education.